Disclaimer: This is Untrue.
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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