Action of NMDA receptors agonists on amplitude of miniature endplate potentials in PRiMA and ColQ genes knockout mice

Abstract

Previously it was shown that activation of NMDA receptors at neuromuscular junction can enhance nitric oxide (NO) production. NO, in turn, able to inhibit synaptic acetylcholinesterase activity and increases amplitude of synaptic responses In this study we tested a hypothesis that molecular form of acetylcholinesterase anchored in plasma membrane could be more sensitive to endogenous NO inhibition than molecular form of acetylcholinesterase located on basal lamina Experiments were performed on extensor digitorum longus of (-/-) PRiMA, (-/-) ColQ and wild type mice Miniature endplate potentials were recorded using standard microelectrode technique. After application of NMDA receptors agonists (glutamate and glycine) amplitude and decay time of miniature endplate potentials did not change in synapses of PRiMA or ColQ knock-out mice. Obtained results show that nitric oxide production owing to the activation of enzyme NO-synthase, which is initiated by glutamate mediated excitation of synaptic NMDA receptors, does not affect selectively one of molecular forms of acetylcholinesterase

Keywords

NMDA receptor / glutamate / nitric oxide / acetylcholinesterase / neuromuscular synapse

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