The human eye can see 'invisible' infrared light
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The human eye can see 'invisible' infrared light
The human eye can see 'invisible' infrared light
December 1, 2014, Washington University School of Medicine
The human eye can see 'invisible' infrared light
The eye can detect light at wavelengths in the visual spectrum. Other wavelengths, such as infrared and ultraviolet, are supposed to be invisible to the human eye, but Washington University scientists have found that under certain conditions, it's possible for us to see otherwise invisible infrared light. Credit: Sara Dickherber
Any science textbook will tell you we can't see infrared light. Like X-rays and radio waves, infrared light waves are outside the visual spectrum. But an international team of researchers co-led by scientists at Washington University School of Medicine in St. Louis has found that under certain conditions, the retina can sense infrared light after all.
Using cells from the retinas of mice and people, and powerful lasers that emit pulses of infrared light, the researchers found that when laser light pulses rapidly, light-sensing cells in the retina sometimes get a double hit of infrared energy. When that happens, the eye is able to detect light that falls outside the visible spectrum.
"We're using what we learned in these experiments to try to develop a new tool that would allow physicians to not only examine the eye but also to stimulate specific parts of the retina to determine whether it's functioning properly," said senior investigator Vladimir J. Kefalov, PhD, associate professor of ophthalmology and visual sciences at Washington University. "We hope that ultimately this discovery will have some very practical applications."
The findings are published Dec. 1 in the Proceedings of the National Academy of Sciences (PNAS) Online Early Edition. Collaborators include scientists in Cleveland, Poland, Switzerland and Norway,
The research was initiated after scientists on the research team reported seeing occasional flashes of green light while working with an infrared laser. Unlike the laser pointers used in lecture halls or as toys, the powerful infrared laser the scientists worked with emits light waves thought to be invisible to the human eye.
The human eye can see 'invisible' infrared light
Frans Vinberg, PhD (left), and Vladimir J. Kefalov, PhD, sit in front of a tool they developed that allows them to detect light responses from retinal cells and photopigment molecules. Credit: Robert Boston
"They were able to see the laser light, which was outside of the normal visible range, and we really wanted to figure out how they were able to sense light that was supposed to be invisible," said Frans Vinberg, PhD, one of the study's lead authors and a postdoctoral research associate in the Department of Ophthalmology and Visual Sciences at Washington University.
Vinberg, Kefalov and their colleagues examined the scientific literature and revisited reports of people seeing infrared light. They repeated previous experiments in which infrared light had been seen, and they analyzed such light from several lasers to see what they could learn about how and why it sometimes is visible.
"We experimented with laser pulses of different durations that delivered the same total number of photons, and we found that the shorter the pulse, the more likely it was a person could see it," Vinberg explained. "Although the length of time between pulses was so short that it couldn't be noticed by the naked eye, the existence of those pulses was very important in allowing people to see this invisible light."
Normally, a particle of light, called a photon, is absorbed by the retina, which then creates a molecule called a photopigment, which begins the process of converting light into vision. In standard vision, each of a large number of photopigments absorbs a single photon.
Our eyes aren't supposed to be able to see infrared light because infrared light waves are longer than the waves in the visual spectrum, but new work from vision researchers at Washington University School of Medicine in St. Louis finds that sometimes we can see infrared light. and those researchers have figured out how it is that our eyes do that. Credit: Washington University BioMed Radio
But packing a lot of photons in a short pulse of the rapidly pulsing laser light makes it possible for two photons to be absorbed at one time by a single photopigment, and the combined energy of the two light particles is enough to activate the pigment and allow the eye to see what normally is invisible.
"The visible spectrum includes waves of light that are 400-720 nanometers long," explained Kefalov, an associate professor of ophthalmology and visual sciences. "But if a pigment molecule in the retina is hit in rapid succession by a pair of photons that are 1,000 nanometers long, those light particles will deliver the same amount of energy as a single hit from a 500-nanometer photon, which is well within the visible spectrum. That's how we are able to see it."
(more at link:
https://phys.org/news/2014-12-human-eye-invisible-infrared.html
)
Re: The human eye can see 'invisible' infrared light
.
Hey Cr6, what a surprise, if we just add the right amount of energy to infrared light, we may actually see it.
I have a similar example, under special conditions I’m able to see ultra-violet. This is the first time I’ve thought to mention it to anyone. I see it sometimes while reading in bed, depending on the paper the book is made with. Believe it or not, the effect was the most visible when I read Miles’ Navigating the Nucleus. When the book is open about 90 degrees, well illuminated from a compact fluorescent lamp from just above and behind my head, but not overly bright, where the pages join together I can clearly see an ultraviolet glow. I imagine visible light energy is amplified by many reflections of visible light occurring in the angle between the two halves of the open book.
.
Hey Cr6, what a surprise, if we just add the right amount of energy to infrared light, we may actually see it.
I have a similar example, under special conditions I’m able to see ultra-violet. This is the first time I’ve thought to mention it to anyone. I see it sometimes while reading in bed, depending on the paper the book is made with. Believe it or not, the effect was the most visible when I read Miles’ Navigating the Nucleus. When the book is open about 90 degrees, well illuminated from a compact fluorescent lamp from just above and behind my head, but not overly bright, where the pages join together I can clearly see an ultraviolet glow. I imagine visible light energy is amplified by many reflections of visible light occurring in the angle between the two halves of the open book.
.
LongtimeAirman- Admin
- Posts : 2074
Join date : 2014-08-10
Re: The human eye can see 'invisible' infrared light
Well LTAM...I've always believed the "photon" as a way of illuminating the "truth"...
Re: The human eye can see 'invisible' infrared light
Wouldn't that just be a violet glow, though? I'm curious.
Jared Magneson- Posts : 525
Join date : 2016-10-11
Re: The human eye can see 'invisible' infrared light
.
I've been tested, I know I've been blessed with exceptional color vision. The color I see is indeed a violet glow, but is it ultra-violet? Of course I don't know. Where did it come from? Given the article at the top of this string, I can imagine how we might be able to see photons at other than visible radii.
There's another place I see the same violet glow - when I tear/cut the plastic seal off the the lid of the ice cream container with a knife - thrown in the sink in direct sunlight - a beautiful violet glow. In previous posts, articles and discussions here at the site, plastic is a special substance, pulling off scotch tape gives off light.
Back to the book, the glow I see, but didn't get around to describe, seems to come from the air above where the pages join together. I believe each page in the book might offer another phase front source that may help explain what I'm seeing. I'm not necessarily making a claim, so much as sharing an interesting observation. In light of the charge field.
.
I've been tested, I know I've been blessed with exceptional color vision. The color I see is indeed a violet glow, but is it ultra-violet? Of course I don't know. Where did it come from? Given the article at the top of this string, I can imagine how we might be able to see photons at other than visible radii.
There's another place I see the same violet glow - when I tear/cut the plastic seal off the the lid of the ice cream container with a knife - thrown in the sink in direct sunlight - a beautiful violet glow. In previous posts, articles and discussions here at the site, plastic is a special substance, pulling off scotch tape gives off light.
Back to the book, the glow I see, but didn't get around to describe, seems to come from the air above where the pages join together. I believe each page in the book might offer another phase front source that may help explain what I'm seeing. I'm not necessarily making a claim, so much as sharing an interesting observation. In light of the charge field.
.
LongtimeAirman- Admin
- Posts : 2074
Join date : 2014-08-10
Re: The human eye can see 'invisible' infrared light
You know LTAM and Jared there's surprisingly a lot of recent research on BioPhotons:
(cough...they are just saying... )
----------
Human high intelligence is involved in spectral redshift of biophotonic activities in the brain
Zhuo Wang, Niting Wang, Zehua Li, Fangyan Xiao, and Jiapei Dai
PNAS August 2, 2016 113 (31) 8753-8758; published ahead of print July 18, 2016 https://doi.org/10.1073/pnas.1604855113
Edited by Michael A. Persinger, Laurentian University, Canada, and accepted by Editorial Board Member Marlene Behrmann May 20, 2016 (received for review March 24, 2016)
http://www.pnas.org/content/113/31/8753.abstract
Significance
It is still unclear why human beings hold higher intelligence than other animals on Earth and which brain properties might explain the differences. The recent studies have demonstrated that biophotons may play a key role in neural information processing and encoding and that biophotons may be involved in quantum brain mechanism; however, the importance of biophotons in relation to animal intelligence, including that of human beings, is not clear. Here, we have provided experimental evidence that glutamate-induced biophotonic activities and transmission in brain slices present a spectral redshift feature from animals (bullfrog, mouse, chicken, pig, and monkey) to humans, which may be a key biophysical basis for explaining why human beings hold higher intelligence than that of other animals.
Abstract
Human beings hold higher intelligence than other animals on Earth; however, it is still unclear which brain properties might explain the underlying mechanisms. The brain is a major energy-consuming organ compared with other organs. Neural signal communications and information processing in neural circuits play an important role in the realization of various neural functions, whereas improvement in cognitive function is driven by the need for more effective communication that requires less energy. Combining the ultraweak biophoton imaging system (UBIS) with the biophoton spectral analysis device (BSAD), we found that glutamate-induced biophotonic activities and transmission in the brain, which has recently been demonstrated as a novel neural signal communication mechanism, present a spectral redshift from animals (in order of bullfrog, mouse, chicken, pig, and monkey) to humans, even up to a near-infrared wavelength (∼865 nm) in the human brain. This brain property may be a key biophysical basis for explaining high intelligence in humans because biophoton spectral redshift could be a more economical and effective measure of biophotonic signal communications and information processing in the human brain.
-------
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0148336
https://emmind.net/endogenous_fields-mind-ebp-biophotons_bokkon_theory_vision.html
Biophotonic Activity and Transmission Mediated by Mutual Actions of Neurotransmitters are Involved in the Origin and Altered States of Consciousness
http://www.sciencedirect.com/science/article/pii/S1011134413002881
Spatiotemporal Imaging of Glutamate-Induced Biophotonic Activities and Transmission in Neural Circuits
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3893221/ (btw...hypoglycemia can cause an abrupt loss of brain bio-available glutamate--Cr6 see: https://experts.umn.edu/en/publications/changes-in-human-brain-glutamate-concentration-during-hypoglycemi)
Photon Entanglement Through Brain Tissue (applied light)
https://www.nature.com/articles/srep37714
Biophotonic Activity and Transmission Mediated by Mutual Actions of Neurotransmitters are Involved in the Origin and Altered States of Consciousness
https://www.researchgate.net/profile/Wang_Zhuo15/publication/323559645_Biophotonic_Activity_and_Transmission_Mediated_by_Mutual_Actions_of_Neurotransmitters_are_Involved_in_the_Origin_and_Altered_States_of_Consciousness/links/5aa795650f7e9bbbff8cfb62/Biophotonic-Activity-and-Transmission-Mediated-by-Mutual-Actions-of-Neurotransmitters-are-Involved-in-the-Origin-and-Altered-States-of-Consciousness.pdf
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3893221/
Convergence of Numbers of Synapses and Quantum Foci Within Human Brain Space: Quantitative
Implications of the Photon as the Source of Cognition
http://www.scipress.com/ILCPA.30.59.pdf
-------
Biophotons Contribute to Retinal Dark Noise
1.Wuhan Institute for Neuroscience and NeuroengineeringSouth Central University for NationalitiesWuhanChina
2.Department of Neurobiology, College of Life SciencesSouth Central University for NationalitiesWuhanChina
https://link.springer.com/article/10.1007/s12264-016-0029-6
Report
First Online: 08 April 2016
Abstract
The discovery of dark noise in retinal photoreceptors resulted in a long-lasting controversy over its origin and the underlying mechanisms. Here, we used a novel ultra-weak biophoton imaging system (UBIS) to detect biophotonic activity (emission) under dark conditions in rat and bullfrog (Rana catesbeiana) retinas in vitro. We found a significant temperature-dependent increase in biophotonic activity that was completely blocked either by removing intracellular and extracellular Ca2+ together or inhibiting phosphodiesterase 6. These findings suggest that the photon-like component of discrete dark noise may not be caused by a direct contribution of the thermal activation of rhodopsin, but rather by an indirect thermal induction of biophotonic activity, which then activates the retinal chromophore of rhodopsin. Therefore, this study suggests a possible solution regarding the thermal activation energy barrier for discrete dark noise, which has been debated for almost half a century.
