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Renin Angiotensin Mechanism.

Neuromuscular Junction (NMJ).

 Neuromuscular Junction (NMJ).

Introduction:

  • The neurons attached to skeletal muscles are “Somatic Motor Neurons” and are responsible for their contraction.

  • NMJ is a synapse (Small gap) present between the motor neuron and skeletal muscle.

  • The space of the synapse is called synaptic cleft and contains various enzymes responsible for neurotransmitter breakdown.

  • At the NMJ the axon of the motor neuron terminates into many synaptic end bulbs.

  • The synaptic end bulbs contain a special chemical called “Neurotransmitter” contained in vesicles, here in case of the NMJ it is AcetylCHoline (Ach).

  • When the action potential reaches synaptic end bulbs the neurotransmitter vesicles are emptied in the synaptic cleft.

  • The region opposite of the synaptic end bulb is Sarcolemma (muscle cell membrane) of the skeletal muscle fiber, it is called “Motor End Plate”.

  • Each motor end plate contains  million Ach receptors.

  • Hence NMJ contains Synaptic End Bulbs of Motor Neurons on one side and Motor End Plate of the Skeletal Muscle Fiber on the other end, both are separated by Synaptic cleft.

Generation of Muscle Action Potential.

  • The impulse or message of muscle contraction is called an action potential.

  • The skeletal muscles being voluntary in nature the impulses for the muscle contraction are sent by the brain.

  • This journey of the muscle action potential is can be summarized into the following steps,

    1. Release of AcetylCholine.

    2. Activation of the Ach receptors.

    3. Production of the muscle action potential.

    4. Termination of the Ach activity.

  1. Release of AcetylCholine:

  • The impulse from the brain reaches the terminal end of the axon of the motor neuron.

  • This impulse cause release of the neurotransmitter i.e. AcetylCholine (Ach) in the synaptic cleft by exocytosis.

  • The released Ach diffuses to its receptors present on the Motor end plate on the other side of the synapse.

  1. Activation of the Ach receptors:

  • The Ach attaches with the Ach receptors present on the Motor End Plate and causes opening of Ion Channels.

  • The opening of ion channels causes influx of the Na+ ions inside the muscle cell.

  1. Production of the muscle action potential:

  • The influx of the Na+ ions inside the muscle cell increases positive charge on the muscle cell.

  • This change in membrane potential generates the action potential for the muscle contraction.

  • The generated action potential spreads along the sarcolemma.

  • This causes the sarcoplasmic reticulum to release stored Calcium ions (Ca++) in the sarcoplasm and the muscle contraction starts.

  1. Termination of the Ach activity:

  • The synaptic cleft contains an enzyme “Acetylcholine Esterase (AchE)” which causes breakdown of Ach into acetic acid and Choline.

  • When Ach dissociates from the receptor it gets metabolized by the AchE in the synaptic cleft hence terminating the action of the Ach.

  • The AchE also breaks down the excess of Ach released by the neuron.

  • The increased activity of AchE is one of the causes of Myasthenia gravis.

  • The breakdown product Choline is collected by the synaptic end bulbs and is used to produce Ach again.

Commonly Asked Questions.

  1. Write a note on Neuromuscular Junction.
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