[Postsynaptic metabolic monoamine modulation of effects mediated by NMDA glutamate receptors in spinal motoneurons of the frog].

Monoamines, their agonists and antagonists have been investigated for their influence on responses of spinal motoneurons in frog mediated by NMDA-glutamate receptors (late components of dorsal root polysynaptic EPSP's and depolarizing responses evoked by L-aspartate). Monoamine responses which promoted an increase of intracellular concentration of cAMP and Ca2+ in the motoneurons (activation of alpha- and beta-adrenoreceptors, D1-dopamine and 5-hydroxytryptamine-receptors) reinforced the studied spinal motoneuron responses of frog. These responses were weakened by the monoamine action which led to a decrease of the intracellular concentration of cAMP and Ca2+ (activation of D2-dopamine and 5-hydroxytryptamine1A-receptors). The monoamine effects were inhibited by specific monoamine antagonists, tolbutamide and trifluoperazine. It is supposed that NMDA receptor-channel complex is exposed by cAMP- and Ca(2+)-calmodulin-dependent phosphorylation induced by activation of membrane monoamine receptors.