a0053z
(connected with note a0272z: Taste & Hearing: Sensory Input Quantification)
(oscillation magnitude)
Amplitude Action Potential Magnitude Effect (APME)
Its possible that a high magnitude vesicle release is more likely to open potassium/sodium channels at the same time in some instances. This could cause the inhibitory or shutdown effect. Like overwhelming or flooding the gates, which would take more time to clear & reset. Temporarily slowing down that gear in the clock mechanism so to speak. So my hypothesis or conjecture is that the phasic or high phase action potential burst leaves the calcium channels open longer resulting in 2 or 3 vesicle sacks being released, resulting in inhibition of array represented by the exit terminal of that neuron.
The high phasic burst could potentially slow down the firing of many of its exit terminal neighbors by inhibiting them with a flood of extra neurotransmitters.
And the slowing effect would have a higher spatial magnitude than the smaller but faster phasic bursts.
Phasic burst might be characterized as being higher frequency but also causing a greater magnitude distribution of vesicles and neurotransmitters.
The signals that cause a Phasic or High Phasic spike might require higher frequency signalling that has a lower magnitude of neurotransmitters per interval.
Perhaps the phasic & high phasic signals, at least as soliton waves across the electromagnetic spectrium, might have a longer range, they would travel across longer distances of the network before eventually being dissipated by the rest of the oscillating groups of cells.
The higher magnitude tonic signals are the oscillating groups of cells that are leveling out or dissipating the energy which represents the incoming phasic signals.
As if the relationship between the phasic signals and the tonic signals was like an Etch in Sketch toy, the magnetic pin is etching with phasic burstlets, and shaking the toy is dissipating the learned signal back into an equilibrium state or an empty slate. That's kind of a rough analogy.
It would be the phasic signals that travel between oscillators, cortical columns, rich clubs, default mode network, majority networking areas, and interneuron neural circuits. I think there is research to back this up, if I remember correctly, so search for citations to bolster this.
Recapping the Phasic Tonic Relationship, the high phasic spike, creates a burstlet, that creates an inhibitory wave (a sharp wave ripple across the brain) that starts with it's direct exit terminal array, the phasic spikes are dissipated into the tonic oscillation, so there is a relationship between the tonic brainwave pattern (like the theta brainwave pattern) and the incoming sensory pathways.
I think this paper below describes one example of how that relationship between phasic spikes from incoming senses, from the eyes, interfaces with an organisms actions, the steps that it takes, to navigate.
""One of the most remarkable aspects of our finding is that this network supports walking on two different timescales simultaneously," said Chiappe. "It operates on a fast timescale to monitor and correct each step while promoting the animal's behavioral goal."" ""Vision and action may seem unrelated, but they are actually tightly associated; just choose a point on the wall and try placing your finger on it with your eyes closed,"" ""The longer the fly has been walking fast, the higher are the chances that it would need help to maintain this action plan. Therefore, the neurons become increasingly 'more alert' and ready to be recruited for movement control."" https://medicalxpress.com/news/2022-05-newly-neural-network-visual-motor.html?fbclid=IwAR2dMsG-yutGOa6UFIIevxUjqy2O3P9DweYSVG9-ZEJ5VVyzuehWlrT21Jg
"Calcium-activated non-selective cation currents are involved in generation of tonic and bursting activity in dopamine neurons of the substantia nigra pars compacta"
"Nigral dopamine neurons are transiently activated by high frequency glutamatergic inputs relaying reward-predicting sensory information. The tonic firing pattern of dopamine cells responds to these inputs with a transient burst of spikes that requires NMDA receptors. Here, we show that NMDA receptor activation further excites the cell by recruiting a calcium-activated non-selective cation current (ICAN) capable of generating a plateau potential." "An animal's behaviour is altered by the temporal pattern of DA release, and it has been proposed that tonic dopamine levels provide a general motivating function while phasic DA permits the corticostriatal plasticity necessary for habit learning (Reynolds & Wickens, 2000; Wise, 2004; Niv et al. 2007)." "Thus, burst firing may encode a ‘reward’ signal during normal reinforcement learning and also pathological addictions (Mirenowicz & Schultz, 1996; Phillips et al. 2003)." " Calcium influx through NMDA receptors and/or voltage-gated calcium channels causes a depolarization that is terminated by the subsequent activation of calcium-activated potassium channels (Overton & Clark, 1997). " "It is generally believed that CAN channels are activated downstream of glutamate receptors to drive plateau potentials and boost burst firing."
