Presynaptic inhibition of glutamatergic synaptic transmission to rat motoneurons by serotonin

摘要: 1. In a brain stem slice preparation, we recorded glutamatergic excitatory postsynaptic currents (EPSCs) in hypoglossal motoneurons (HMs) evoked by extracellular stimulation the reticular formation just ipsilateral to motor nucleus (n. XII). Serotonin (5-HT) inhibited synaptic transmission dose-dependent fashion as indicated reduction EPSC (eEPSC) peak amplitude 46 +/- 2% (mean SE, n = 26) of control (5-HT 10 microM). This effect was not voltage dependent, eEPSC reversal potential altered (n 5). Additionally, 5-HT decreased rate rise 41 14). Blockade N-methyl-D-aspartate-receptor-channels D(-)-2-amino-5-phosphonopentanoic acid (50 microM) or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate receptor-channels 6,7-dinitro-quinoxaline (20 did alter relative 7 and 3, respectively). 2. presence tetrodotoxin (1 microM), bath application reduce glutamate elicited pressure ejection L-glutamate mM) onto HMs 5), it increased median interevent interval spontaneous miniature EPSCs (mEPSCs) 178 12% 4), suggesting that acts presynaptically probability vesicle release. mEPSC slightly three four cells (median 92 3% control). 3. The specific 5-HT1B receptor agonist [3-(1,2,5,6-tetrahydropyrid-4-yl)pyrrolo[3,2-b]pyrid-5-one] mimicked its on eEPSCs (eEPSC reduced 31 5% control; 40 4% control, 5, respectively) mEPSCs 231 36% 102 5-HT-mediated inhibition blocked coapplication 1-(2-methoxyphenyl)-4-[4-(2-phthalimido) butyl] piperazine hydrobromide 5-HT1A antagonist, 3-[2-[4-(4-flurobenzoyl)-1-piperdinyl]ethyl]-2,4(1H,3H)-quin azolinedione tartrate 5-HT2A/2C antagonist 4). These data indicate is primarily mediated. 4. We conclude 5-HT, acting through presynaptic receptors, inhibits reducing