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2.5.3 Signal Transmission and Potentiation

2.5.3.1 Overview

As mentioned before, Neurons gain basic Electric Potential Difference. Based on the Electric Potential Difference, signals are created and transmitted. In addition, when a signal is created in a neuron, efficiency of transmission is enhanced at the synapse that caused the signal. It contributes to mechanism of memorization. Furthermore, another device regulating signal transmission is prepared.

2.5.3.2 Details

2.5.3.2.1 Signal Transmission through Excitatory Chemical Synapse

Based on Electric Potential Difference, Voltage-Gated Ion Channels and Ligand-Gated Ion Channels cause signal transmission through Excitatory Chemical Synapse as follows. (As mentioned later, some chemical synapses inhibit other chemical synapses from transmitting signals. This type of synapses is called Inhibitory Chemical Synapses. In contrast, common chemical synapses intending to transmit signals explained here are called Excitatory Chemical Synapses, since signals would be, in a sense, excitations.)

Specifically, a signal is rapid rise and fall of intracellular Electric Potential Difference. According to a simple model, the rise and fall of intracellular Electric Potential Difference is shown like in the following '"Schematic" Action Potential.' On the other hand, it is in fact affected by various elements and is shown like in the following '"Real" Action Potential.' A signal is also called a "Fire" or a "Spike." Otherwise, creating a signal is called "Firing."




*Attribution: https://en.wikipedia.org/wiki/File:Action_potential_vert.png

Then the signal as rise and fall of intracellular Electric Potential Difference is transmitted as follows from the dendrites and the cell body to the axon terminals. Since the inside of the neuron is commonly negatively charged, " - " are commonly shown on the inside of neuron's phospholipid bilayer. In contrast, " + " are commonly shown on the outside of neuron's phospholipid bilayer.

*Attribution: https://en.wikipedia.org/wiki/File:Action_Potential.gif

The mechanism of the rise and fall is as follows.

First, fig. (1) shows a simplified diagram of a chemical synapse in resting state. The upper part of (1) shows 2 presynaptic neurons' axon terminals. The lower half of (1) shows part of a postsynaptic neuron's dendrite. As far as positive ions, the inside of the neurons are mostly filled with Potassium ions. Other major electrolytes (ions) are placed following the analyzed abundance. As far as positive ions, outside of the neurons is mosty filled with Sodium ions, while a small quantity of Potassium ions, Calcium ions, and Magnesium ions follow. Similarly, other major electrolytes (ions) are placed following the analyzed abundance. Sodium-Potassium Transporters (in black) reside among the phospholipid bilayers of both neurons. Voltage-Gated Calcium (Ion) Channels (in brown) reside among the phospholipid bilayer of the axon terminals. Neurotransmitters such as glutamic acids are held in packs called Synaptic Vesicles made of phospholipid bilayer at the axon terminals. Ligand-Gated Sodium (Ion) Channels with AMPA Receptors, Voltage-Gated Sodium (Ion) Channels, Voltage-Gated (Ion) Channels, and Ligand-Gated Cation (positive ion) Channels with NMDA Receptors reside among the phospholipid bilayer of the postsynaptic neuron's dendrites. Ligand-Gated Sodium (Ion) Channels with AMPA Receptors held in vesicles made of phospholipid bilayer drift in the postsynaptic neuron near the dendrites. These Transporters, Channels, and Receptors are all a kind of enzymes.

* "AMPA Receptor in Wikipedia" https://en.wikipedia.org/wiki/AMPA_receptor
* "NMDA Receptor in Wikipedia" https://en.wikipedia.org/wiki/NMDA_receptor

In (2), when electric charge in the cell body of the left presynaptic neuron became positive and Sodium ions reach the left axon terminal, the electric potential of the left axon terminal rises, Voltage-Gated Calcium (Ion) Channels open and Calcium ions flow in.

In (3), Calcium ions (in orange) flow in, protein kinases are activated, affinity between the presynaptic neuron's phospholipid bilayer and the vesicles' phospholipid bilayer rise, and they approach.

In (4), the Neurotransmitter Vesicle fuse with the presynaptic neuron's phospholipid bilayer and the Neurotransmitters such as glutamic acids are released.


In (5) and (6), AMPA Receptors of Ligand-Gated Sodium Channels receive Neurotransmitters such as glutamic acids and the channel open, Sodium ions flow in. Then the electric potential in the postsynapyic neuron around the channels rises to a certain extent.





In many cases, the rise by some Ligand-Gated Sodium Channels might be insufficient to reach "threshold level." In this situation, if additional Ligand-Gated Sodium Channels are opened almost at the same time by other Neurotransmitters from other (right) axon terminal as in (7) and (8), additional Sodium ions flow in, the electric potential rise over "threshold level."





In (9) and (10), when the electric potential rises to a certain extent over "threshold level," the Voltage-Gated Sodium Channels open and Sodium ions additionally flow in. Then the electric potential in the postsynaptic neuron additionally rises (Fires) and the rise is transmitted to the axon terminals of the postsynaptic neuron. Thus signals as electric potential are transmitted from neurons to another neuron. (For simplification, behavior of Ligand-Gated Cation (positive ion) Channels with NMDA Receptors about memorization is left out for now.)





In (11), because the electric potential rose, Voltage-Gated Potassium Channels open and Potassium ions flow out.


