This document contains a summary of the lecture 4 and book of the course the adaptive brain. This summary is about chapter 6 in the book Neuroscience by Purves.
Summary of Purves Chapter 22: Early Brain Development
Samenvatting Fundamentals of Neuroscience, UvA
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Vrije Universiteit Amsterdam (VU)
Neuroscience minor
The Adaptive Brain
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Neurotransmitters chapter 6
Learning objectives Acetylcholine
• You can explain what the difference is between ionotropic and Acetylcholine is released by neuromuscular junctions and works
metabotropic neurotransmitter receptors and you can explain on the skeletal muscles (contractions), smooth muscle cells (heart
their function muscle relaxation), and also on the salivary glands. The ruffled
• You can name the different classes of neurotransmitters and structure of the motor end plate makes the area for the fusion
explain their main function in the brain of neurotransmitters bigger. Acetylcholine is synthesised out of
• You can analyse the action of different drugs or poisons on the choline and acetyl-CoA of the Krebs cycle and locally
nervous system concentrated in vesicles. Many cells can make acetylcholine which
is not specifically used, but it is used by a lot of neuronal cells.
Ionotropic neurotransmitters The signal is terminated by acetylcholinesterase.
These are ion channels that are operated by the presence of
neurotransmitters. They are often specific and only let through
certain ions and evoke an action potential. Sodium, potassium,
chloride and calcium determine the generation of an action
potential.
Neurotransmitter
Present =
Conductivity high
Acetylcholine and other small neurotransmitters are concentrated
in vesicles by H+ gradient-derived exchange molecules.
Metabotropic neurotransmitters
They use a secondary messenger system, such as the G-proteins. Nerve gas
Second messengers are molecules that amplify the signal and The breakdown of acetylcholine is essential. The nerve gas Sarin
trigger an intracellular response. Examples of second messengers or Novichok are acetylcholinesterase blockers. What these gasses
are cAMP, diacylglycerol, and calcium. Examples of cellular do is block the breakdown of acetylcholine, which causes a
responses are protein phorylation, gene transcription, and the continuous contraction of your muscles. This could have
opening of ion channels. When a neurotransmitter binds to this paralysing effects, but also the muscles that are used for
receptor, G-proteins get activated and dissociate from the breathing are affected in this way.
receptor. They can now interact with ion channels or bind to
other effector proteins such as enzymes that make intracellular Acetylcholinesterase blockers in Alzheimer’s therapy
messengers that open or close ion channels. Metabotropic In Alzheimer’s, the acetylcholine input in the central nervous
neurotransmitters are also called G-protien coupled receptors. system is decreased. Acetylcholinesterase blockers can be used
These receptors can trigger multiple pathways parallel! to keep acetylcholine, which is being released, intact. This way
the neurons are being maintained a little bit longer and
symptomatically treat Alzheimer’s symptoms. Though this therapy
does not last forever.
Nicotinic acetylcholine receptor
Amplification of neurotransmitter signals The nicotinic receptor is ionotropic and is comprised out of 5
subunits that make up the pore. When acetylcholine binds to
those subunits they start to rotate around their axis which
makes the pore domains point outward. This way the ions can
flow through. This is very typical for ionotropic receptors. The 5
subunits have different varieties of which you can build the
receptor, which can influence the affinity for certain substances
or could keep the pore open longer, which is important for
synaptic plasticity.
, Muscarinic acetylcholine receptor The ionotropic glutamate receptors depolarise neurons. The AMPA
This type of receptor is a metabotropic receptor/G-protein receptor has a large amplitude and stays open for a short time
coupled receptor. This is a 7 transmembrane receptor that can be and turns the synapse on and off immediately. The NMDA receptor
activated by exchange from GDP > GTP. There are also multiple is a little bit slower and stays open for a longer time. This type of
variants of this receptor but you cannot change the affinity of receptor is mostly used for synaptic plasticity where you have
this receptor. more long-term excitation. The kainate receptor opens quickly and
closes slowly (in the middle). This receptor plays a role mostly in
epilepsy.
The expression of these receptors determines the cellular
response of the cell. Neurotransmitters themselves do not contain
this information.
Excitotoxicity
Natural substances that affect ACh receptors When a blood clot forms in the brain it cuts off the blood supply
The ACh system is targeted by many natural poisons due to its to a certain area in the brain, which could lead to dying cells.
central role in neuromuscular junctions. When this concerns glutamatergic neurons, glutamate leaks into
• Tobacco plant, nicotinia tabacum, agonists ionotropic AChR the environment and will activate all sorts of neurons. Glutamate
• Fly amanita, Amanita muscaria, agonist for metabotropic AChR cannot be pumped away and there is too much glutamate present.
• α-bungarotoxin (snake venom), antagonist nicotinic receptor This in turn could lead to lipid and protein breakdown, and more
• Curare, plant extract C. Tomentosum, antagonist nicotinic apoptosis. When apoptosis is not controlled there will be more
receptor glutamate leaking out, which in turn could lead to a snowballing
• Atropine (belladonna), antagonist of the muscarinic receptor effect and leads to a huge cleft in the brain. Glial cells are
present in the brain to prevent this.
Glutamate
Glutamate is an amino acid that is present in every cell in your
body. Glutamate is concentrated in synaptic vesicles, which works
with the same mechanism as acetylcholine, but instead, uses a
VGLUT transporter that pumps in glutamate in exchange for H+.
The glutamate signal is terminated a little bit differently, they
depend on transporters, the excitatory amino acid transporter
(EAAT) that are located on glial cells. In these cells, the Ionotropic glutamate receptors
glutamate is first converted to glutamine and transported to the The AMPA and NMDA receptor has a similar structure compared
presynapse. Glutamine is converted into glutaminase in the to the nicotinic acetylcholine receptor, but are composed of
presynaptic cell. different proteins. Positively charged ions such as sodium (drives
depolarisation) bind to the AMPA receptor. The NMDA receptors
are opened by glutamate and depolarization. When glutamate binds
the pore does not open yet, there is a magnesium ion blocking the
flow of the ions through the pore. To open the pore, the cell
needs to be depolarised (become more positive) so the magnesium
can dissociate and the ions can flow through.
How you could test this in an experiment is
When you look at the current that goes
through the receptor and you compare
that to the potential difference in the
Glutamate neurotransmitter receptors membrane. Normal ion pores are linear.
• AMPA, NMDA, kainate: ionotropic receptors When the cell becomes more and more
• Metabotropic glutamate receptors (mGLuRs) negative it starts to attract more and more
Glutamate mediates excitatory input in the brain. The function is magnesium, and the flow of ions gets
to evoke an action potential in the postsynaptic cell. It is the on blocked (resting cells).
signal in the brain.
This is all related to synaptic plasticity
and LTP, which is the synaptic basis of
learning and memory.
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