In humans, of course.

You seem to have lots of questions. Not to be a complete a**, but the answers to your questions can be found relatively easy using Google.

 

Nevertheless: you have to look up neuromuscular neurotransmission in order to get this, or else I might answer your question, with the risk of you merely accepting my answer, not giving it thoughts and basically not understanding it (because I'm not going to explain the whole neuromuscular neurotransmission system, lots of (online) sources are doing that just fine).

 

Anyways, I'm not a heartless bastard. I've marked things you certainly do have to look up yourself in bold.

 

Neurons at neurmuscular junctions (cf. synapse between motoneuron and its target muscle cell) release acetylcholine (ACh), which binds to its receptor (AChR), here of nicotinic type (nAChR) (which means activation of the receptor it is also potentiated by nicotine). The receptor is an ion channel coupled receptor, coupled to an non-specific ion channel. Once activated, the channel opens and sodium (Na) flows into the cell, potassium (K) flows out of the cell, but to a much less extent, resulting in a net positive ion influx, resulting in a depolarization of the cell (membrane). Needless to say what a depolarization of a muscle cell will do to that cell. Please, look up how this happens.

 

Myasthenia gravis is an autoimmune disease in which antibodies attack own AChRs, leaving it impossible (or much less possible) for motoneurons to activate muscle cells.

 

I might also explain the therapeutic place of drugs targeting (inhibiting, more specifically) acetylcholinesterase in patients with myasthenia gravis, but then I'd need you to look up the function of acetylcholinesterase, and think for yourself why inhibiting this enzyme will be somewhat beneficial for pts with myasthenia gravis.

Edited August 6, 20169 yr by Function