A central part of my argument is that a group of oscillating fireflies act as a single sensor, unified via oscillation, so that if one of them is excited by food, or eaten by a frog, that disturbs the oscillating firing pattern of the entire hive or flock of fireflies, in other words they all notice, via oscillation the fireflies are entified,
(Later on I want to expand this concept to atomically homogenous materials, to say something like here is a sheet of graphite because it has an array of atoms that are united by a common oscillatory pattern. What effects part of the sheet sends a signal rippling across the whole sheet, so the sheet of graphine atoms is an entified sensor, something like that)
My argument is that the rendering output that makes up our internal representations, and our mind, is in the phase variations between the normal tonic oscillating pattern, and the phasic bursts that alter that tonic pattern. The tonic pattern is not just pink noise. It's an attractor state for the neural oscillations of cell assemblies. Like clocks or fireflies as described in the book Sync these tonic oscillations are dissipating energy from the phasic & high phasic spikes, but they also notice when neurons are inhibited because that is a phase change also that effects the group. To finish the thought, the rendering output is then read by the next array of sensors, in this case the receptors on the receiving dendritic array.
(Insert Link to research on the dendritic arrays on the bodies of Zebrafish)
"NMDA caused a switch from tonic to burst firing A, NMDA (15 μm, in the bath) caused the tonic firing and stable resting potential from time point i to depolarize and switch to high-frequency burst firing with regenerative oscillations of membrane potential (mean: 0.3 Hz ± 0.02, n = 88) by time point ii. Lower trace: DC injection was slowly ramped to −100 pA in order to hyperpolarize the cell and induce stronger oscillations starting at time point ii. B, ISI histograms of firing activity for a representative DA neuron. Tonic spiking had a unimodal distribution of ISIs at 250 ms (CV = 0.15). C, NMDA caused strong bursting with a bimodal ISI distribution, with peaks at 150 ms (ISI within a burst) and 2100 ms (ISI between bursts)."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3115821/
Share link from iphone & upload photo about pace setter potentials, plateau potentials, and action potentials.
Perhaps I can think of pace setter potentials as tonic firing, plateau potential as phasic firing, and action potentials as high phasic firing?
DOI:10.1146/annurev-biophys-111521-102500 "Embryonic Development hinges on effect coordination of molecular events across space and time. Waves can help synchronize signals across large spatial scales (hundreds of microns across for embryos, and organize signalling dynamics to ensure proper patterning of repeated structures)
If Embryonic waves can do that, then tonic brainwaves, or pacesetter electrical wave currents in the brain can do that. They can synchronize signals across space & time, and ensure patterning of repeated biological structures.
Now you throw in some patterns like inhibitions, phase plateau potentials, and high phasic spike potentials and well you have more complex patterns being embedded into the biological structure of your brain.
Plateau Potentials pacesetter potential action potential https://www.sciencedirect.com/topics/biochemisPhasictry-genetics-and-molecular-biology/plateau-potentials
Know your potentials: Slow waves are Pacesetter Potentials. Fast waves are Spike Potentials. In the middle are Plateau Potentials.
Reference Plateau image from book pictures and or twitter. http://twitter.com/worksalt/status/1557769028873072640?s=21
"Molecular Mechanisms of Memory J. Waters, ... F. Helmchen, in Learning and Memory: A Comprehensive Reference, 2008 4.39.3.4.3 NMDA spikes Another mode of dendritic regenerativity involves the voltage dependence of the N-methyl-d-aspartate receptor (NMDAR). Schiller et al. (2000) noticed that glutamate uncaging at dendritic sites can elicit plateau potentials at the soma that depend nonlinearly on stimulus intensity. Similar results were obtained with focal synaptic stimulation, and these potentials depend on NMDAR activation (Schiller and Schiller, 2001). NMDA spikes result in plateau potentials with large dendritic depolarizations (around 30 mV). These spikes are less attenuated en route to the soma than subthreshold EPSPs and therefore represent a mechanism by which dendrite-to-soma coupling is greatly enhanced (Nevian et al., 2007)."
