Neuromuscular junction is the is the synapse between axons of motorneurons and muscle.
Events occuring during Neuromuscular Transmission.
- when a action potential is produced in a axon it travels down towards the motor axon terminal.It depolarizes the presynaptic terminal that open Ca2+ channels and Ca2+ ions moves into the presynaptic terminal down it's electrochemical gradient.
- Ca2+ uptake causes release of ACh into the synaptic cleft by exocytosis.
- ACh diffuse to the postsynaptic membrane,ACh bind to it's receptors which opens ligand gated Na+ and Ka+ channels and Na+ influx occurs.
- Influx of Na+ causes local depolarization.The magnitude of depolarization produced is referred to as End Plate Potential(EPP).EPP is not a action potential,but a local depolarization.
- when the end plates depolarizes,local currents causes depolarization and action potential in the adjacent muscle tissue.
- ACh is degraded by acetylcholinestrase(AChE ) into acetyl CoA and choline on the muscle end plate.
Agents interfering Neuromuscular junction:
- Botulinus toxin-it blocks the release of ACh from presynaptic terminal.
- Curare-it binds with the ACh receptors on motor end plate.
- Neostigmine-it prevents the ACh degradation by inhibiting the AChE.
- Hemicholinium-blocks reuptake of choline into presynaptic terminal.
No comments:
Post a Comment