Final answer:
The problematic neurotransmitter in myasthenia gravis (MG) is acetylcholine, as it's the target of autoimmune antibodies that block, alter, or destroy its receptors at the neuromuscular junction, leading to muscle weakness.
Step-by-step explanation:
The neurotransmitter that is problematic in myasthenia gravis (MG) is acetylcholine. MG is characterized by weakness and rapid fatigue of any of the muscles under your voluntary control. It is caused by an error in the transmission of nerve impulses to muscles. Normally, when electrical signals or impulses travel down a motor nerve, the nerve endings release acetylcholine.
Acetylcholine travels from the nerve ending and binds to acetylcholine receptors on the muscle, which leads to muscle contraction. In MG, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction which prevents the muscle from contracting. This is why acetylcholine is considered problematic in MG.