[Early post-denervation depolarization: effect of NO, acetylcholine and glutamate on chloride transporter].
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 motoneurones 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.
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Katedra fyziologie zivocichů a vývojové biologie. Prírodovĕdecká fakulta UK, Praha.
D000109:Acetylcholine / Q000502:physiology*; D000818:Animals; D002712:Chlorides / Q000378:metabolism*; D004594:Electrophysiology; D018698:Glutamic Acid / Q000502:physiology*; D017136:Ion Transport; D008564:Membrane Potentials / Q000502:physiology; D009121:Muscle Denervation; D018482:Muscle, Skeletal / Q000294:innervation*; D009569:Nitric Oxide / Q000502:physiology*
D002712:Chlorides; D009569:Nitric Oxide; D018698:Glutamic Acid; D000109:Acetylcholine