ABSTRACT
L-glutamate released from the motor nerve terminal seems to be involved in the maintenance of resting potential (RP) in skeletal muscles via the N-methyl-D-aspartate (NMDA)-activated influx of Ca2+ to the cytoplasm with subsequent activation of NO-synthase and production of the NO which could act as a messenger providing the control of the membrane ion-transporting proteins.
Subject(s)
Glutamic Acid/pharmacology , Muscle Fibers, Skeletal/drug effects , Neurotransmitter Agents/pharmacology , Animals , Diaphragm/innervation , In Vitro Techniques , Male , Membrane Potentials/drug effects , Membrane Potentials/physiology , Microelectrodes , Muscle Denervation , Muscle Fibers, Skeletal/physiology , Rats , Receptors, N-Methyl-D-Aspartate/drug effects , Receptors, N-Methyl-D-Aspartate/physiologyABSTRACT
The early postdenervation depolarization of rat diaphragm muscle fibres (8-10 mV) is substantially smaller (3 mV) when muscle strips are bathed with 1 mM L-glutamate (GLU) or N-methyl-D-aspartate (NMDA). The effects of GLU and NMDA are not seen in the presence of aminophosphonovaleric acid (APV), a blocker of NMDA-subtype of glutamate receptors, 5 mM Mg2+ (which blocks NMDA-controlled ion channels) and L-nitroarginine methylester (NAME), an inhibitor of NO-synthase. This indicates that NMDA-subtype of GLU receptors might be involved in the regulation of the membrane potential in muscle fibres, most probably through the NO-synthase system.