-------
Speculative but interesting:
https://hipmonkey.wordpress.com/2014/02/08/biophotons-the-human-body-emits-communicates-with-and-is-made-from-light/
-------
Node of Ranvier as an Array of Bio-Nanoantennas for Infrared Communication in Nerve Tissue
Andrea Zangari, Davide Micheli, Roberta Galeazzi & Antonio Tozzi
Scientific Reportsvolume 8, Article number: 539 (2018) | Download Citation
Abstract
Electromagnetic radiation, in the visible and infrared spectrum, is increasingly being investigated for its possible role in the most evolved brain capabilities. Beside experimental evidence of electromagnetic cellular interactions, the possibility of light propagation in the axon has been recently demonstrated using computational modelling, although an explanation of its source is still not completely understood. We studied electromagnetic radiation onset and propagation at optical frequencies in myelinated axons, under the assumption that ion channel currents in the node of Ranvier behave like an array of nanoantennas emitting in the wavelength range from 300 to 2500 nm. Our results suggest that the wavelengths below 1600 nm are most likely to propagate throughout myelinated segments. Therefore, a broad wavelength window exists where both generation and propagation could happen, which in turn raises the possibility that such a radiation may play some role in neurotransmission.
Introduction
The intriguingly complex nature of the brain has always encouraged extensive studies on neuronal communication, aiming to understand signaling mechanisms and their integration into neural functions of the highest level. New perspectives have been revealed by approaching different biophysical mechanisms, which may coexist with the established chemical and electrical properties of cellular membranes1. In this context, previous studies on the electromagnetic properties of neurons gained increasing interest, resulting in further achievements and new open questions2,3,4. It seems therefore appropriate to explore the possible implications, which may add further knowledge to the current theoretical and experimental work in this direction.
Since early decisive studies, electrochemical phenomena have been shown to be predominant in the generation and traveling of information5.
The conduction of signals within neurons is sustained by a propagating phenomenon known as action potential (AP), which is a sharp change in the electrical potential across the cell membrane, in which different ionic species are involved. Once triggered, this process travels down the whole axon towards synapses. Some axons are coated with myelin, a multilayered lipid envelope, provided by surrounding glial cells and interrupted at regular distances. These gaps are called nodes of Ranvier (NR)6. In myelinated fibers the AP is triggered in the axon initial segment (AIS) and in the NR, where ion channels are concentrated, and leaps from node to node at a rate significantly higher than in unmyelinated axons. This process is known as “saltatory conduction”7.
The original Hodgkin–Huxley (HH) theory models each component of an excitable cell as an electrical element, taking into account the concentration of the main ionic species involved5. The transmission of APs in myelinated fibers has been described borrowing some concepts of the cable theory to simulate impulse initiation and saltatory propagation8.
Beside the fundamental mechanisms of neuronal membrane excitability described by the HH model, a number of other biophysical phenomena are associated with neuronal activity1.
Different physical approaches to these processes, which take into account mechanical forces, thermodynamics and electromagnetism, drew growing interest from researchers and may provide further understanding of the mechanisms underlying neuronal signaling and encoding of information2,9.
We focused our attention on the possible electromagnetic (EM) aspects of axonal impulse conduction, which have been investigated so far. Optical propagation of photons through myelinic waveguides has been recently shown to be possible by detailed modeling, and therefore raising the question of what could be the source of such radiation4.
Like any other cellular process, axonal activity involves energy generation and exchange. Since early investigations on neuronal function, measurements during action potential revealed the production of heat10, while infrared radiation transfer between nerve ends, following stimulation, has been experimentally detected11.
Beyond these reports, many researchers have been considering a possible role of EM radiation, either of the infrared or visible spectrum, in neural excitability and signaling, resulting in theoretical work on what has been referred to as an electromagnetic theory of neural communication2.
Actually, the existence and transport of infrared and visible light have been recently demonstrated in different tissues and even in nerves3,12,13.
Next to the studies on the existence of photon emissions as possible carriers of cellular information, different hypotheses of EM propagation through membranes or axonal structures have been advanced14, until recently, when a comprehensive model described the possible propagation of EM waves through optical communication pathways in the axon4. Alongside a growing interest in the interaction between EM radiations and biological tissues for its diagnostic and therapeutic implications, some evidence of axonal response to infrared and visible light has been observed, adding a further step towards an EM interpretation of neuronal signaling15.
(more at: https://www.nature.com/articles/s41598-017-18866-x )
(cough...they are just saying... )
----------
Human high intelligence is involved in spectral redshift of biophotonic activities in the brain
Zhuo Wang, Niting Wang, Zehua Li, Fangyan Xiao, and Jiapei Dai
PNAS August 2, 2016 113 (31) 8753-8758; published ahead of print July 18, 2016 https://doi.org/10.1073/pnas.1604855113
Edited by Michael A. Persinger, Laurentian University, Canada, and accepted by Editorial Board Member Marlene Behrmann May 20, 2016 (received for review March 24, 2016)
http://www.pnas.org/content/113/31/8753.abstract
Significance
It is still unclear why human beings hold higher intelligence than other animals on Earth and which brain properties might explain the differences. The recent studies have demonstrated that biophotons may play a key role in neural information processing and encoding and that biophotons may be involved in quantum brain mechanism; however, the importance of biophotons in relation to animal intelligence, including that of human beings, is not clear. Here, we have provided experimental evidence that glutamate-induced biophotonic activities and transmission in brain slices present a spectral redshift feature from animals (bullfrog, mouse, chicken, pig, and monkey) to humans, which may be a key biophysical basis for explaining why human beings hold higher intelligence than that of other animals.
Abstract
Human beings hold higher intelligence than other animals on Earth; however, it is still unclear which brain properties might explain the underlying mechanisms. The brain is a major energy-consuming organ compared with other organs. Neural signal communications and information processing in neural circuits play an important role in the realization of various neural functions, whereas improvement in cognitive function is driven by the need for more effective communication that requires less energy. Combining the ultraweak biophoton imaging system (UBIS) with the biophoton spectral analysis device (BSAD), we found that glutamate-induced biophotonic activities and transmission in the brain, which has recently been demonstrated as a novel neural signal communication mechanism, present a spectral redshift from animals (in order of bullfrog, mouse, chicken, pig, and monkey) to humans, even up to a near-infrared wavelength (∼865 nm) in the human brain. This brain property may be a key biophysical basis for explaining high intelligence in humans because biophoton spectral redshift could be a more economical and effective measure of biophotonic signal communications and information processing in the human brain.
-------
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0148336
https://emmind.net/endogenous_fields-mind-ebp-biophotons_bokkon_theory_vision.html
Biophotonic Activity and Transmission Mediated by Mutual Actions of Neurotransmitters are Involved in the Origin and Altered States of Consciousness
http://www.sciencedirect.com/science/article/pii/S1011134413002881
Spatiotemporal Imaging of Glutamate-Induced Biophotonic Activities and Transmission in Neural Circuits
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3893221/ (btw...hypoglycemia can cause an abrupt loss of brain bio-available glutamate--Cr6 see: https://experts.umn.edu/en/publications/changes-in-human-brain-glutamate-concentration-during-hypoglycemi)
Photon Entanglement Through Brain Tissue (applied light)
https://www.nature.com/articles/srep37714
Biophotonic Activity and Transmission Mediated by Mutual Actions of Neurotransmitters are Involved in the Origin and Altered States of Consciousness
https://www.researchgate.net/profile/Wang_Zhuo15/publication/323559645_Biophotonic_Activity_and_Transmission_Mediated_by_Mutual_Actions_of_Neurotransmitters_are_Involved_in_the_Origin_and_Altered_States_of_Consciousness/links/5aa795650f7e9bbbff8cfb62/Biophotonic-Activity-and-Transmission-Mediated-by-Mutual-Actions-of-Neurotransmitters-are-Involved-in-the-Origin-and-Altered-States-of-Consciousness.pdf
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3893221/
Convergence of Numbers of Synapses and Quantum Foci Within Human Brain Space: Quantitative
Implications of the Photon as the Source of Cognition
http://www.scipress.com/ILCPA.30.59.pdf
-------
Biophotons Contribute to Retinal Dark Noise
1.Wuhan Institute for Neuroscience and NeuroengineeringSouth Central University for NationalitiesWuhanChina
2.Department of Neurobiology, College of Life SciencesSouth Central University for NationalitiesWuhanChina
https://link.springer.com/article/10.1007/s12264-016-0029-6
Report
First Online: 08 April 2016
Abstract
The discovery of dark noise in retinal photoreceptors resulted in a long-lasting controversy over its origin and the underlying mechanisms. Here, we used a novel ultra-weak biophoton imaging system (UBIS) to detect biophotonic activity (emission) under dark conditions in rat and bullfrog (Rana catesbeiana) retinas in vitro. We found a significant temperature-dependent increase in biophotonic activity that was completely blocked either by removing intracellular and extracellular Ca2+ together or inhibiting phosphodiesterase 6. These findings suggest that the photon-like component of discrete dark noise may not be caused by a direct contribution of the thermal activation of rhodopsin, but rather by an indirect thermal induction of biophotonic activity, which then activates the retinal chromophore of rhodopsin. Therefore, this study suggests a possible solution regarding the thermal activation energy barrier for discrete dark noise, which has been debated for almost half a century.
-------
Speculative but interesting:
https://hipmonkey.wordpress.com/2014/02/08/biophotons-the-human-body-emits-communicates-with-and-is-made-from-light/
-------
Node of Ranvier as an Array of Bio-Nanoantennas for Infrared Communication in Nerve Tissue
Andrea Zangari, Davide Micheli, Roberta Galeazzi & Antonio Tozzi
Scientific Reportsvolume 8, Article number: 539 (2018) | Download Citation
Abstract
Electromagnetic radiation, in the visible and infrared spectrum, is increasingly being investigated for its possible role in the most evolved brain capabilities. Beside experimental evidence of electromagnetic cellular interactions, the possibility of light propagation in the axon has been recently demonstrated using computational modelling, although an explanation of its source is still not completely understood. We studied electromagnetic radiation onset and propagation at optical frequencies in myelinated axons, under the assumption that ion channel currents in the node of Ranvier behave like an array of nanoantennas emitting in the wavelength range from 300 to 2500 nm. Our results suggest that the wavelengths below 1600 nm are most likely to propagate throughout myelinated segments. Therefore, a broad wavelength window exists where both generation and propagation could happen, which in turn raises the possibility that such a radiation may play some role in neurotransmission.
