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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