In myasthenia gravis, what deficiency leads to early fatigue in skeletal muscles?

In myasthenia gravis, the primary issue is a deficiency or blockage of acetylcholine at the neuromuscular junction. This autoimmune disorder causes the body to produce antibodies that attack acetylcholine receptors, which impairs the ability of nerve impulses to stimulate muscle contraction. As a result, skeletal muscles experience weakness and fatigue, particularly during periods of activity. This leads to the characteristic early fatigue observed in individuals with the condition because their muscles are unable to receive the necessary signals to contract effectively.

The other neurotransmitters mentioned, such as serotonin, dopamine, and norepinephrine, do not play a direct role in the muscular effects seen in myasthenia gravis. Their functions pertain to other aspects of neurotransmission and brain function, but they are not responsible for the specific muscle fatigue associated with this autoimmune disorder.