"Long-Term Depression: Possible Cellular Mechanism for Learning Mediated by the Cerebellum Masao Ito, in Neural Models of Plasticity, 1989 IV Involvement of Ca2+ Inflow in LTD LTD has been shown to be abolished when climbing-fiber impulses are conditioned with postsynaptic inhibition of Purkinje cell dendrites through stellate cells (Ekerot and Kano, 1985). Since stellate-cell inhibition depresses both the Ca2+ spikes and subsequent Ca2+-dependent plateau potentials induced in Purkinje cell dendrites by climbing-fiber impulses, the above observation suggests that Ca2+ inflow into Purkinje cell dendrites plays an essential role in inducing LTD. More direct evidence for the role of Ca2+ inflow has recently been obtained by intradendritic injection of a Ca2+ chelator, EGTA (M. Sakurai, personal communication). Iontophoretic injection of EGTA through an electrode containing EGTA plus "potassium" acetate abolished the LTD, whereas control injection of acetate ions did not affect the LTD"
- Spikes are followed by Plateau Potentials
- Lack of Potassium K+ leads to inhibited Ca2+ spikes and to LTD in the post synapse dendrite.
The Potassium K+ Channel might be the most important part of the human brain in the context to what it adds.
I think of the original artificial neuron, the Perceptron, and the idea of the All or Nothing action potential, which is sort of like summing up everything the neuron could sense as an accumulation of charges that would result in an all or nothing spike, essentially an on or off switch.
That model of a neuron, which might similar to the Hodgkin & Huxley model of a neuron has Sodium channels as the star of the show, the neuron fills up with charge, it spikes, and then neurotransmitters flow through the synaptic cleft to the next neuron. In that model the Potassium channel is not more important than the Sodium channel, it's just another pump helping to lower the neurons positive charge so the neuron can be reset again.
We know now, and I am presenting more of this research today, that the all or nothing action potential isn't an all or nothing event in the computational sense. The reason is because the potassium channels are doing more than just repolarization & hyperpolarization, the potassium channels are manipulated by metabotropic receptors that affect cAMP Cascades and this manipulation can change the duration of the action potential, changing the magnitude of the AP wave shape, causing calcium channels to open longer, releasing more exosomes or synaptic vesicles. There is a lot more happening with Potassium channels and it affects the signals that the cell is sending to other cells.
In otherwords Potassium channels are the key to phase variations in the signal transmittion between nerve cells, and phase variations are how the rendering of the mind is tomographically computed & perceived by oscillating networks of neurons that are each computing and each perceiving a small part of the conscious mind (a volumetric tomographic pattern) that is being computationally rendered by the brain (or alternatively by an artificial neural network if you have one of those.)
The work on The Self Aware Networks began with understanding MVR Multi-Vesicle Released undermined the Synaptic Unrealiability which undermined the Perceptron that was still the basis of Artificial (Deep) Neural Networks today in 2022, 79 years after the Perceptron was invented.
I'm calling the new model of the Neuron the Metatron, but right now the pieces of the Metatron exist across several notes so I want to bring it together under one roof.
Cardiac Delayed Rectifier Potassium Channels in Health and Disease https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4893812/
Paraphasing the article: Delayed rectifier potassium channels conduct outward potassium currents during the plateau phase of action potentials and play pivotal roles in repolarization.
"during the plateau phase calcium entry via L-type calcium channels triggers contraction. counter balancing the calcium influx potassium ions pass through the membrane in the outward direction. the plateau phase is a balance of inward & outward currents"
Paraphrasing the article: The plateau phase is after the initial depolarization of the action potential, it is prolongation of the duration of depolarization phase before the repolarization phase begins.
Paraphrasing: Sodium channels terminate quickly, initiating the repolarization phase, but slower potassium channels currents persist during the plateau phase, the repolarization phase, and the hyperpolarization phase.
"The delayed rectifiers essentially determine the waveform as well as action potential duration (APD)."
doi:10.1016/j.ccep.2016.01.004.
"In the nervous system, Src family tyrosine kinases are thought to be involved in cell growth, migration, differentiation, apoptosis, as well as in myelination and synaptic plasticity."
"Emerging evidence indicates that K+ channels are crucial targets of Src tyrosine kinases."
"The present study shows that a Src family tyrosine kinase constitutively activates delayed rectifier K channels (IK)."
"IK currents are markedly downregulated upon exposure of cells to the tyrosine kinase inhibitors herbimycin A and genistein, while a potent upregulation of IK is observed when recombinant Fyn kinase is introduced through the patch pipette."
https://www.researchgate.net/publication/247089844 DOI: 10.1016/S0304-3940(97)90197-X
Not only are potassium channels key to APD, action potential duration, but they can be upregulated or downregulated by the signals they receive.
Listen to 2 audio recordings about this paper "Voltage-gated potassium channels are modulated by Fyn tyrosine kinase in Schwann cells" Regulation of potassium channels in myelin-forming glial cells Part 1 https://youtu.be/bCzWOtvMdFc Part 2 https://youtu.be/mQi3Smz0lGA