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Chemical Synaptic Transmission 1 (11) - Coggle Diagram
Chemical Synaptic Transmission 1 (11)
Transmission at typical chemical synapse
pre synaptic neurone - signal arrives
post synaptic neurone - signal recieved
glial cells - surround synapses and have role in supporting transmission
neurotransmitter is synthesised, packed into synaptic vesicles, released into the synaptic cleft, response occurs from post synaptic cleft, neurotransmitter must be removed, if neurotransmitter stays for too long, transmission won't work properly
Neurotransmitters
must be present at the synapse
must be released in response to the appropriate stimuli
specific post-synaptic receptors must be present
Structure of the mammalian neuromuscular junction
it is large, accessible, simple
nerve terminal has many mitochondria to provide energy to support neurotransmitter release, restoring ion gradients after activity, neurotransmitter synthesis and packaging, vesicle recycling and calcium handling
synthesise 2. loading onto vesicles 3. pre-synaptic action potential, terminal depolarisation, VGCC opening, calcium influx, calcium induced vesicle fusion and transmitter exocytosis 4. transmitter binding to postsynaptic receptors, postsynaptic channel opening or closing, ion flux, current flow, modulation of postsynaptic cell excitability, synaptic deactivation by transmitter removal or enzymatic degradation and vesicular recycling
Synthesis
enzyme that catalyses synthesis of acetylcholine is choline acetyl transferase
choline and acetyl coA are catalysed by ChAT to form ACh
ChAT is synthesised in the cell body and transported to the synapse by slow axonal transport (0.5 to 5mm per day)
Packing
ACh is package into vesicles by the vesicular acetylcholine transporter, this concentrates ACh in the vesicle (about 10,000 molecules per vesicle) by exchanging for vesicular H+
Release
calcium dependent process
vesicles are held close to the membrane by snare proteins
when calcium channels open, calcium enters the cell, a conformational change occurs in the snare proteins, the proteins pull the vesicle towards the membrane
sodium is required for AChR release
tetrodotoxin prevents an AP from being generated in the motorneurone by blocking voltage gated sodium ion channels, thus blocking AP dependent release of ACh from the terminal
Calcium
transmitter release is dependent on the entry of calcium via voltage-gate calcium channels
vesicle docks, snare complexes form to pull membranes closer together, entering calcium binds to synaptotagmin, calcium bound synaptotagmin catalyses membrane fusion by binding to snares and the plasma membrane
botulinum toxins lead to muscle weakness and paralysis by cleaving snare proteins that control exocytosis
if you artificially increase the voltage of the presynaptic cell, there is an influx of calcium ions
Response
there are acetylcholine receptors in the postsynaptic membrane made of five subunits
when ACh binds, a conformation change happens, this makes it permeable to ions, sodium, and potassium, sodium first flows into postsynaptic cell, becomes more positive
Remove
nmj acts with a high safety factor because sustained activation of the synapses is required
synaptic deactivation by transmitter removal or enzymatic degradation using acetylcholinesterase, choline is taken back up by the presynaptic neurone, process is extremely fast
high safety factor leads to sustained tetanic (full strength) muscle contraction
Quantal theory
cells release neurotransmitter in discrete quanta rather than in a continuous flow
1 quantum is the contents of 1 synaptic vesicle, postsynaptic responses are built from sums of these units
Molecular machinery mediating vesicle endocytosis
clathrin attaches to the vesicle membrane aided by adaptor proteins, polymerisation of clathrin causes membrane curvature and eventual pinching off of the vesicle by dynamin, clathrin is then stripped off by Hsc-70/auxilin and the synaptic vesicle is generated