Agents Affecting NM Transmission

i) Botulinum toxin : block release of Ach

ii) Curare : Competes with Ach for receptors

iii) Neostigmine : Anticholinesterase prolongs the action of Ach

iv) Hemicholinium : blocks reuptake of choline into presynapticterminal

Myasthenia gravis: It is caused by the formation of circulating antibodies to nicotinic acetylcholine receptors present on the muscle. These antibodies destroy some of the receptors and bind others to neighboring receptors, triggering their removal by endocytosis.

Lambert—Eaton Syndrome: In this condition, muscle weakness is caused by an autoimmune attack against one of the Ca+2 channels in the nerve endings at the neuromuscular junction.

Tetanus toxin, which is produced by the bacterium Clostridium tetani, can result in tetany throughout all the skeletal muscles of the body (toxin travels to the spinal cord where it blocks inhibitory nerves, allowing the excitatory motor neurons to fire rapidly. Rapidly firing motor neurons summate to produce tetany).

Denervation hypersensitivity or supersensitivity: When the motor nerve to skeletal muscle is cut and allowed to degenerate, the muscle gradually becomes extremely sensitive to acetylcholine.

Neurotransmitters and neuromodulators are divided into two major categories:

  • Small-molecule transmitters (monoamines, catecholamines, and amino acids) and large-molecule transmitters (neuropeptides).
  • Monoamines include acetylcholine, serotonin, and histamine. Catecholamines include norepinephrine, epinephrine, and dopamine. Amino acids include glutamate, GABA, and glycine.

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