Introduction
The intriguingly complex nature of the brain has always encouraged extensive studies on neuronal communication, aiming to understand signaling mechanisms and their integration into neural functions of the highest level. New perspectives have been revealed by approaching different biophysical mechanisms, which may coexist with the established chemical and electrical properties of cellular membranes1. In this context, previous studies on the electromagnetic properties of neurons gained increasing interest, resulting in further achievements and new open questions2,3,4. It seems therefore appropriate to explore the possible implications, which may add further knowledge to the current theoretical and experimental work in this direction.
Since early decisive studies, electrochemical phenomena have been shown to be predominant in the generation and traveling of information5.
The conduction of signals within neurons is sustained by a propagating phenomenon known as action potential (AP), which is a sharp change in the electrical potential across the cell membrane, in which different ionic species are involved. Once triggered, this process travels down the whole axon towards synapses. Some axons are coated with myelin, a multilayered lipid envelope, provided by surrounding glial cells and interrupted at regular distances. These gaps are called nodes of Ranvier (NR)6. In myelinated fibers the AP is triggered in the axon initial segment (AIS) and in the NR, where ion channels are concentrated, and leaps from node to node at a rate significantly higher than in unmyelinated axons. This process is known as “saltatory conduction”7.
The original Hodgkin–Huxley (HH) theory models each component of an excitable cell as an electrical element, taking into account the concentration of the main ionic species involved5. The transmission of APs in myelinated fibers has been described borrowing some concepts of the cable theory to simulate impulse initiation and saltatory propagation8.
Beside the fundamental mechanisms of neuronal membrane excitability described by the HH model, a number of other biophysical phenomena are associated with neuronal activity1.
Different physical approaches to these processes, which take into account mechanical forces, thermodynamics and electromagnetism, drew growing interest from researchers and may provide further understanding of the mechanisms underlying neuronal signaling and encoding of information2,9.
We focused our attention on the possible electromagnetic (EM) aspects of axonal impulse conduction, which have been investigated so far. Optical propagation of photons through myelinic waveguides has been recently shown to be possible by detailed modeling, and therefore raising the question of what could be the source of such radiation4.
Like any other cellular process, axonal activity involves energy generation and exchange. Since early investigations on neuronal function, measurements during action potential revealed the production of heat10, while infrared radiation transfer between nerve ends, following stimulation, has been experimentally detected11.
Beyond these reports, many researchers have been considering a possible role of EM radiation, either of the infrared or visible spectrum, in neural excitability and signaling, resulting in theoretical work on what has been referred to as an electromagnetic theory of neural communication2.
Actually, the existence and transport of infrared and visible light have been recently demonstrated in different tissues and even in nerves3,12,13.
Next to the studies on the existence of photon emissions as possible carriers of cellular information, different hypotheses of EM propagation through membranes or axonal structures have been advanced14, until recently, when a comprehensive model described the possible propagation of EM waves through optical communication pathways in the axon4. Alongside a growing interest in the interaction between EM radiations and biological tissues for its diagnostic and therapeutic implications, some evidence of axonal response to infrared and visible light has been observed, adding a further step towards an EM interpretation of neuronal signaling15.
(more at: https://www.nature.com/articles/s41598-017-18866-x )
Last edited by Cr6 on Thu Sep 20, 2018 10:08 pm; edited 1 time in total
Re: The human eye can see 'invisible' infrared light
Also this is a good summary article:
------------
https://emmind.net/endogenous_fields-mind-ebp-biophotons_bokkon_theory_vision.html
Biophotons Bókkon's Theory of Vision
Photons are also internally generated to form biophysical pictures during visual imagery
It is possible that visual perception is based upon biophotonic representations of reality inside the brain. Various findings on exogenously applied light and endogenously generated biophotons make the basis for the theory, the visual sensation of light (phosphenes) is likely to be due to the inherent perception of ultraweak photon emissions of cells in the visual system.
In Bókkon's words the theory can summarized as follows:
" The retina absorbs external photons during vision, and then transforms photon signals into electrical signals that are carried to the V1. ... "
(Moreover, it has been demonstrated that biophotons can be guided along the neural fibers. Latest experiments have provide evidence that the glutamate-induced biophotonic activities reflect biophotonic transmission along the axons and in neural circuits, by which may be a new mechanism for the processing of neural information. Since regulated electrical signals of neurons can be converted into regulated biophoton signals, external photonic representation can emerge not only as electrical signals but also as regulated biophoton signals in the brain).
" ... Then, V1 retinotopic electrical signals (spike-related electrical signals along classical axonal-dendritic pathways) can be converted into regulated biophotons within retinotopic neurons that make it possible to create internal biophysical pictures (intrinsic re-representation of perceived external objects) during visual perception and imagery. Therefore, information in the brain appears not only as electrical (chemical) signal but also as a controlled biophoton signal of synchronized V1 neurons." [15]
For the developers of the theory the detailed and realistic visual representation in early V1 and V2 areas cannot be guaranteed by mere electrical representations. However, the biophysical picture concept may guarantee the detailed and realistic visual representation of objects in retinotopic V1 and V2 areas by congruent patterns of regulated biophotons.
There exists some findings that underpin some aspects of the theory and some of them with surprising results, a theoretical work [1] related to the retinal discrete dark noise effect demonstrated that thermal activation approach is mathematically incongruent and but that the discrete components of noise are indistinguishable in shape and duration from those produced by real photon induced photo-isomerization, so it's proposed that the retinal discrete dark noise is most likely due to "photons" inside cells instead "heat" for thermal activation of visual pigments..
It must be said in that sense that now exist experimental evidence of biophotonic activity in the retina [2]:
" Here, we used a novel ultra-weak biophoton imaging system (UBIS) to detect biophotonic activity (emission) under dark conditions in rat and bullfrog (Rana catesbeiana) retinas in vitro. We found a significant temperature-dependent increase in biophotonic activity that was completely blocked either by removing intracellular and extracellular Ca2+ together or inhibiting phosphodiesterase 6. These findings suggest that the photon-like component of discrete dark noise may not be caused by a direct contribution of the thermal activation of rhodopsin, but rather by an indirect thermal induction of biophotonic activity, which then activates the retinal chromophore of rhodopsin. Therefore, this study suggests a possible solution regarding the thermal activation energy barrier for discrete dark noise, which has been debated for almost half a century."
But this not invalidate that a visual representation made by biphotons or ultraweak photon emissions (UPE) is also taking place with neurons of the V1 and V2 areas as a source.
A very curious phenomena is detected in [16]; they design an experiment based in the premise that in visual projection a physical electromagnetic component is present so they put or not put mirrors in front of subject of the test (which is unaware of those changes) affecting the subject's perception of his mental projection as it is doubled or distorted when mirror is put:
" As the results of both the experiments have showed, when the mental image was projected on the mutually reflective mirrors, a duplication or a multiplication of the subjective perception like mental image appeared. This phenomenon did not appear sending the image toward the two not reflecting panels. The mental image projected on the mirrors would act in a similar way to a light beam generating an optical reflection phenomenon."
Some propositions that the eye itself emit energy of some kind have been done previously, and that this emission is involved in visual perception, or in the creation of "sense of being watched" in the objective has been stipulated [3].
Here it can be pointed out the following experiment [17] where biophotons are also reflected in mirrors, which causes an augmented effect on sender (in this case HepG2 cells).
In [9] photons (biophotons) are detected from subject imagining white light:
" The quantitative convergence of the energies associated with photon emission, change in cerebral power, and the minute decrease in the local adjacent geomagnetic field in the same plane as the photon emission, suggests that experience of an “inner light” may reflect actual photon production whose energies are shared with changes in the proximal intensity of the geomagnetic field in the plane associated with photon emission."
While in [18] is suggested that LSD-induced visual hallucinations can be due to transient enhancement of bioluminescent photons in the early retinotopic visual system; LSD can generate biophotons when is metabolized by peroxidase so, for the authors, the visual hallucinogenic effect may be due that there are several sources of biophotons producing mechanisms in the brain in parallel, especially in the early visual system.
Very related to this in [11] hallucinogens are proposed to exert effect via a biophysical interference, but in this case because their intrinsic fluorescence:
" ... of importance in this context, are the strong flurescence properties of the major hallucinogens: LSD, bufetonine, dimethyl-tryptamine, psilocybine, psilocin, iboguanin, harmine, cannabidinol and mescaline. Furthermore it has been shown that hallucinogenic properties of these substances have a direct correlation to their fluorescence properties and their readyness to donate electrons. As hypothesis we propose that the fluorescence interacts physically with the proposed Biophoton mediated cell to cell communication thus producing hallucinations."
In [19] authors summarize some luminescence-dependent phenomena in the eye, so they review the profs available for understanding discrete dark noise as ultraweak photon emission produced by lipid peroxidation of rods, retinal phosphenes as ultraweak photon emission generated from excess free radicals and negative afterimage as a result of delayed luminescence in the eye, among them.
In this compendium [13] of various aspects of the theory, made by Bókkon himself, there are mentioned various other facts that can support the theory. Also several proposals are reviewed of how this kind of visual representations can work in other situations apart of representations of the external world, for example: as a biophysical picture during visual imagery or also as the human memory (unconscious) that can operate through intrinsic dynamic pictures and then link these picture-representations to each other during language learning processes.
Apart from the endogenously generated photons, which it is undoubtedly the area of study for this theory, maybe is interesting to note how exogenously generated photons affects the brain when is exposed to them because its sensitivity may be indicative that there are endogenous photonic pathways working in normal brain functioning. To get started with this it must be taken into account that humans can detect a single-photon, at least when incident on the cornea [4], as demonstrated in an experiment that shows that the probability of reporting a single photon is modulated by the presence of an earlier photon.
Also there are interesting experiments that demonstrate that applying temporally patterned light over skull (without eyes intervention) resulted in suppression of gamma activity within the right cuneus (including the extrastriate area), beta activity within the left angular and right superior temporal regions, and alpha power within the right parahippocampal region [5] and as mentioned in the paper, that photons can traverse the skull and influence biochemical and biophysical functions within brain space has been known or suspected by many previous researchers. In [6] it is shown that transcranial light affects plasma monoamine levels and expression of brain encephalitic pain in mouse.
Extraocular light, but in this case directed trough ear canals, is also used in various experiments. In [7] extraocular light delivered via ear canals abolished normal emotional modulation of attention related brain responses. In [8] is showed that transcranial bright light treatment may have antidepressant and anxiolytic effect in seasonal affective disorder patients.
There are also some ideas (that with some experimental evidences are all compiled in a section [10]) that also can be take in consideration, like as mentioned previously, the discovery that biophotons can be conducted along neural fibers [12]:
" ... the detected biophotonic activities in the corpus callosum and thalamus in sagittal brain slices mostly originate from axons or axonal terminals of cortical projection neurons, and that the hyperphosphorylation of microtubule-associated protein tau leads to a significant decrease of biophotonic activities in these two areas. Furthermore, the application of glutamate in the hippocampal dentate gyrus results in increased biophotonic activities in its intrahippocampal projection areas. These results suggest that the glutamate-induced biophotonic activities reflect biophotonic transmission along the axons and in neural circuits, which may be a new mechanism for the processing of neural information."
The relationship between an electromagnetic theory of mind and this biophysical representation is that this representation, being made by biophotons, can be part of the consciousness itself forming a layer of a multilayered (or multifrequency) electromagnetic mind. Other frequencies, as classical low frequencies generated in the brain, can interact with this layer [14].
