NDLI: Early Postdenervation Depolarization Is Controlled by Acetylcholine and Glutamate via Nitric Oxide Regulation of the Chloride Transporter

Content Provider	Springer Nature Link
Author	Vyskočil, František
Copyright Year	2003
Abstract	Resting non-quantal acetylcholine (ACh) and probably glutamate (Glu) release from nerve endings activates M1- and NMDA receptor-mediated Ca$^{2+}$ 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.
Starting Page	575
Ending Page	585
Page Count	11
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	28
Issue Number	3-4
e-ISSN	15736903
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	2003-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Neurosciences Neurology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
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Early Postdenervation Depolarization Is Controlled by Acetylcholine and Glutamate via Nitric Oxide Regulation of the Chloride Transporter