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This document was created by Alex Yartsev ([email protected]); if I have used your data or images and forgot to reference you, please email me. THE NEUROMUSSCULAR JUNCTION - Action Potential - - Voltagegated Ca++ channel Nicotinic Acetylcholine receptor - An axon of a motor neuron loses its myelin as it approaches a muscle fiber It divides into several terminal boutons, or “endfeet”, which contain acetylcholine The endfeet fit into folds of the thickened MOTOR END PLATE which is the part of the muscle fiber Only one fiber ends at one end plate; there is no convergence of input When an action potential arrives, ity triggers voltage gated calcium channels These channels activate the protein machinery (SNAPs , synaptosomal nerve associated proteins, and VAMPs, vesicleassociated membrane proteins) which drags the vesicles to the surface of the synapse The vesicles release acetylcholine The acetylcholine binds to the postsynaptic acetylcholine receptor The receptor becomes conductive to Na+ and K+ The current sink created by this brings the adjacent membrane to firing level The acetylcholine is rapidly degraded by acetylcholinestrase Acetylcholinesterase END PLATE POTENTIAL - The end plate contains about 15-40 million Ach receptors Each nerve impulse releases about 60 vesicles Each vesicle contains about 10,000 molecules of Ach This amount is about 10 times what you actually need to reach a full end plate potential QUANTAL RELEASE OF NEUROTRANSMITTER - The synapse RANDOMLY releases Ach at rest. This produces minute depolarizing spikes, each about 0.5 mV The size of the quanta varies DIRECTLY with the Ca++ concentration and INVERSELY with Mg++ concentration Something very similar seems to happen at all synaptic junctions MYASTHENIA GRAVIS: antibodies to the acetylcholine receptor LAMBERT-EATON SYNDROME: antibodies to the voltage-gated calcium channel