References:
1. Salari, Vahid, et al. "The Physical Mechanism for Retinal Discrete Dark Noise: Thermal Activation or Cellular Ultraweak Photon Emission?." PloS one 11.3 (2016): e0148336.
2. Li, Zehua, and Jiapei Dai. "Biophotons Contribute to Retinal Dark Noise." Neuroscience bulletin 32.3 (2016): 246-252.
3. Ross, Colin A. "Traditional beliefs and electromagnetic fields." AIBR: Revista de Antropología Iberoamericana 6.3 (2011): 269-286.
4. Tinsley, Jonathan N., et al. "Direct detection of a single photon by humans." Nature Communications 7 (2016).
5. Karbowski, Lukasz M., et al. "LORETA indicates frequency-specific suppressions of current sources within the cerebrums of blindfolded subjects from patterns of blue light flashes applied over the skull." Epilepsy & Behavior 51 (2015): 127-132.
6. Flyktman, Antti, et al. "Transcranial light affects plasma monoamine levels and expression of brain encephalopsin in the mouse." Journal of Experimental Biology 218.10 (2015): 1521-1526.
7. Sun, Lihua, et al. "Human Brain Reacts to Transcranial Extraocular Light." PloS one 11.2 (2016): e0149525.
8. Jurvelin, Heidi, et al. "Transcranial bright light treatment via the ear canals in seasonal affective disorder: a randomized, double-blind dose-response study." BMC psychiatry 14.1 (2014): 1.
9. Saroka, Kevin S., Blake T. Dotta, and Michael A. Persinger. "Concurrent photon emission, changes in quantitative brain activity over the right hemisphere, and alterations in the proximal geomagnetic field while imagining white light." International Journal of Life Science and Medical Research 3.1 (2013): 30.
10. EMMIND › Endogenous Fields & Mind › Endogenous Biophotons › Biophotons, Microtubules & Brain
11. Grass, F. "P03-33-Biophotons, hallucinogens, and fluorescence." European Psychiatry 26 (2011): 1202.
12. Tang, Rendong, and Jiapei Dai. "Spatiotemporal imaging of glutamate-induced biophotonic activities and transmission in neural circuits." PloS one 9.1 (2014): e85643.
13. Bókkon, Istvan. "Explanations step by step about Bókkon's biophysical picture representation model (also called intrinsic biophysical virtual visual reality) during visual perception and imagery." (2013)
14. Bereta, Martin, et al. "Low frequency electromagnetic field effects on ultra-weak photon emission from yeast cells." 2016 ELEKTRO. IEEE, 2016.
15. Bókkon, I., et al. "Estimation of the number of biophotons involved in the visual perception of a single-object image: Biophoton intensity can be considerably higher inside cells than outside." Journal of Photochemistry and Photobiology B: Biology 100.3 (2010): 160-166.
16. Ruggieri, Vezio. "Psycho-Physiological Hypothesis about Visual Mental Images Projection." Academy of Social Science Journal 2.9 (2017).
17. Zamani, M., Etebari, M., & Moradi, S. (2017). The Increment of Genoprotective Effect of Melatonin due to “Autooptic” Effect versus the Genotoxicity of Mitoxantron. Journal of Biomedical Physics and Engineering.
18. Kapócs, Gábor, et al. "Possible role of biochemiluminescent photons for lysergic acid diethylamide (LSD)-induced phosphenes and visual hallucinations." Reviews in the Neurosciences 28.1 (2017): 77-86.
19. Salari, Vahid, et al. "Phosphenes, retinal discrete dark noise, negative afterimages and retinogeniculate projections: A new explanatory framework based on endogenous ocular luminescence." Progress in retinal and eye research 60 (2017): 101-119.
------------
https://emmind.net/endogenous_fields-mind-ebp-biophotons_bokkon_theory_vision.html
Biophotons Bókkon's Theory of Vision
Photons are also internally generated to form biophysical pictures during visual imagery
It is possible that visual perception is based upon biophotonic representations of reality inside the brain. Various findings on exogenously applied light and endogenously generated biophotons make the basis for the theory, the visual sensation of light (phosphenes) is likely to be due to the inherent perception of ultraweak photon emissions of cells in the visual system.
In Bókkon's words the theory can summarized as follows:
" The retina absorbs external photons during vision, and then transforms photon signals into electrical signals that are carried to the V1. ... "
(Moreover, it has been demonstrated that biophotons can be guided along the neural fibers. Latest experiments have provide evidence that the glutamate-induced biophotonic activities reflect biophotonic transmission along the axons and in neural circuits, by which may be a new mechanism for the processing of neural information. Since regulated electrical signals of neurons can be converted into regulated biophoton signals, external photonic representation can emerge not only as electrical signals but also as regulated biophoton signals in the brain).
" ... Then, V1 retinotopic electrical signals (spike-related electrical signals along classical axonal-dendritic pathways) can be converted into regulated biophotons within retinotopic neurons that make it possible to create internal biophysical pictures (intrinsic re-representation of perceived external objects) during visual perception and imagery. Therefore, information in the brain appears not only as electrical (chemical) signal but also as a controlled biophoton signal of synchronized V1 neurons." [15]
For the developers of the theory the detailed and realistic visual representation in early V1 and V2 areas cannot be guaranteed by mere electrical representations. However, the biophysical picture concept may guarantee the detailed and realistic visual representation of objects in retinotopic V1 and V2 areas by congruent patterns of regulated biophotons.
There exists some findings that underpin some aspects of the theory and some of them with surprising results, a theoretical work [1] related to the retinal discrete dark noise effect demonstrated that thermal activation approach is mathematically incongruent and but that the discrete components of noise are indistinguishable in shape and duration from those produced by real photon induced photo-isomerization, so it's proposed that the retinal discrete dark noise is most likely due to "photons" inside cells instead "heat" for thermal activation of visual pigments..
It must be said in that sense that now exist experimental evidence of biophotonic activity in the retina [2]:
" Here, we used a novel ultra-weak biophoton imaging system (UBIS) to detect biophotonic activity (emission) under dark conditions in rat and bullfrog (Rana catesbeiana) retinas in vitro. We found a significant temperature-dependent increase in biophotonic activity that was completely blocked either by removing intracellular and extracellular Ca2+ together or inhibiting phosphodiesterase 6. These findings suggest that the photon-like component of discrete dark noise may not be caused by a direct contribution of the thermal activation of rhodopsin, but rather by an indirect thermal induction of biophotonic activity, which then activates the retinal chromophore of rhodopsin. Therefore, this study suggests a possible solution regarding the thermal activation energy barrier for discrete dark noise, which has been debated for almost half a century."
But this not invalidate that a visual representation made by biphotons or ultraweak photon emissions (UPE) is also taking place with neurons of the V1 and V2 areas as a source.
A very curious phenomena is detected in [16]; they design an experiment based in the premise that in visual projection a physical electromagnetic component is present so they put or not put mirrors in front of subject of the test (which is unaware of those changes) affecting the subject's perception of his mental projection as it is doubled or distorted when mirror is put:
" As the results of both the experiments have showed, when the mental image was projected on the mutually reflective mirrors, a duplication or a multiplication of the subjective perception like mental image appeared. This phenomenon did not appear sending the image toward the two not reflecting panels. The mental image projected on the mirrors would act in a similar way to a light beam generating an optical reflection phenomenon."
Some propositions that the eye itself emit energy of some kind have been done previously, and that this emission is involved in visual perception, or in the creation of "sense of being watched" in the objective has been stipulated [3].
Here it can be pointed out the following experiment [17] where biophotons are also reflected in mirrors, which causes an augmented effect on sender (in this case HepG2 cells).
In [9] photons (biophotons) are detected from subject imagining white light:
" The quantitative convergence of the energies associated with photon emission, change in cerebral power, and the minute decrease in the local adjacent geomagnetic field in the same plane as the photon emission, suggests that experience of an “inner light” may reflect actual photon production whose energies are shared with changes in the proximal intensity of the geomagnetic field in the plane associated with photon emission."
While in [18] is suggested that LSD-induced visual hallucinations can be due to transient enhancement of bioluminescent photons in the early retinotopic visual system; LSD can generate biophotons when is metabolized by peroxidase so, for the authors, the visual hallucinogenic effect may be due that there are several sources of biophotons producing mechanisms in the brain in parallel, especially in the early visual system.
Very related to this in [11] hallucinogens are proposed to exert effect via a biophysical interference, but in this case because their intrinsic fluorescence:
" ... of importance in this context, are the strong flurescence properties of the major hallucinogens: LSD, bufetonine, dimethyl-tryptamine, psilocybine, psilocin, iboguanin, harmine, cannabidinol and mescaline. Furthermore it has been shown that hallucinogenic properties of these substances have a direct correlation to their fluorescence properties and their readyness to donate electrons. As hypothesis we propose that the fluorescence interacts physically with the proposed Biophoton mediated cell to cell communication thus producing hallucinations."
In [19] authors summarize some luminescence-dependent phenomena in the eye, so they review the profs available for understanding discrete dark noise as ultraweak photon emission produced by lipid peroxidation of rods, retinal phosphenes as ultraweak photon emission generated from excess free radicals and negative afterimage as a result of delayed luminescence in the eye, among them.
In this compendium [13] of various aspects of the theory, made by Bókkon himself, there are mentioned various other facts that can support the theory. Also several proposals are reviewed of how this kind of visual representations can work in other situations apart of representations of the external world, for example: as a biophysical picture during visual imagery or also as the human memory (unconscious) that can operate through intrinsic dynamic pictures and then link these picture-representations to each other during language learning processes.
Apart from the endogenously generated photons, which it is undoubtedly the area of study for this theory, maybe is interesting to note how exogenously generated photons affects the brain when is exposed to them because its sensitivity may be indicative that there are endogenous photonic pathways working in normal brain functioning. To get started with this it must be taken into account that humans can detect a single-photon, at least when incident on the cornea [4], as demonstrated in an experiment that shows that the probability of reporting a single photon is modulated by the presence of an earlier photon.
Also there are interesting experiments that demonstrate that applying temporally patterned light over skull (without eyes intervention) resulted in suppression of gamma activity within the right cuneus (including the extrastriate area), beta activity within the left angular and right superior temporal regions, and alpha power within the right parahippocampal region [5] and as mentioned in the paper, that photons can traverse the skull and influence biochemical and biophysical functions within brain space has been known or suspected by many previous researchers. In [6] it is shown that transcranial light affects plasma monoamine levels and expression of brain encephalitic pain in mouse.
Extraocular light, but in this case directed trough ear canals, is also used in various experiments. In [7] extraocular light delivered via ear canals abolished normal emotional modulation of attention related brain responses. In [8] is showed that transcranial bright light treatment may have antidepressant and anxiolytic effect in seasonal affective disorder patients.
There are also some ideas (that with some experimental evidences are all compiled in a section [10]) that also can be take in consideration, like as mentioned previously, the discovery that biophotons can be conducted along neural fibers [12]:
" ... the detected biophotonic activities in the corpus callosum and thalamus in sagittal brain slices mostly originate from axons or axonal terminals of cortical projection neurons, and that the hyperphosphorylation of microtubule-associated protein tau leads to a significant decrease of biophotonic activities in these two areas. Furthermore, the application of glutamate in the hippocampal dentate gyrus results in increased biophotonic activities in its intrahippocampal projection areas. These results suggest that the glutamate-induced biophotonic activities reflect biophotonic transmission along the axons and in neural circuits, which may be a new mechanism for the processing of neural information."
