title: Early postdenervation depolarization is controlled by acetylcholine and glutamate via nitric oxide regulation of the chloride transporter.
abstract: Resting non-quantal acetylcholine (ACh) and probably glutamate (Glu) release from nerve endings activates M1- and NMDA receptor-mediated Ca2+ entry into the sarcoplasm with following activation of NOS and production of NO. This is a trophic message from motoneurons, which keeps the Cl- transport inactive in the innervated sarcolemma. After denervation, the secretion of ACh and Glu at the neuromuscular junction is eliminated within 3-4 h and the production of NO in the sarcoplasm is lowered. As a result, the Cl- influx is probably activated by dephosphorylation of the Cl- transporter with subsequent elevation of intracellular Cl- concentration. The equilibrium Cl- potential becomes more positive and the muscle membrane becomes depolarized.
authors.affiliation: Institute of Physiology, Academy of Sciences of the Czech Republic, Vídenská 1083, Prague, Czech Republic. vyskocil@biomed.cas.cz
authors.forename: Frantisek
authors.initials: F
authors.lastname: Vyskocil
mesh_terms: D000109:Acetylcholine / Q000502:physiology*; D000818:Animals; D002352:Carrier Proteins / Q000502:physiology*; D002712:Chlorides / Q000378:metabolism*; D004594:Electrophysiology; D018698:Glutamic Acid / Q000502:physiology*; D009121:Muscle Denervation; D018482:Muscle, Skeletal / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism*
chemical_list: D002352:Carrier Proteins; D002712:Chlorides; D009569:Nitric Oxide; D018698:Glutamic Acid; D000109:Acetylcholine