Myasthenia gravis is a chronic autoimmune neuromuscular disease that causes weakness and rapid fatigue and results from disrupted communication between nerves and muscles. With myasthenia gravis, antibodies block or destroy muscle receptor sites for the neurotransmitter acetylcholine, so the muscles receive fewer signals that prevent the muscles from contracting. This is likely the result of an enlarged thymus, which seems to be the case with many myasthenia gravis patients. The antibodies can also block the function of muscle-specific receptor tyrosine kinase, which resides in the nerve-muscular junction. Other symptoms of myasthenia gravis include droopy eyelids, and difficulty speaking, swallowing, chewing, and creating facial expressions.
Finding suggests cannabis limits acetylcholine degradation by inhibiting the enzyme acetylcholinesterase, thereby facilitating muscle and nerve communication. When cannabis inhibits this enzyme, acetylcholine has time to interact with its receptor before its breakdown, thereby overcoming the blocked receptor and causing muscle contractions. Cannabis consists of many cannabinoids that can demonstrate this effect, like THC, CBD, and CBN. Interestingly enough, it does not appear that cannabis' effects on enzymes and neurotransmitters is the result of its interactions with CB1 and CB2 receptors in the endocannabinoid system. This leaves much to be desired when it comes to cannabis and the mechanism responsible for its ability to inhibit enzymes and facilitate the interaction between muscle and nerve communication.
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