The relationship between an electromagnetic theory of mind and this biophysical representation is that this representation, being made by biophotons, can be part of the consciousness itself forming a layer of a multilayered (or multifrequency) electromagnetic mind. Other frequencies, as classical low frequencies generated in the brain, can interact with this layer [14].
References:
1. Salari, Vahid, et al. "The Physical Mechanism for Retinal Discrete Dark Noise: Thermal Activation or Cellular Ultraweak Photon Emission?." PloS one 11.3 (2016): e0148336.
2. Li, Zehua, and Jiapei Dai. "Biophotons Contribute to Retinal Dark Noise." Neuroscience bulletin 32.3 (2016): 246-252.
3. Ross, Colin A. "Traditional beliefs and electromagnetic fields." AIBR: Revista de Antropología Iberoamericana 6.3 (2011): 269-286.
4. Tinsley, Jonathan N., et al. "Direct detection of a single photon by humans." Nature Communications 7 (2016).
5. Karbowski, Lukasz M., et al. "LORETA indicates frequency-specific suppressions of current sources within the cerebrums of blindfolded subjects from patterns of blue light flashes applied over the skull." Epilepsy & Behavior 51 (2015): 127-132.
6. Flyktman, Antti, et al. "Transcranial light affects plasma monoamine levels and expression of brain encephalopsin in the mouse." Journal of Experimental Biology 218.10 (2015): 1521-1526.
7. Sun, Lihua, et al. "Human Brain Reacts to Transcranial Extraocular Light." PloS one 11.2 (2016): e0149525.
8. Jurvelin, Heidi, et al. "Transcranial bright light treatment via the ear canals in seasonal affective disorder: a randomized, double-blind dose-response study." BMC psychiatry 14.1 (2014): 1.
9. Saroka, Kevin S., Blake T. Dotta, and Michael A. Persinger. "Concurrent photon emission, changes in quantitative brain activity over the right hemisphere, and alterations in the proximal geomagnetic field while imagining white light." International Journal of Life Science and Medical Research 3.1 (2013): 30.
10. EMMIND › Endogenous Fields & Mind › Endogenous Biophotons › Biophotons, Microtubules & Brain
11. Grass, F. "P03-33-Biophotons, hallucinogens, and fluorescence." European Psychiatry 26 (2011): 1202.
12. Tang, Rendong, and Jiapei Dai. "Spatiotemporal imaging of glutamate-induced biophotonic activities and transmission in neural circuits." PloS one 9.1 (2014): e85643.
13. Bókkon, Istvan. "Explanations step by step about Bókkon's biophysical picture representation model (also called intrinsic biophysical virtual visual reality) during visual perception and imagery." (2013)
14. Bereta, Martin, et al. "Low frequency electromagnetic field effects on ultra-weak photon emission from yeast cells." 2016 ELEKTRO. IEEE, 2016.
15. Bókkon, I., et al. "Estimation of the number of biophotons involved in the visual perception of a single-object image: Biophoton intensity can be considerably higher inside cells than outside." Journal of Photochemistry and Photobiology B: Biology 100.3 (2010): 160-166.
16. Ruggieri, Vezio. "Psycho-Physiological Hypothesis about Visual Mental Images Projection." Academy of Social Science Journal 2.9 (2017).
17. Zamani, M., Etebari, M., & Moradi, S. (2017). The Increment of Genoprotective Effect of Melatonin due to “Autooptic” Effect versus the Genotoxicity of Mitoxantron. Journal of Biomedical Physics and Engineering.
18. Kapócs, Gábor, et al. "Possible role of biochemiluminescent photons for lysergic acid diethylamide (LSD)-induced phosphenes and visual hallucinations." Reviews in the Neurosciences 28.1 (2017): 77-86.
19. Salari, Vahid, et al. "Phosphenes, retinal discrete dark noise, negative afterimages and retinogeniculate projections: A new explanatory framework based on endogenous ocular luminescence." Progress in retinal and eye research 60 (2017): 101-119.
Re: The human eye can see 'invisible' infrared light
Interesting that Glutamate is regulated closely by axons/brain cells...probably involved in bio-photon reception:
----------
Inside the Glutamate Storm
http://www.dana.org/Cerebrum/Default.aspx?id=39382
The amino acid glutamate is the major signaling chemical in nature. All invertebrates (worms, insects, and the like) use glutamate for conveying messages from nerve to muscle. In mammals, glutamate is mainly present in the central nervous system, brain, and spinal cord, where it plays the role of a neuronal messenger, or neurotransmitter. In fact, almost all brain cells use glutamate to exchange messages. Moreover, glutamate can serve as a source of energy for the brain cells when their regular energy supplier, glucose, is lacking. However, when its levels rise too high in the spaces between cells—known as extracellular spaces—glutamate turns its coat to become a toxin that kills neurons.*
As befits a potentially hazardous substance, glutamate is kept safely sealed within the brain cells. A healthy neuron releases glutamate only when it needs to convey a message, then immediately sucks the messenger back inside. Glutamate concentration inside the cells is 10,000 times greater than outside them. If we follow the dam analogy, that would be equivalent to holding 10,000 cubic feet of glutamate behind the dam and letting only a trickle of one cubic foot flow freely outside. A clever pumping mechanism makes sure this trickle never gets out of hand: When a neuron senses the presence of too much glutamate in the vicinity—the extracellular space—it switches on special pumps on its membrane and siphons the maverick glutamate back in.
----------
Inside the Glutamate Storm
http://www.dana.org/Cerebrum/Default.aspx?id=39382
The amino acid glutamate is the major signaling chemical in nature. All invertebrates (worms, insects, and the like) use glutamate for conveying messages from nerve to muscle. In mammals, glutamate is mainly present in the central nervous system, brain, and spinal cord, where it plays the role of a neuronal messenger, or neurotransmitter. In fact, almost all brain cells use glutamate to exchange messages. Moreover, glutamate can serve as a source of energy for the brain cells when their regular energy supplier, glucose, is lacking. However, when its levels rise too high in the spaces between cells—known as extracellular spaces—glutamate turns its coat to become a toxin that kills neurons.*
As befits a potentially hazardous substance, glutamate is kept safely sealed within the brain cells. A healthy neuron releases glutamate only when it needs to convey a message, then immediately sucks the messenger back inside. Glutamate concentration inside the cells is 10,000 times greater than outside them. If we follow the dam analogy, that would be equivalent to holding 10,000 cubic feet of glutamate behind the dam and letting only a trickle of one cubic foot flow freely outside. A clever pumping mechanism makes sure this trickle never gets out of hand: When a neuron senses the presence of too much glutamate in the vicinity—the extracellular space—it switches on special pumps on its membrane and siphons the maverick glutamate back in.
Re: The human eye can see 'invisible' infrared light
DMT release is likely involved at a limited scale with "imaging" and bio-photons:
------
PINEAL DMT: BLINDED BY THE LIGHT
SOMA PINOLINE: BLINDED BY THE LIGHT
Prophets, Procreation, & Parallel Worlds
by Iona Miller, (c)2006 - 2013
The groundbreaking work of Dr. Rick Strassman (2001) focuses on the role natural body chemistry plays in creating spiritual life. He calls DMT the Spirit Molecule; an endogenous hallucinogen, which he boldly asserts, is an active agent in a variety of altered states including mystical experience. To explore his theory, Strassman conducted extensive testing, injecting volunteers with the powerful psychedelic, synthetic DMT (N,N-dimethyltryptamine; N,N-DMT).
DMT is so powerful it is physically immobilizing, and produces a flood of unexpected and overwhelming visual and emotional imagery. Taking it is like an instantaneous LSD peak. DMT crosses the usually impenetrable blood-brain-barrier, suggesting its fundamental role in consciousness. But, concluding his 5-year studies early, Strassman admitted despite their growth potential, there were no viable therapeutic or neurological applications. He does NOT recommend recreational use.
DMT production is stimulated, in the extraordinary conditions of birth, sexual ecstasy, childbirth, extreme physical stress, near-death, and death, as well as meditation. Pineal DMT also plays a significant role in dream consciousness. This chemical messenger links body and spirit. Pineal activation awakens normally latent neural pathways.
"All spiritual disciplines describe quite psychedelic accounts of the transformative experiences, whose attainment motivate their practice. Blinding white light, encounters with demonic and angelic entities, ecstatic emotions, timelessness, heavenly sounds, feelings of having died and being reborn, contacting a powerful and loving presence underlying all of reality--these experiences cut across all denominations. They also are characteristic of a fully psychedelic DMT experience. How might meditation evoke the pineal DMT experience?"
"Meditative techniques using sound, sight, or the mind may generate particular wave patterns whose fields induce resonance in the brain. Millennia of human trial and error have determined that certain "sacred" words, visual images, and mental exercises exert uniquely desired effects. Such effects may occur because of the specific fields they generate within the brain. These fields cause multiple systems to vibrate and pulse at certain frequencies. We can feel our minds and bodies resonate with these spiritual exercises. Of course, the pineal gland also is buzzing at these same frequencies. . .The pineal begins to "vibrate" at frequencies that weaken its multiple barriers to DMT formation: the pineal cellular shield, enzyme levels, and quantities of anti-DMT. The end result is a psychedelic surge of the pineal spirit molecule, resulting in the subjective states of mystical consciousness." (Strassman, 2001).
Natural hallucinogens may belong to the tryptamine or beta-carboline family of compounds. One compound (6-methoxy-1,2,3,4-tetra-hydro-beta-carboline) has been implicated in rapid eye movement sleep (REM). It is concentrated in the retinae of mammals, which may be related to its visual effects.There are several ways in which either psychoactive tryptamines and/or beta-carbolines may be produced within the central nervous system and pineal from precursors and enzymes that are known to exist in human beings. In addition, nerve fibers leave the pineal and make synaptic connections with other brain sites through traditional nerve-to-nerve connections, not just through endocrine secretions.
https://ionamiller2017.weebly.com/pineal-dmt.html
------
PINEAL DMT: BLINDED BY THE LIGHT
SOMA PINOLINE: BLINDED BY THE LIGHT
Prophets, Procreation, & Parallel Worlds
by Iona Miller, (c)2006 - 2013
The groundbreaking work of Dr. Rick Strassman (2001) focuses on the role natural body chemistry plays in creating spiritual life. He calls DMT the Spirit Molecule; an endogenous hallucinogen, which he boldly asserts, is an active agent in a variety of altered states including mystical experience. To explore his theory, Strassman conducted extensive testing, injecting volunteers with the powerful psychedelic, synthetic DMT (N,N-dimethyltryptamine; N,N-DMT).
DMT is so powerful it is physically immobilizing, and produces a flood of unexpected and overwhelming visual and emotional imagery. Taking it is like an instantaneous LSD peak. DMT crosses the usually impenetrable blood-brain-barrier, suggesting its fundamental role in consciousness. But, concluding his 5-year studies early, Strassman admitted despite their growth potential, there were no viable therapeutic or neurological applications. He does NOT recommend recreational use.
DMT production is stimulated, in the extraordinary conditions of birth, sexual ecstasy, childbirth, extreme physical stress, near-death, and death, as well as meditation. Pineal DMT also plays a significant role in dream consciousness. This chemical messenger links body and spirit. Pineal activation awakens normally latent neural pathways.
