What is primarily disrupted in the neuromuscular junction in Myasthenia gravis?

In Myasthenia gravis, the primary disruption at the neuromuscular junction involves a deficiency in acetylcholine receptors. This condition is characterized by an autoimmune response in which antibodies target and bind to the nicotinic acetylcholine receptors on the postsynaptic membrane of the muscle. As a result, the number of functional acetylcholine receptors decreases.

This deficiency impairs the ability of acetylcholine, released from the presynaptic motor neuron, to effectively stimulate muscle contraction. With fewer receptors available, the muscle fibers do not receive adequate signals despite normal release of acetylcholine, leading to weakness and rapid fatigue of the skeletal muscles.

Understanding this mechanism is crucial because it highlights the importance of acetylcholine in neuromuscular transmission and the specific role that receptor availability plays in muscle function. This explanation underscores the pathophysiology behind the symptoms experienced by individuals with Myasthenia gravis.