This page is the first part of a study of the article :
Is plasticity of synapses the mechanism of long-term memory storage? By Wickliffe C. Abraham, Owen D. Jones and David L. Glanzman
In this paper, several mechanisms that may be the key to long term storage are presented in an attempt to understand the process of human memory and especially the storage of information in the brain. This first part is about how LTP works.
Changes in synapses
The changes that happen to synapses are either strengthening or weakening changes.
Strengthening changes are called Long term potentiation (LTP) in which case, the connection between the two cells becomes more efficient and the electric signals, used for many cell to cell communications, are passed on more smoothly.
Synapse
the connection between two neurons or a neuron and another cell where molecules are passed on to send a signal
For invertebrate animals, this is called Long term facilitation (LTF) though we will mostly focus on LTP and LTD.
Weakening changes, called Long term depression (LTD) on the other hand do the opposite and the communication becomes less efficient leading to nearly nonexistent synapses in extreme cases.
These two types of plasticity are closely linked to memory storage and studied by high frequency electrical stimulations of a pathway in the brain or by repeating the pairing of pre and postsynaptic neuron firings.
These are thought to simulate the learning experience in the real world.
The repeated pairing of neuron firing induces LTD or LTP based on the timing of the activation of each cell. LTP occurs when the presynaptic neuron fires before and LTD occurs when the postsynaptic neuron fires after.
There are several other factors in the induction of these states.
One is called metaplasticity.
Metaplasticity
This is when a certain activity in the past causes the synapse to be more or less susceptible to LTP or LTD.
Neuromodulators can also direct a synapse towards one of the two states independently to the traditional routes which usually require an NMDA receptor.
Neuromodulator
molecules that act on neurons in a way similar to both neurotransmitters and hormones
NMDA receptor
=N-Methyl-D-aspatate receptor
an ionotropic glutamate receptor involved in most kinds of synaptic plasticity
Receptors are chemical structures found on or in cells that react to specific molecules.
In neurons, they bind to neurotransmitters to create an electric signal activating or blocking the neuron
The receptors
LTP and LTD, found throughout the brain and nervous system, can be triggered by many receptors.
They can be triggered by both ionotropic receptors
Ionotropic receptors
a receptor that forms an ion channel that opens or closes in reaction to a molecule/ neurotransmitter
A.K.A. ligand gated ion channels
and metabotropic receptors.
Metabotropic receptor
A receptor that is on the membrane of a cell that in reaction to a neurotransmitter will cause certain activities inside, such as activate enzymes or proteins.
a GPCR ( G-protein-coupled-receptor.
GPCRs are receptors on the membrane made of seven segments that will release a G protein in response to a molecule binding to it. This protein acts on other proteins and enzymes.
The most studied one is the NMDA receptor which creates an ion channel for calcium ions .
Ion channel
a structure that lets specific ions go through them.
This changes the electrical charge of the cell that becomes a signal
GABAergic synapses have been found to have a high plasticity, which means they can easily change.
GABA is often found in interneurons and being an inhibitory neurotransmitter, it can block the activation of the latter neuron to block the message from getting passed on.
GABA
Gamma Amino butyric acid
The most common inhibitory neurotransmitter, meaning it blocks neurons receiving GABA from transmitting a signal
Interneuron
neurons that don’t receive sensory information or send a message to a muscle, they relay the message between the sensory neurons and motor neurons
Other types of neurons are Sensory neurons that receive sensual information such as vision, touch, smell… and Motor neurons that send a signal to muscle cells to contract or relax to create a movement
This would mean inhibition of emotions or movements, thoughts can be strengthened or weakened by experience.
LTP in this kind of neuron would lead to a certain message to be rarely passed on.
This high plasticity is thought to be mostly to maintain a precise timing for neuronal firing by keeping a balance between excitatory signals and inhibitory signals.
The stages of LTP
LTP is said to work in 3 stages for the storage of information. These 3 stages depend on its duration.
The 1 st stage is called early LTP or LTP1. This one lasts for several hours and no longer.
The next stages are both included in what is called late LTP.
Late LTP depends on the synthesis ( creation ) of new proteins, something early LTP doesn’t have.
The first part is LTP2, which doesn’t need or use transcription and synthesises proteins from existing mRNA. The mechanism that creates the proteins is found in the synapto-dendritic compartments.
Transcription
a process in which DNA gets copied onto RNA before being decoded to create proteins in the next process called translation
mRNA
the RNA that is created during transcription
Dendrite
The terminal on neurons that receive neurotransmitters.
The terminals that send are called axons
Then comes LTP3 which depends on transcription and modifies genes and proteins.
Which stage a synapse goes to is determined by the stimulation it received.
However, a synapse that was only stimulated to early LTP can reach late LTP in a specific case.
This is called the synaptic tag and capture hypothesis (STC).
In this hypothesis, weakly stimulated synapses can set tags that will capture proteins produced by the late LTP of surrounding neurons to reach the late stages.
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