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Muscle NMDA receptors regulate the resting membrane potential through NO-synthase
A K Urazaev1, S T Magsumov, G I Poletayev
1Kazan Medical University, Russia.
Physiological Research
|January 1, 1995
Summary
L-glutamate and NMDA significantly reduce postdenervation depolarization in rat muscle fibers. This effect, mediated by NMDA-subtype glutamate receptors and NO-synthase, suggests a role in regulating muscle fiber membrane potential.
Area of Science:
- Neuroscience
- Muscle Physiology
- Cellular Signaling
Background:
- Denervation of skeletal muscle leads to early postdenervation depolarization.
- The precise mechanisms regulating this depolarization are not fully understood.
Purpose of the Study:
- To investigate the role of L-glutamate (GLU) and N-methyl-D-aspartate (NMDA) in modulating postdenervation depolarization of rat diaphragm muscle fibers.
- To explore the involvement of NMDA-subtype glutamate receptors and NO-synthase in this process.
Main Methods:
- Measurement of muscle fiber membrane potential in rat diaphragm.
- Application of L-glutamate (GLU) and N-methyl-D-aspartate (NMDA) to muscle strips.
- Use of specific antagonists: aminophosphonovaleric acid (APV) and L-nitroarginine methylester (NAME).
- Inclusion of Mg2+ to block NMDA-controlled ion channels.
Main Results:
- Early postdenervation depolarization (8-10 mV) was reduced to 3 mV in the presence of 1 mM L-glutamate or NMDA.
- The effects of GLU and NMDA were abolished by APV, Mg2+, and NAME.
- This suggests that NMDA-subtype glutamate receptors and NO-synthase are involved.
Conclusions:
- NMDA-subtype glutamate receptors play a role in regulating the membrane potential of muscle fibers.
- The NO-synthase system is likely involved in the mechanism by which these receptors modulate membrane potential.
- These findings shed light on the neurochemical regulation of muscle excitability after denervation.