Which neurotransmitter is primarily affected in Myasthenia Gravis?

Myasthenia Gravis is a chronic autoimmune neuromuscular disorder characterized by weakness and rapid fatigue of voluntary muscles. The primary neurotransmitter affected in this condition is acetylcholine. In Myasthenia Gravis, the body's immune system mistakenly creates antibodies that block or destroy the receptors for acetylcholine at the neuromuscular junction. This interference prevents acetylcholine from effectively binding to its receptors, which is necessary for muscle contraction. As a result, the transmission of nerve impulses to the muscles is impaired, leading to muscle weakness.

The rationale for choosing acetylcholine is rooted in its critical role in muscle activation. Acetylcholine is released from motor neurons and binds to receptors on muscle fibers to initiate contraction. Without adequate binding due to receptor blockage, muscle weakness ensues, which is the hallmark of Myasthenia Gravis. Understanding this mechanism is essential for grasping the nature of the disorder and its symptoms, which typically include muscle weakness that worsens after periods of activity and improves after rest.