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Neuromuscular Junc.

Physiology and Pharmacology

QuestionAnswer
Role of neuromuscular junction Connects motor neurons to muscle. Controls fast and precise muscle contraction Skeletal muscles only receive impulses from one neuron at a time Converts electrical energy in the nerve to mechanical energy in the muscle 40 um long (same as a cell)
3 main areas of a NMJ Nerve terminal Apposition Post synaptic membrane
Apposition Contains the endplates (where nerves meet the muscle) Motor neurons make contact with 1 muscle fibre each to allow a coordinated response
How to study NMJ Can be studied in vitro as muscles cells are large so can easily be isolated. Can be studied by stimulating the motor axon and recording membrane depolarisation in the muscle fibre at two points to view changes in membrane potential
Measuring endplate potentials - Von Gersadorff 2008 In resting muscles you get endplate potentials - these are background and do not form an AP. When stimulated there is a small delay for the EPP to form before the AP is generated. Further down the axon there is no EPP formed, only AP is detected
Why not just use electrical signalling Impendence matching - the presynaptic current is not enough to charge the membrane capacitance of the much larger muscle cell We need chemical signalling to retrigger and AP
Evidence for chemical transmission Delay (>500us) between terminal activation and muscle response Motor axon terminals release acetylcholine upon stimulation Exogenous application of ACh excited muscle fibres Toxins including curare block neurotransmitter transmission so prevent APs
Structure of an end plate Folded membrane to form invaginations increase SA to allow maximal sensitivity in a small area. ACh receptors and Na channels are close together so small depolarisations at the receptors are transmitted to the channels.
Structure of ACh receptor 5 subunits with 2 being identical Spans the membrane 4 times Permeable to Na+, K+ and Cl- so acts as an ion channel
Stages of neurotransmitter release AP invades nerve terminal.VDCC opens Ca2+ enters terminal.Ca2+ binds to docking proteins-causes vesicle fusion with pre synaptic membrane.ACh diffuses across synapse to bind to receptor on post synaptic membrane Influx of Na+ depolarises muscle-forms EPP
Calcium dependence of neurotransmitter release Varied [Ca2+] in surrounding fluid. Linear relationship between [Ca2+]^4 and voltage of EPP. This suggests that 4 Ca2+ ions are needed to release one vesicle
Quantal nature of the NMJ Enough vesicles must be released in order for an AP to be generated. If not enough are released an end plate potential is seen with no corresponding AP
Why are NMJs the high fidelity synapse 3 factors must be suffice for an AP to be triggered: 1. Number of vesicles released 2. Quantal amplitude (release of neurotransmitter) 3. Release probability of neurotransmitter
The vesical cycle Neurotransmitter loading Clustering Docking at active zone Priming to allow release Fusion pore opening Then one of: Kiss and stay, Kiss and run or Reacidify and back to endosome
SNARE proteins Soluble NSF Attachment Protein Receptors Attached to vesicles, binds to syntaxin, changing its conformation to pull the vesicle to the membrane. 4 Ca2+ are needed to allow fusion pore opening and NT release. ATP is then used to allow the vesicle to bud
What happens to acetycholine After dissociation from the AChR, immediate hydrolysis of ACh ensures rapid termination of transmission > temporal precision of signal Broken down by acetylcholinesterase - constantly expressed so is present before binding to allow rapid termination
What happens after ACh is broken down Forms Choline and Acetyl CoA which are taken back up into the presynaptic neuron and recycled
Drugs and toxins affecting NMJ Dendrotoxin - affects K+ channels Botulism toxin - Cleaves SNARE proteins preventing NT release Physostigmine inhibits acetylcholinesterase, causing ACh build up and spasms Tetrodoxin - Inhibit Na+ channels, so prevent AP formation
Lambert-Eaton Myasthenic Syndrome Antibodies against pre-synaptic voltage gated Ca2+ channels prevent Ca2+ influx, depolarisation and ACh release Symptoms: Proximal arms and legs most effected. Most cases have an underlying maligancy e.g. small call lung cancer
Myasthenia Gravis IgG autoantibodies targeting post synaptic ACh receptors prevent ACh from binding. Symptoms:Eyelid drooping, swallowing difficulty (dysphagia), changes in speech (dysarthria and hypophonia) Babies with mothers affected are born with a temporary version
Effect of Myasthenia Gravis on post synaptic membrane Remodelling occurs. Less folds are present so less AChRs. This is difficult to treat as the remodelling is usually irreversible
How does malignancy cause LEM syndrome Immune surveillance leads to presentation of tumour derived antigens Leads to production of antibodies which respond to nearby healthy cells
Botulism Caused by a toxin produced by a bacterium. Causes constipation, floppy movements due to muscle weakness and paralysis. Common in honey, so should not be fed to babies.
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