Influence of the Activation of NMDA Receptors on the Resting Membrane Potential of the Postsynaptic Cell at the Neuromuscular Junction

Abstract

Impaired function or insufficient expression of glutamate N-methyl-D-aspartate (NMDA) receptors underlies a number of brain pathologies; these receptors are, therefore, regarded as a pharmacological target for many neuroactive drugs. It was shown that in the CNS, this type of glutamate receptors participate in the processes of neuronal excitation, synaptic plasticity [1, 2], and excitotoxicity in neurodegenerative diseases and are also involved in the pathogenesis of epilepsy and seizures. However, until recently, the presence and activity of NMDA receptors beyond the CNS had never been considered. This research shows that activation of NMDA receptors at the mammalian neuromuscular junction alters the resting membrane potential of the postsynaptic cell evoked by cation entry through the receptor-associated channel.

Neuromuscular recovery from botulism involves multiple forms of compensatory plasticity

“…Considering the speed of RMP reduction after BoNT/A intoxication, local signaling mechanisms that are independent from transcription may contribute to changes in RMP. In denervated rat diaphragms, RMP is modulated by the loss of glutamatergic and cholinergic anterograde signaling ( Urazaev et al, 1995 , 1997 ; Proskurina et al, 2018 ), and recent work has identified a pathway by which AChRs directly modify RMP through altering Na,K-ATPase pump activity ( Krivoi et al, 2006 ; Heiny et al, 2010 ; Kravtsova et al, 2016 ). More work is needed to determine the functional consequences of these changes on muscle excitability.…”