"All spiritual disciplines describe quite psychedelic accounts of the transformative experiences, whose attainment motivate their practice. Blinding white light, encounters with demonic and angelic entities, ecstatic emotions, timelessness, heavenly sounds, feelings of having died and being reborn, contacting a powerful and loving presence underlying all of reality--these experiences cut across all denominations. They also are characteristic of a fully psychedelic DMT experience. How might meditation evoke the pineal DMT experience?"
"Meditative techniques using sound, sight, or the mind may generate particular wave patterns whose fields induce resonance in the brain. Millennia of human trial and error have determined that certain "sacred" words, visual images, and mental exercises exert uniquely desired effects. Such effects may occur because of the specific fields they generate within the brain. These fields cause multiple systems to vibrate and pulse at certain frequencies. We can feel our minds and bodies resonate with these spiritual exercises. Of course, the pineal gland also is buzzing at these same frequencies. . .The pineal begins to "vibrate" at frequencies that weaken its multiple barriers to DMT formation: the pineal cellular shield, enzyme levels, and quantities of anti-DMT. The end result is a psychedelic surge of the pineal spirit molecule, resulting in the subjective states of mystical consciousness." (Strassman, 2001).
Natural hallucinogens may belong to the tryptamine or beta-carboline family of compounds. One compound (6-methoxy-1,2,3,4-tetra-hydro-beta-carboline) has been implicated in rapid eye movement sleep (REM). It is concentrated in the retinae of mammals, which may be related to its visual effects.There are several ways in which either psychoactive tryptamines and/or beta-carbolines may be produced within the central nervous system and pineal from precursors and enzymes that are known to exist in human beings. In addition, nerve fibers leave the pineal and make synaptic connections with other brain sites through traditional nerve-to-nerve connections, not just through endocrine secretions.
https://ionamiller2017.weebly.com/pineal-dmt.html
Re: The human eye can see 'invisible' infrared light
Just wanted to add this college research site on Color Reception (photon reception) by cones-rods in the human eye. This brings up the question of "photon-collision" with the fovea centralis and color-movement in the human brain. Still, how do we remember scenes of our lives in "color" how do our memories fuel the "colors" if the eye isn't involved in remembering...via photons?
---------
http://hyperphysics.phy-astr.gsu.edu/hbase/vision/cie.html#c2
Approximate colors can be assigned to areas on the CIE Chromaticity Diagram. These are rough categories, and not to be taken as precise statements of color. The boundaries and the color names are adapted from Brand Fortner, "Number by Color", Part 5, SciTech Journal 6, p32, May/June 1996.
Any attempt to depict the gamut of human color vision on a computer monitor must be accompanied by numerous qualifications and exceptions. In the first place, you cannot display the range of human color perception on an RGB monitor - the gamut of normal human vision covers the entire CIE diagram while the gamut of an RGB monitor can be displayed as a triangular region within the CIE diagram. Another qualification is that the hue and saturation associated with a given color name can vary over a considerable range. Add to that the variations with different kinds of display monitors, and you rightly conclude that an accurate rendition is impossible. With all those excuses, however, it still might be instructive to provide a rough idea of the regions of the CIE Diagram associated with common color names.
The display here was created by choosing representative RGB values for the color regions from a rendition of the 1976 CIE Chromaticity Diagram provided by Photo Research, Inc. Note that one representative value in about the middle of the hue and saturation ranges was chosen for each section of the diagram. The point chosen was just a visual judgment of a representative color in the range. The RGB values obtained are listed in the table at right. A different observer would likely have chosen different points to represent the color names, but at least these values might provide a starting point for preferred variations.
One characteristic of the commonly used 1931 CIE Chromaticity Diagram that is evident even from this crude portrayal is that the green takes up far too much of the landscape compared to the number of visually different colors in the region. That was one of the shortcomings that the 1960 and 1976 revisions sought to address.
The C.I.E. Color Space
The CIE system characterizes colors by a luminance parameter Y and two color coordinates x and y which specify the point on the chromaticity diagram. This system offers more precision in color measurement than do the Munsell and Ostwald systems because the parameters are based on the spectral power distribution (SPD) of the light emitted from a colored object and are factored by sensitivity curves which have been measured for the human eye.
Based on the fact that the human eye has three different types of color sensitive cones, the response of the eye is best described in terms of three "tristimulus values". However, once this is accomplished, it is found that any color can be expressed in terms of the two color coordinates x and y.
The colors which can be matched by combining a given set of three primary colors (such as the blue, green, and red of a color television screen) are represented on the chromaticity diagram by a triangle joining the coordinates for the three colors.
Also:
https://micro.magnet.fsu.edu/primer/lightandcolor/humanvisionintro.html
Wikipedia:
In the light
In summary: Light closes cGMP-gated sodium channels, reducing the influx of both Na+ and Ca2+ ions. Stopping the influx of Na+ ions effectively switches off the dark current. Reducing this dark current causes the photoreceptor to hyperpolarise, which reduces glutamate release which thus reduces the inhibition of retinal nerves, leading to excitation of these nerves. This reduced Ca2+ influx during phototransduction enables deactivation and recovery from phototransduction, as discussed below in § Deactivation of the phototransduction cascade.
A light photon interacts with a retinal molecule in an opsin complex in a photoreceptor cell. The retinal undergoes isomerisation, changing from the 11-cis-retinal to the all-trans-retinal configuration.
Opsin therefore undergoes a conformational change to metarhodopsin II.
Metarhodopsin II activates a G protein known as transducin. This causes transducin to dissociate from its bound GDP, and bind GTP; then the alpha subunit of transducin dissociates from the beta and gamma subunits, with the GTP still bound to the alpha subunit.
The alpha subunit-GTP complex activates phosphodiesterase, also known as PDE6. It binds to one of two regulatory subunits of PDE (which itself is a tetramer) and stimulates its activity.
PDE hydrolyzes cGMP, forming GMP. This lowers the intracellular concentration of cGMP and therefore the sodium channels close.[3]
Closure of the sodium channels causes hyperpolarization of the cell due to the ongoing efflux of potassium ions.
Hyperpolarization of the cell causes voltage-gated calcium channels to close.
As the calcium level in the photoreceptor cell drops, the amount of the neurotransmitter glutamate that is released by the cell also drops. This is because calcium is required for the glutamate-containing vesicles to fuse with cell membrane and release their contents (see SNARE proteins).
A decrease in the amount of glutamate released by the photoreceptors causes depolarization of on-center bipolar cells (rod and cone On bipolar cells) and hyperpolarization of cone off-center bipolar cells.
https://en.wikipedia.org/wiki/Visual_phototransduction
https://en.wikipedia.org/wiki/Cone_cell
https://en.wikipedia.org/wiki/Vertebrate_visual_opsin#Cone_opsins
Keep in mind the fovea centralis.
http://hyperphysics.phy-astr.gsu.edu/hbase/vision/retina.html#c2
Though the eye receives data from a field of about 200 degrees, the acuity over most of that range is poor. To form high resolution images, the light must fall on the fovea, and that limits the acute vision angle to about 15 degrees. In low light, this fovea constitutes a second blind spot since it is exclusively cones which have low light sensitivity. At night, to get most acute vision one must shift the vision slightly to one side, say 4 to 12 degrees so that the light falls on some rods.
A "dimple on the retina" provides our highest resolution vision.
"Just about at the center of the retina is a small depression from 2.5 to 3 mm in diameter known as the yellow spot, or macula. There is a tiny rod-free region about 0.3mm in diameter at its center, the fovea centralis. (In comparison the image of the full Moon on the retina is about 0.2 mm in diameter.) Here the cones are thinner (with diameters of 0.0030mm to 0.0015mm) and more densely packed than anywhere else in the retina. Since the fovea provides the sharpest and most detailed information, the eyeball is continuously moving, so that light from the object of primary interest falls on this region. ...the rods are multiply connected to nerve fibers, and a single such fiber can be activated by any one of about a hundred rods. By contrast, cones in the fovea are individually connected to nerve fibers. The actual perception of a scene is constructed by the eye-brain system in a continuous analysis of the time-varying retinal image."(Hecht)
---------
http://hyperphysics.phy-astr.gsu.edu/hbase/vision/cie.html#c2
Approximate colors can be assigned to areas on the CIE Chromaticity Diagram. These are rough categories, and not to be taken as precise statements of color. The boundaries and the color names are adapted from Brand Fortner, "Number by Color", Part 5, SciTech Journal 6, p32, May/June 1996.
Any attempt to depict the gamut of human color vision on a computer monitor must be accompanied by numerous qualifications and exceptions. In the first place, you cannot display the range of human color perception on an RGB monitor - the gamut of normal human vision covers the entire CIE diagram while the gamut of an RGB monitor can be displayed as a triangular region within the CIE diagram. Another qualification is that the hue and saturation associated with a given color name can vary over a considerable range. Add to that the variations with different kinds of display monitors, and you rightly conclude that an accurate rendition is impossible. With all those excuses, however, it still might be instructive to provide a rough idea of the regions of the CIE Diagram associated with common color names.
The display here was created by choosing representative RGB values for the color regions from a rendition of the 1976 CIE Chromaticity Diagram provided by Photo Research, Inc. Note that one representative value in about the middle of the hue and saturation ranges was chosen for each section of the diagram. The point chosen was just a visual judgment of a representative color in the range. The RGB values obtained are listed in the table at right. A different observer would likely have chosen different points to represent the color names, but at least these values might provide a starting point for preferred variations.
One characteristic of the commonly used 1931 CIE Chromaticity Diagram that is evident even from this crude portrayal is that the green takes up far too much of the landscape compared to the number of visually different colors in the region. That was one of the shortcomings that the 1960 and 1976 revisions sought to address.
The C.I.E. Color Space
The CIE system characterizes colors by a luminance parameter Y and two color coordinates x and y which specify the point on the chromaticity diagram. This system offers more precision in color measurement than do the Munsell and Ostwald systems because the parameters are based on the spectral power distribution (SPD) of the light emitted from a colored object and are factored by sensitivity curves which have been measured for the human eye.
Based on the fact that the human eye has three different types of color sensitive cones, the response of the eye is best described in terms of three "tristimulus values". However, once this is accomplished, it is found that any color can be expressed in terms of the two color coordinates x and y.
The colors which can be matched by combining a given set of three primary colors (such as the blue, green, and red of a color television screen) are represented on the chromaticity diagram by a triangle joining the coordinates for the three colors.
Also:
https://micro.magnet.fsu.edu/primer/lightandcolor/humanvisionintro.html
Wikipedia:
In the light
In summary: Light closes cGMP-gated sodium channels, reducing the influx of both Na+ and Ca2+ ions. Stopping the influx of Na+ ions effectively switches off the dark current. Reducing this dark current causes the photoreceptor to hyperpolarise, which reduces glutamate release which thus reduces the inhibition of retinal nerves, leading to excitation of these nerves. This reduced Ca2+ influx during phototransduction enables deactivation and recovery from phototransduction, as discussed below in § Deactivation of the phototransduction cascade.
A light photon interacts with a retinal molecule in an opsin complex in a photoreceptor cell. The retinal undergoes isomerisation, changing from the 11-cis-retinal to the all-trans-retinal configuration.
Opsin therefore undergoes a conformational change to metarhodopsin II.
Metarhodopsin II activates a G protein known as transducin. This causes transducin to dissociate from its bound GDP, and bind GTP; then the alpha subunit of transducin dissociates from the beta and gamma subunits, with the GTP still bound to the alpha subunit.
