Author:
Adámek S,Shakirzyanova AV,Malomouzh AI,Naumenko NV,Vyskočil F
Abstract
In a frog neuromuscular preparation of m. sartorius, glutamate
had a reversible dose-dependent inhibitory effect on both
spontaneous miniature endplate potentials (MEPP) and nerve
stimulation-evoked endplate potentials (EPP). The effect of
glutamate on MEPP and EPP is caused by the activation of
metabotropic glutamate receptors, as it was eliminated by MCPG,
an inhibitor of group I metabotropic glutamate receptors. The
depression of evoked EPP, but not MEPP frequency was removed
by inhibiting the NO production in the muscle by L-NAME and by
ODQ that inhibits the soluble NO-sensitive guanylyl cyclase. The
glutamate-induced depression of the frequency of spontaneous
MEPP is apparently not caused by the stimulation of the NO
cascade. The particular glutamate-stimulated NO cascade
affecting the evoked EPP can be down-regulated also by
adenosine receptors, as the glutamate and adenosine actions are
not additive and application of adenosine partially prevents the
further decrease of quantal content by glutamate. On the other
hand, there is no obvious interaction between the glutamatemediated inhibition of EPP and inhibitory pathways triggered by
carbacholine and ATP. The effect of glutamate on the evoked
EPP release might be due to NO-mediated modulation
(phosphorylation) of the voltage-dependent Ca2+ channels at the
presynaptic release zone that are necessary for evoked quantal
release and open during EPP production.
Publisher
Institute of Physiology of the Czech Academy of Sciences
Subject
General Medicine,Physiology
Cited by
10 articles.
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