In (12), because Potassium ions flew out, the electric potential in the postsynaptic neuron is reduced. Subsequently, Sodium-Potassium Transporters work, the postsynaptic neuron becomes resting state like in (1).


2.5.3.2.2 Basic Mechanism of Memorization (Potentiation)

When some presynaptic neurons transmit signals almost at the same time or repeatedly to a postsynaptic neuron, efficiency of the transmission between the neurons at specific synapses rises, being called "potentiation," mediated by Ligand-Gated Cation (positive ion) Channels with NMDA Receptors and AMPA Receptor-containing vesicles. This is the basic mechanism of memorization.
Specifically, as electric potential of the postsynaptic neuron rises, Calcium ions enter through Ligand-Gated Ion Channels with NMDA Receptors among the phospholipid bilayer, Calcium ions activate protein kinases (a kind of enzymes), AMPA Receptor-containing vesicles' Ligand-Gated Sodium Channels move to the postsynaptic neurons' phospholipid bilayer, and Sodium ion inflow is amplified. This instantaneous capacity amplification is called "E-LTP (early-form long time potentiation)," while this could be basically same as Short-Term Memorization, which is generated instantly.
In addition, activated some protein kinases encourage unspecified protein synthesis mechanism to create additional Ligand-Gated Sodium Channels near the Ligand-Gated Cation (positive ion) Channel with NMDA Receptor after several hours. This time-consuming additional creation would contribute to lomg-term improvement of transmission called "L-LTP (late long time potentiation)." Then the synapse becomes to be "Potentiated Synapse," where efficiency of transmission is enhanced.

More specifically, as mentioned above in (5) and (7), when glutamic acids are released from the presynaptic neuron, Ligand-Gated Sodium Channels with AMPA Receptor receive glutamic acids, the channels open, Sodium ions flow in. If the inflow is sufficient, the intracellular electric potential rises, then next to (8), the Magnesium ion is released from the NMDA Receptor as in [9]. Then when the NMDA Receptor receives a glutamic acid, the channel opens, various positive ions including Calcium ions pass through the channel as in [10], Calcium ions activate protein kinases, affinity between the postsynaptic neuron's phospholipid bilayer and vesicles' phospholipid bilayer rises, they fuse, AMPA Receptor-containing vesicles' Ligand-Gated Sodium Channels move to the postsynaptic neurons' phospholipid bilayer as in [11], and Sodium ion inflow is promptly amplified as E-LTP.







Next to [11], specifically then (9), (10), (11), and (12) are experienced and after a while, some activated protein kinases encourage unspecified protein synthesis mechanism, proteins are synthesized, additional Ligand-Gated Sodium Channels are created as in [13] as L-LTP. Thus the synapse becomes to be "Potentiated Synapse," where efficiency of transmission is enhanced. Dendrite spines could be formed in association with the creation.


Thus, efficiency of the transmission between neurons at specific synapses near Ligand-Gated Cation (positive ion) Channels with NMDA Receptors rises, this is the basic mechanism of memorization.
* "Long-Term Potentiation in Wikipedia" https://en.wikipedia.org/wiki/Long-term_potentiation
* "Short-Term Memory in Wikipedia" https://en.wikipedia.org/wiki/Short-term_memory
* "Protein Kinase in Wikipedia" https://en.wikipedia.org/wiki/Protein_kinase

2.5.3.2.3 Signal Inhibition through Inhibitory Chemical Synapses

As mentioned above, some Chemical Synapses inhibit other Chemical Synapses from transmitting signals. They are called Inhibitory Chemical Synapses. Inhibitory Chemical Synapses inhibit signals interfering with rise of intracellular Electric Potential Difference.
Like Excitatory Chemical Synapses, Inhibitory Chemical Synapses contains Neurotransmitters in the axon terminals of the presynaptic neurons. However, Neurotransmitters of Inhibitory Chemical Synapses are different from those of Excitatory Chemical Synapses such as glutamic acids. The Neurotransmitters of Inhibitory Chemical Synapses are GABA (gamma-aminobutyric acid), Glycine, and so on. They are called Inhibitory Neurotransmitters.
* "Gamma-Aminobutyric Acid in Wikipedia" https://en.wikipedia.org/wiki/Gamma-Aminobutyric_acid

Specifically, in ⑥, unlike in (6), the right axon terminal of the presynaptic neuron forms an Inhibitory Chemical Synapse allied with Ligand-Gated Chloride Channels. In this case, the Neurotransmitters of the right axon terminal are GABAs.
In ⑥, the left axon terminal just released the Neurotransmitters such as glutamic acids, Sodium ions flew in, the electric potential rose to a certain extent.

In ⑦, when electric charge in the cell body of the right presynaptic neuron become positive and Sodium ions reach the right axon terminal, Calcium ions (in orange) flow in, GABAs as (Inhibitory) Neurotransmitters are released, Ligand-Gated Chloride Channels receive GABAs, Ligand-Gated Chloride Channels open, Chloride ions (in blue) flow in. Since Chloride ions are negatively charged, the intracellular electric potential is reduced.

Then in ⑨, unlike (9), although the left Excitatory Chemical Synapse tried to send a signal, the postsynaptic neuron wouldn't send a signal (Fire) inhibited by the right Inhibitory Chemical Synapse.







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