The alpha subunit-GTP complex activates phosphodiesterase, also known as PDE6. It binds to one of two regulatory subunits of PDE (which itself is a tetramer) and stimulates its activity.
PDE hydrolyzes cGMP, forming GMP. This lowers the intracellular concentration of cGMP and therefore the sodium channels close.[3]
Closure of the sodium channels causes hyperpolarization of the cell due to the ongoing efflux of potassium ions.
Hyperpolarization of the cell causes voltage-gated calcium channels to close.
As the calcium level in the photoreceptor cell drops, the amount of the neurotransmitter glutamate that is released by the cell also drops. This is because calcium is required for the glutamate-containing vesicles to fuse with cell membrane and release their contents (see SNARE proteins).
A decrease in the amount of glutamate released by the photoreceptors causes depolarization of on-center bipolar cells (rod and cone On bipolar cells) and hyperpolarization of cone off-center bipolar cells.
Representation of molecular steps in photoactivation (modified from Leskov et al., 2000[2]). Depicted is an outer membrane disk in a rod. Step 1: Incident photon (hν) is absorbed and activates a rhodopsin by conformational change in the disk membrane to R*. Step 2: Next, R* makes repeated contacts with transducin molecules, catalyzing its activation to G* by the release of bound GDP in exchange for cytoplasmic GTP, which expels its β and γ subunits. Step 3: G* binds inhibitory γ subunits of the phosphodiesterase (PDE) activating its α and β subunits. Step 4: Activated PDE hydrolyzes cGMP. Step 5: Guanylyl cyclase (GC) synthesizes cGMP, the second messenger in the phototransduction cascade. Reduced levels of cytosolic cGMP cause cyclic nucleotide gated channels to close preventing further influx of Na+ and Ca2+.
https://en.wikipedia.org/wiki/Visual_phototransduction
https://en.wikipedia.org/wiki/Cone_cell
https://en.wikipedia.org/wiki/Vertebrate_visual_opsin#Cone_opsins
Keep in mind the fovea centralis.
http://hyperphysics.phy-astr.gsu.edu/hbase/vision/retina.html#c2
Though the eye receives data from a field of about 200 degrees, the acuity over most of that range is poor. To form high resolution images, the light must fall on the fovea, and that limits the acute vision angle to about 15 degrees. In low light, this fovea constitutes a second blind spot since it is exclusively cones which have low light sensitivity. At night, to get most acute vision one must shift the vision slightly to one side, say 4 to 12 degrees so that the light falls on some rods.
A "dimple on the retina" provides our highest resolution vision.
"Just about at the center of the retina is a small depression from 2.5 to 3 mm in diameter known as the yellow spot, or macula. There is a tiny rod-free region about 0.3mm in diameter at its center, the fovea centralis. (In comparison the image of the full Moon on the retina is about 0.2 mm in diameter.) Here the cones are thinner (with diameters of 0.0030mm to 0.0015mm) and more densely packed than anywhere else in the retina. Since the fovea provides the sharpest and most detailed information, the eyeball is continuously moving, so that light from the object of primary interest falls on this region. ...the rods are multiply connected to nerve fibers, and a single such fiber can be activated by any one of about a hundred rods. By contrast, cones in the fovea are individually connected to nerve fibers. The actual perception of a scene is constructed by the eye-brain system in a continuous analysis of the time-varying retinal image."(Hecht)
Chromium6- Posts : 811
Join date : 2019-11-29
Re: The human eye can see 'invisible' infrared light
Interestingly, cGMP and Calcium interplay with serverity of Alzheimer's disease from a few reported papers. Keep in mind that the NF-κB inhibition can be done with cheap Syrian-Rue/Harmine/Harmaline as well:
https://en.wikipedia.org/wiki/Harmaline
Keep in mind about HSV-1 and Alzheimer's:
https://www.nature.com/articles/s41598-021-87963-9
The Interplay between cGMP and Calcium Signaling in Alzheimer’s Disease
by Aileen Jehle andOlga Garaschuk *
Department of Neurophysiology, Institute of Physiology, Eberhard Karls University of Tübingen, 72074 Tübingen, Germany
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2022, 23(13), 7048; https://doi.org/10.3390/ijms23137048
Received: 5 April 2022 / Revised: 31 May 2022 / Accepted: 22 June 2022 / Published: 24 June 2022
(This article belongs to the Special Issue Alzheimer's disease: From Molecular Basis to Therapy)
Abstract
Cyclic guanosine monophosphate (cGMP) is a ubiquitous second messenger and a key molecule in many important signaling cascades in the body and brain, including phototransduction, olfaction, vasodilation, and functional hyperemia. Additionally, cGMP is involved in long-term potentiation (LTP), a cellular correlate of learning and memory, and recent studies have identified the cGMP-increasing drug Sildenafil as a potential risk modifier in Alzheimer’s disease (AD). AD development is accompanied by a net increase in the expression of nitric oxide (NO) synthases but a decreased activity of soluble guanylate cyclases, so the exact sign and extent of AD-mediated imbalance remain unclear. Moreover, human patients and mouse models of the disease present with entangled deregulation of both cGMP and Ca2+ signaling, e.g., causing changes in cGMP-mediated Ca2+ release from the intracellular stores as well as Ca2+-mediated cGMP production. Still, the mechanisms governing such interplay are poorly understood. Here, we review the recent data on mechanisms underlying the brain cGMP signaling and its interconnection with Ca2+ signaling. We also discuss the recent evidence stressing the importance of such interplay for normal brain function as well as in Alzheimer’s disease.
Keywords: cyclic guanosine-3′,5′-monophosphate; nitric oxide; neurodegeneration; neuroinflammation; astrocytes; microglia; phosphodiesterase inhibitors
1. Introduction
Cyclic guanosine monophosphate (cGMP) is one of the ubiquitous second messengers of the body and brain. It targets a manifold of downstream pathways, thus eliciting a broad variety of cellular/tissue effects. The role of cGMP has been extensively studied in the periphery, where it has important physiological functions in the vasculature, heart, pulmonary arteries, and gastrointestinal tract [1]. The dysfunction of the aforementioned pathways (e.g., in the cardiovascular domain) is common and the development of drugs, targeting these pathways, has substantial therapeutic implications. The most known are phosphodiesterase (PDE) inhibitors (e.g., PDE5 inhibitor Sildenafil), used in erectile dysfunction [2]. In the brain, cGMP is involved in signal transduction in the retina as well as synaptic plasticity, learning and memory formation, activity-dependent hyperemia, and inflammation [3,4]. Therefore, it has gained attention as a possible druggable target for treating neurodegenerative diseases.
In neuro-glial brain networks, the production of cGMP is modulated in an activity-dependent manner, with increases in synaptic transmission as well as second messenger-mediated rises in the cytosolic free Ca2+ concentration ([Ca2+]i) enhancing the production of cGMP [5,6,7]. Both neuronal activity and Ca2+ signaling are affected in Alzheimer’s disease (AD) patients or mouse models of the disease [7,8,9]. In fact, AD patients are known to have an increased incidence of epileptic seizures, which is independent of the disease stage and highest in cases with early disease onset [7,10,11,12]. The vicinity of amyloid plaque deposits, studied in animal models of the disease, is known for its profound neuronal, astrocytic, and microglial hyperactivity [8,10,12]. AD is the most common form of dementia, and it is expected that the number of AD cases will rise significantly in the years to come due to the aging of the Western population, consequences of the COVID-19 pandemic, and profound inflammation/brain traumata obtained during war [13,14,15], making this disease a major concern for modern society.
The cGMP signaling pathway is reportedly affected during the early stages of AD [16], making it an interesting target for developing new treatment strategies. In this review, we summarize the physiological roles of the cGMP signaling pathway in different constituents of the neuro-glial brain network, its interconnection with Ca2+ signaling, its implications in AD, and the current attempts in developing new AD therapies targeting the cGMP signaling pathway.
2. cGMP Toolkit in the Brain
There are two main pathways for cGMP production (Figure 1). The first pathway is mediated by NO. This short-lived free radical molecule is mainly produced through nitric oxide synthases (NOS). Like other tissues, the brain contains two types of the constitutively expressed NOS (neuronal (nNOS) and endothelial (eNOS)) as well as the inducible NOS (iNOS), whose expression is triggered by different stimuli. The nNOS is widely expressed throughout the brain and is abundant in neurons, but it is also found in other brain cells such as astrocytes and endothelial cells. eNOS is most commonly expressed in endothelial cells [17], but also in blood vessel-associated astrocytes as well as in the layer II–IV cortical neurons [18,19]. The activity of both types of constitutively expressed NOS is regulated by Ca2+ and calmodulin [20,21]. This mechanism of activation enables a fast and transient increase in the intracellular NO concentration in response to cells’ activity. In contrast to constitutively expressed NOS isoforms, the expression of iNOS is triggered. This form of NOS is part of the immune response machinery and therefore is mainly found in astrocytes and microglia [22]. To a smaller degree, it is also expressed in neurons and endothelial cells of the blood–brain barrier (BBB) [23]. The main stimuli inducing iNOS activity are tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), interferon-gamma (IFN-γ), lipopolysaccharide (LPS), and double-strand RNA (dsRNA) [22,24,25]. The subsequent NO production is primarily regulated at the transcriptional level through binding sites for the nuclear factor κB (NF-κB) and the phosphorylated cyclic adenosin monophosphate (cAMP) response element-binding protein (pCREB) in the promoter region of the iNOS gene [26,27]. Once the expression of iNOS is triggered, it generates NO over a prolonged period of time. One factor controlling the expression of iNOS via NF-κB is the nuclear factor erythroid 2-related factor 2 (Nrf2). This transcription factor can be activated by NO [28,29] and causes, among others, the expression of heme oxygenase 1. This protein is known to inhibit NF-κB, thus causing a NO-coupled reduction in iNOS expression in case of inflammation (Figure 1).
https://www.mdpi.com/1422-0067/23/13/7048
Memory Enhancers for Alzheimer's Dementia: Focus on cGMP - PMC
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7828493/
Improved Long-Term Memory via Enhancing cGMP-PKG Signaling
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207334/
https://en.wikipedia.org/wiki/Cyclic_guanosine_monophosphate
Chemical formula C10H12N5O7P
Protein kinase activation
cGMP is involved in the regulation of some protein-dependent kinases. For example, PKG (protein kinase G) is a dimer consisting of one catalytic and one regulatory unit, with the regulatory units blocking the active sites of the catalytic units.
cGMP binds to sites on the regulatory units of PKG and activates the catalytic units, enabling them to phosphorylate their substrates. Unlike with the activation of some other protein kinases, notably PKA, the PKG is activated but the catalytic and regulatory units do not disassociate.
https://www.nature.com/articles/s41401-021-00639-y
https://en.wikipedia.org/wiki/Harmaline
The harmala alkaloids are psychoactive in humans.[1] Harmaline is shown to act as an acetylcholinesterase inhibitor.[3] Harmaline also stimulates striatal dopamine release in rats at very high dose levels.[4] Since harmaline is a reversible inhibitor of monoamine oxidase A, it could, in theory, induce both serotonin syndrome and hypertensive crises in combination with tyramine, serotonergics, catecholaminergics drugs or prodrugs. Harmaline-containing plants and tryptamine-containing plants are used in ayahuasca brews. The inhibitory effects on monoamine oxidase allows dimethyltryptamine (DMT), the psychoactively prominent chemical in the mixture, to bypass the extensive first-pass metabolism it undergoes upon ingestion, allowing a psychologically active quantity of the chemical to exist in the brain for a perceivable period of time.[5] Harmaline forces the anabolic metabolism of serotonin into N-acetylserotonin (normelatonin), and then to melatonin, the body's principal sleep-regulating hormone and a powerful antioxidant.
