title: Interaction of glutamate- and adenosine-induced decrease of acetylcholine quantal release at frog neuromuscular junction.
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 glutamate-mediated 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.
authors.affiliation: Third Surgical Department, First Faculty of Medicine, Charles University, Prague, Czech Republic.
authors.forename: S
authors.initials: S
authors.lastname: Adámek
authors.forename: A V
authors.initials: AV
authors.lastname: Shakirzyanova
authors.forename: A I
authors.initials: AI
authors.lastname: Malomouzh
authors.forename: N V
authors.initials: NV
authors.lastname: Naumenko
authors.forename: F
authors.initials: F
authors.lastname: Vyskočil
mesh_terms: D000109:Acetylcholine / Q000378:metabolism*; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000241:Adenosine / Q000494:pharmacology*; D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D015220:Calcium Channels / Q000502:physiology; D002217:Carbachol / Q000494:pharmacology; D018679:Cholinergic Agonists / Q000494:pharmacology; D002799:Cholinergic Fibers / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D019054:Evoked Potentials, Motor / Q000187:drug effects; D018698:Glutamic Acid / Q000494:pharmacology*; D006162:Guanylate Cyclase / Q000378:metabolism; D009045:Motor Endplate / Q000187:drug effects* / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism; D011895:Rana ridibunda; D017470:Receptors, Glutamate / Q000502:physiology
chemical_list: D015220:Calcium Channels; D018679:Cholinergic Agonists; D017470:Receptors, Glutamate; D009569:Nitric Oxide; D018698:Glutamic Acid; D000255:Adenosine Triphosphate; D002217:Carbachol; D006162:Guanylate Cyclase; D000241:Adenosine; D000109:Acetylcholine