Myasthenia gravis (MG) is an autoimmune disorder affecting which receptors?

Myasthenia gravis (MG) is primarily characterized by the body's immune system producing antibodies that attack acetylcholine receptors located at the neuromuscular junction. This autoimmune response decreases the effectiveness of acetylcholine, a neurotransmitter responsible for stimulating muscle contraction. As a result, individuals with MG experience varying degrees of muscle weakness and fatigue, particularly after periods of activity.

The role of acetylcholine receptors is central to the condition because they are essential for transmitting signals from nerves to muscles. When these receptors are blocked or destroyed by antibodies, muscle contractions become less effective, leading to the hallmark symptoms of the disease. This specific targeting of acetylcholine receptors distinguishes myasthenia gravis from other disorders affecting different types of receptors, such as beta-adrenergic, dopamine, or GABA receptors. Understanding this mechanism is crucial for recognizing the clinical manifestations and treatment approaches for myasthenia gravis.