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| Question | Answer |
| Motor unit | - Motor unit= motor nerve + the skeletal muscle fibres it controls - They are myelinated nerves originating in the nervous system - Control skeletal muscle movement - rapidly conducting - synapse with induvidual skeletal muscle fibres - Nerve comes together with muscle fibre at specialised junction; the neuromuscular junction |
| Neuromuscular junction structure - schwann cell forms lid over junctional cleft -membrane thrown into junctional folds to increase SA - acetylcholine diffuses through junctional cleft | |
| How drugs can modify synaptic (neuromuscular) transmission | - Presynaptically: interfering with the synthesis, storage and/or release of neurotransmitter - Postsynaptically (post junctionally); interfering with receptors and/or removal mechanism of the neurotransmitter |
| Key steps in neuromuscular transmission | 1. Action potential reaches motor neuron 2. Depolarisation of nerve terminal 3. Opening of voltage gated calcium channels 4. Calcium entry into nerve terminal 5. Release of acetylcholine into nerve terminal by exocytosis - diffusion of ach across cleft- 6. activation of nicotinic Ach receptors on muscle membrane (post synaptically) |
| Prejunctional events of neuromuscular transmission | - Choline taken in from outside the cell - Ach synthesised from choline and acetylcoenzyme A by the enzyme CAT (choline-acetyl-transferase) - Ach is stored in synaptic vesicles until it is released by exocytosis |
| Drugs acting prejunctionally to inhibit neuromuscular transmission | - Hemicholiniums: Plant toxins that block uptake of choline. Not clinically effective as too slow. - AH5183: blocks storage of Ach in vesicles. Not clinically effective as too slow. - Botulinium toxin; delays ach release as it destroys key proteins involved in exocytosis. |
| Post-junctional events in neuromuscular transmission | - Once released, Ach diffuses across junctional cleft, activating nicotinic Ach receptors on muscle membrane. - This release is caused by the action potential. - Most Ach is broken down by acetylcholinestherase before it even reaches the receptor |
| The nicotinic ach receptor | - Consists of 5 protein subunits around non-selective cation channels, permeable to Na+ and K+ - Activated by the agonist nicotine - the non-selective cation channel in the centre opens when 2 molecules of Ach bind to the protein complex; one to each subunit. - Opening channel results in depolarisation of the endplate region of the muscle membrane. This is an endplate potential. |
| Drugs acting postjunctionally to inhibit neuromuscular transmission | - reversible competitive antagonists; bind to nicotinic Ach receptor and block it. Have no efficacy so do not activate it. This prevents the channel being activated by ach. - Turbocurarine (posion darts) |
| Clinical uses of reversible competitive antagonists | - used alongside anaesthetics as muscle relaxants during surgery - Lasts about 10-15 minutes depending on drug - Patients cant breathe so must be artificially ventilated - Effects can be reversed by neostigmine |
| Depolarising muscle relaxants | - Only one clinical relevance; suxamethoneum - Acts as a agonist at nicotinic Ach receptors; activates receptor - Unlike Ach, is not broken down by AchE so lingers at the neuromuscular junction, causing prolonged depolarisation. - Used clinically for short duration muscle relaxation - Can be broken down by pseudocholinestherase, although this causes initial contraction of muscles (fasiculations) and post-op muscle pain. |
| Anticholinestherase drugs | - The enzyme cholinestherase can be inhibited by a number of drugs, including: - Neostigmine - Edrophonium - These drugs prevent the breakdown of Ach, increasing conc of neurotransmitter at the neuromuscular junction. - HOWEVER they do not reverse the actions of agents that have already depolarised the membrane. |
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