United States Patent Number 5591738 describes a method for treating various chemical dependencies via the administration of harmaline and or other beta-carbolines.[6]
A study has reported the antiviral activity of Harmaline against Herpes Simplex Virus 1 and 2 (HSV-1 and HSV-2) by inhibiting immediate early transcription of the virus at noncytotoxic concentration.[7]
Harmaline is known to act as a histamine N-methyltransferase inhibitor.[8] This explains how harmaline elicits its wakefulness-promoting effects.
Keep in mind about HSV-1 and Alzheimer's:
https://www.nature.com/articles/s41598-021-87963-9
-----------Published: 22 April 2021
Herpes simplex virus 1 and the risk of dementia: a population-based study
Meghan J. Murphy, Lana Fani, M. Kamran Ikram, Mohsen Ghanbari & M. Arfan Ikram
Scientific Reports volume 11, Article number: 8691 (2021) Cite this article
Abstract
Herpes simplex virus 1 (HSV1) is a neuroinvasive virus capable of entering the brain which makes it a candidate pathogen for increasing risk of dementia. Previous studies are inconsistent in their findings regarding the link between HSV1 and dementia, therefore, we investigated how HSV1 relates to cognitive decline and dementia risk using data from a population-based study. We measured HSV1 immunoglobulin (IgG) antibodies in serum collected between 2002 and 2005 from participants of the Rotterdam Study. We used linear regression to determine HSV1 in relation to change in cognitive performance during 2 consecutive examination rounds on average 6.5 years apart. Next, we determined the association of HSV1 with risk of dementia (until 2016) using a Cox regression model. We repeated analyses for Alzheimer’s disease. All models were adjusted for age, sex, cardiovascular risk factors, and apolipoprotein E genotype. Of 1915 non-demented participants (mean age 71.3 years, 56.7% women), with an average follow-up time of 9.1 years, 244 participants developed dementia (of whom 203 Alzheimer’s disease). HSV1 seropositivity was associated with decline in global cognition (mean difference of HSV1 seropositive vs seronegative per standard deviation decrease in global cognition − 0.16; 95% confidence interval (95%CI), − 0.26; − 0.07), as well as separate cognitive domains, namely memory, information processing, and executive function, but not motor function. Finally, HSV1 seropositivity was not associated with risk of dementia (adjusted hazard ratio 1.18, 95% CI 0.83; 1.68), similar for Alzheimer’s disease. HSV1 is associated with cognitive decline but not with incident dementia in the general population. These data suggest HSV1 to be associated only with subtle cognitive disturbances but not with greater cognitive disorders that result in dementia.
The Interplay between cGMP and Calcium Signaling in Alzheimer’s Disease
by Aileen Jehle andOlga Garaschuk *
Department of Neurophysiology, Institute of Physiology, Eberhard Karls University of Tübingen, 72074 Tübingen, Germany
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2022, 23(13), 7048; https://doi.org/10.3390/ijms23137048
Received: 5 April 2022 / Revised: 31 May 2022 / Accepted: 22 June 2022 / Published: 24 June 2022
(This article belongs to the Special Issue Alzheimer's disease: From Molecular Basis to Therapy)
Abstract
Cyclic guanosine monophosphate (cGMP) is a ubiquitous second messenger and a key molecule in many important signaling cascades in the body and brain, including phototransduction, olfaction, vasodilation, and functional hyperemia. Additionally, cGMP is involved in long-term potentiation (LTP), a cellular correlate of learning and memory, and recent studies have identified the cGMP-increasing drug Sildenafil as a potential risk modifier in Alzheimer’s disease (AD). AD development is accompanied by a net increase in the expression of nitric oxide (NO) synthases but a decreased activity of soluble guanylate cyclases, so the exact sign and extent of AD-mediated imbalance remain unclear. Moreover, human patients and mouse models of the disease present with entangled deregulation of both cGMP and Ca2+ signaling, e.g., causing changes in cGMP-mediated Ca2+ release from the intracellular stores as well as Ca2+-mediated cGMP production. Still, the mechanisms governing such interplay are poorly understood. Here, we review the recent data on mechanisms underlying the brain cGMP signaling and its interconnection with Ca2+ signaling. We also discuss the recent evidence stressing the importance of such interplay for normal brain function as well as in Alzheimer’s disease.
Keywords: cyclic guanosine-3′,5′-monophosphate; nitric oxide; neurodegeneration; neuroinflammation; astrocytes; microglia; phosphodiesterase inhibitors
1. Introduction
Cyclic guanosine monophosphate (cGMP) is one of the ubiquitous second messengers of the body and brain. It targets a manifold of downstream pathways, thus eliciting a broad variety of cellular/tissue effects. The role of cGMP has been extensively studied in the periphery, where it has important physiological functions in the vasculature, heart, pulmonary arteries, and gastrointestinal tract [1]. The dysfunction of the aforementioned pathways (e.g., in the cardiovascular domain) is common and the development of drugs, targeting these pathways, has substantial therapeutic implications. The most known are phosphodiesterase (PDE) inhibitors (e.g., PDE5 inhibitor Sildenafil), used in erectile dysfunction [2]. In the brain, cGMP is involved in signal transduction in the retina as well as synaptic plasticity, learning and memory formation, activity-dependent hyperemia, and inflammation [3,4]. Therefore, it has gained attention as a possible druggable target for treating neurodegenerative diseases.
In neuro-glial brain networks, the production of cGMP is modulated in an activity-dependent manner, with increases in synaptic transmission as well as second messenger-mediated rises in the cytosolic free Ca2+ concentration ([Ca2+]i) enhancing the production of cGMP [5,6,7]. Both neuronal activity and Ca2+ signaling are affected in Alzheimer’s disease (AD) patients or mouse models of the disease [7,8,9]. In fact, AD patients are known to have an increased incidence of epileptic seizures, which is independent of the disease stage and highest in cases with early disease onset [7,10,11,12]. The vicinity of amyloid plaque deposits, studied in animal models of the disease, is known for its profound neuronal, astrocytic, and microglial hyperactivity [8,10,12]. AD is the most common form of dementia, and it is expected that the number of AD cases will rise significantly in the years to come due to the aging of the Western population, consequences of the COVID-19 pandemic, and profound inflammation/brain traumata obtained during war [13,14,15], making this disease a major concern for modern society.
The cGMP signaling pathway is reportedly affected during the early stages of AD [16], making it an interesting target for developing new treatment strategies. In this review, we summarize the physiological roles of the cGMP signaling pathway in different constituents of the neuro-glial brain network, its interconnection with Ca2+ signaling, its implications in AD, and the current attempts in developing new AD therapies targeting the cGMP signaling pathway.
2. cGMP Toolkit in the Brain
There are two main pathways for cGMP production (Figure 1). The first pathway is mediated by NO. This short-lived free radical molecule is mainly produced through nitric oxide synthases (NOS). Like other tissues, the brain contains two types of the constitutively expressed NOS (neuronal (nNOS) and endothelial (eNOS)) as well as the inducible NOS (iNOS), whose expression is triggered by different stimuli. The nNOS is widely expressed throughout the brain and is abundant in neurons, but it is also found in other brain cells such as astrocytes and endothelial cells. eNOS is most commonly expressed in endothelial cells [17], but also in blood vessel-associated astrocytes as well as in the layer II–IV cortical neurons [18,19]. The activity of both types of constitutively expressed NOS is regulated by Ca2+ and calmodulin [20,21]. This mechanism of activation enables a fast and transient increase in the intracellular NO concentration in response to cells’ activity. In contrast to constitutively expressed NOS isoforms, the expression of iNOS is triggered. This form of NOS is part of the immune response machinery and therefore is mainly found in astrocytes and microglia [22]. To a smaller degree, it is also expressed in neurons and endothelial cells of the blood–brain barrier (BBB) [23]. The main stimuli inducing iNOS activity are tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), interferon-gamma (IFN-γ), lipopolysaccharide (LPS), and double-strand RNA (dsRNA) [22,24,25]. The subsequent NO production is primarily regulated at the transcriptional level through binding sites for the nuclear factor κB (NF-κB) and the phosphorylated cyclic adenosin monophosphate (cAMP) response element-binding protein (pCREB) in the promoter region of the iNOS gene [26,27]. Once the expression of iNOS is triggered, it generates NO over a prolonged period of time. One factor controlling the expression of iNOS via NF-κB is the nuclear factor erythroid 2-related factor 2 (Nrf2). This transcription factor can be activated by NO [28,29] and causes, among others, the expression of heme oxygenase 1. This protein is known to inhibit NF-κB, thus causing a NO-coupled reduction in iNOS expression in case of inflammation (Figure 1).
https://www.mdpi.com/1422-0067/23/13/7048
Memory Enhancers for Alzheimer's Dementia: Focus on cGMP - PMC
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7828493/
Improved Long-Term Memory via Enhancing cGMP-PKG Signaling
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207334/
https://en.wikipedia.org/wiki/Cyclic_guanosine_monophosphate
Chemical formula C10H12N5O7P
Protein kinase activation
cGMP is involved in the regulation of some protein-dependent kinases. For example, PKG (protein kinase G) is a dimer consisting of one catalytic and one regulatory unit, with the regulatory units blocking the active sites of the catalytic units.
cGMP binds to sites on the regulatory units of PKG and activates the catalytic units, enabling them to phosphorylate their substrates. Unlike with the activation of some other protein kinases, notably PKA, the PKG is activated but the catalytic and regulatory units do not disassociate.
Published: 30 March 2021
Harmine is an effective therapeutic small molecule for the treatment of cardiac hypertrophy
Jie Huang, Yang Liu, Jia-xin Chen, Xin-ya Lu, Wen-jia Zhu, Le Qin, Zi-xuan Xun, Qiu-yi Zheng, Er-min Li, Ning Sun, Chen Xu & Hai-yan Chen
Acta Pharmacologica Sinica volume 43, pages50–63 (2022)Cite this article
1893 Accesses
11 Citations
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Abstract
Harmine is a β-carboline alkaloid isolated from Banisteria caapi and Peganum harmala L with various pharmacological activities, including antioxidant, anti-inflammatory, antitumor, anti-depressant, and anti-leishmanial capabilities. Nevertheless, the pharmacological effect of harmine on cardiomyocytes and heart muscle has not been reported. Here we found a protective effect of harmine on cardiac hypertrophy in spontaneously hypertensive rats in vivo. Further, harmine could inhibit the phenotypes of norepinephrine-induced hypertrophy in human embryonic stem cell-derived cardiomyocytes in vitro. It reduced the enlarged cell surface area, reversed the increased calcium handling and contractility, and downregulated expression of hypertrophy-related genes in norepinephrine-induced hypertrophy of human cardiomyocytes derived from embryonic stem cells. We further showed that one of the potential underlying mechanism by which harmine alleviates cardiac hypertrophy relied on inhibition of NF-κB phosphorylation and the stimulated inflammatory cytokines in pathological ventricular remodeling. Our data suggest that harmine is a promising therapeutic agent for cardiac hypertrophy independent of blood pressure modulation and could be a promising addition of current medications for cardiac hypertrophy.
https://www.nature.com/articles/s41401-021-00639-y
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