NEUROMUSCULAR JUNCTION IT IS THE JUNCTION BETWEEN A
NEUROMUSCULAR JUNCTION
IT IS THE JUNCTION BETWEEN A MOTOR NERVE AND A MUSCLE FIBRE THROUGH WHICH THE NERVE CAN COMMUNICATE WITH MUSCLE
AXON TERMINAL SYNAPTIC VESICLES SYNAPTIC CLEFT MOTOR END PLATE SUBNEURAL CLEFT
AXON TERMINAL q Contains around 3, 000 vesicles which contain the neurotransmitters acetylcholine (Ach) SYNAPTIC CLEFT (20 – 30 nm) q Space between the axon terminal and muscle membrane q Contains the enzyme Cholinesterase which can destroy Ach
MOTOR END PLATE q Thickened part of the muscle membrane q Contains Ach receptors SUBNEURAL CLEFT q Muscle membrane of motor end plate is folded at places known as Subneural cleft (Junctional folds) q Increases the surface area
Nerve impulse reaches nerve terminal § Opening of voltage gated calcium channels § Calcium diffuses from the ECF into the nerve terminal § Release of Ach from the synaptic vesicles into the synaptic cleft by proces of Exocytosis §
§Binding of Ach with receptor, formation of Ach- receptor complex Opening of Ligand gated sodium channels § Entry of sodium ions into the ECF § Development of end plate potential ( EPP ) §
§ End plate potential triggers a muscle action potential. § The impulse spreads down into the muscle and makes it to contract.
After Ach acts on the receptors, it is hydrolyzed by the enzyme cholinesterase into Acetate and Choline § Choline is actively reabsorbed into the nerve terminal to be used again to form Ach § The whole process of Ach release, action and destruction takes about 5 – 10 ms §
MINIATURE END PLATE POTENTIAL Develops normally in the motor End Plate even in the absence of nerve impulse. Due to spontaneous release of small quantities of Ach from the nerve ending.
AGENTS AFFECTING NEUROMUSCULAR JUNCTION DRUGS THAT BLOCK TANSMISSION By inhibiting Ach release Eg: Botulinum toxin By Antagonizing Ach action By competitive inhibition Eg: Curariform drugs By persistant Depolarisation Eg: Succinylcholin DRUGS THAT INACTIVATE CHOLINESTERASES Eg: Neostigmine, Di – Isopropyl Flourophoshate
MYASTHENIA GRAVIS An autoimmune disorder caused by circulating antibodies that block Acetyl Choline receptors at the post synaptic membrane Inhibits the excitatory effects of neurotransmitter Acetyl Choline on Nicotinic receptors
FEATURES Rapid onset of fatigue. Generalized weakness of muscle. Most common affected muscles are Extraocular muscles, Facial muscles, Swallowing and muscles of Mastication In sever form, patient may die from paralysis of Respiratory muscles
LAMBERT - EATON SYNDROME Antibodies against calcium channels Reduced calcium influx and subsequent Ach release Neuromuscular transmission is affected with consequent muscular weakness
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