AI Article Synopsis
- Denervation in rat diaphragm fibers leads to lower resting membrane potential, increased input resistance, and heightened sensitivity to acetylcholine.
- Furosemide (1 X 10(-4) M) reduces the muscle membrane depolarization and acetylcholine sensitivity post-denervation, but does not stop changes in the muscle fiber's electrical properties.
- Chloride ions might act as intracellular messengers in regulating muscle membrane potential and sensitivity to acetylcholine, although they are not crucial for the overall neurotrophic regulation.
Article Abstract
A decrease in resting MP, increase in the input resistance, appearance of anode breakdown APs, and extrajunctional acetylcholine sensitivity following denervation were revealed in the rat diaphragm muscle fibres. Addition of 1 X 10(-4) M furosemide to the culture medium reduced the degree of post-denervation muscle membrane depolarization and of extrajunctional acetylcholine sensitivity, but did not prevent the changes in passive electrical properties and in firing level of the muscle fibre membrane. Chloride ions could serve as intracellular messengers responsible for the neurotrophic control of muscle membrane resting potential and membrane sensitivity to acetylcholine. The Cl- are not essential in neurotrophic regulation of the electrogenic properties of membrane.
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