We tested the effects of microiontophoretic application of serotonin (5-HT) on the firing rate of neurons located in the gracile nucleus (GN) of rats. Application of 5-HT1A and 5-HT2 agonists and antagonists respectively mimicked/ modulated and blocked the effects produced by the amine, respectively. Among the tested neurons, 88.2% modified their background firing activity in the presence of 5-HT. Responsive neurons decreased their mean firing activity (MFA) in 56.7% of cases and increased it in the remaining 43.3%. To ascertain the specificity of the effects induced by 5-HT, we utilized 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) and alpha-methyl-5-hydroxytryptamine (α-MET-5-HT), agonists for 5-HT1A and 5-HT2 receptors, respectively. The microiontophoresis of 8-OH-DPAT modified the background firing rate of all GN neurons (100% of tested neurons) mimicking the decrease of MFA evoked by 5-HT. The application of a-MET-5-HT modified the MFA in 76.9% of tested neurons, decreasing it in 61.5% of cases and increasing in the remaining 23.1%. The decrease of MFA induced by 8-OH-DPAT was antagonized by application of the 5-HT1A receptor antagonist N-[2-[-(2-Methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinylcyclohexanecarboxamide maleate salt (WAY100635), while application of 5-HT2 receptor antagonist ketanserine tartrate (KET) antagonized only the increase of MFA induced by a-MET-5-HT. These results indicate that 5-HT is able to modulate the background firing activity of GN neurons by 5-HT1A and 5-HT2 receptors.

中文翻译：

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5-羟色胺修饰了大鼠幼虫核神经元的自发突触活性：5-HT1A和5-HT2受体的作用。

我们测试了血清素（5-HT）的微离子电渗疗法对位于大鼠细核（GN）的神经元放电速率的影响。5-HT1A和5-HT2激动剂和拮抗剂的应用分别模拟/调节并阻断了胺产生的作用。在测试的神经元中，有88.2％的人在5-HT存在的情况下改变了其背景激发活性。响应神经元在56.7％的患者中降低了平均射击活动（MFA），在其余43.3％的患者中提高了平均射击活动。为了确定5-HT诱导的效应的特异性，我们使用了8-羟基-2-（二正丙基氨基）四氢萘（8-OH-DPAT）和α-甲基-5-羟基色胺（α-MET-5 -HT），分别是5-HT1A和5-HT2受体的激动剂。8-OH-DPAT的微离子电泳改变了所有GN神经元（测试神经元的100％）的本底放电速率，模仿了5-HT引起的MFA降低。使用a-MET-5-HT可以修饰76.9％的受试神经元中的MFA，在61.5％的情况下可降低MFA，在其余的23.1％的情况下可以提高。通过应用5-HT1A受体拮抗剂N- [2-[-（2-甲氧基苯基）-1-哌嗪基]乙基] -N-2-吡啶基环己烷甲酰胺盐（ WAY100635），而使用5-HT2受体拮抗剂酒石酸ketanserine（KET）则只能拮抗由a-MET-5-HT诱导的MFA升高。这些结果表明5-HT能够通过5-HT1A和5-HT2受体调节GN神经元的背景激发活性。使用a-MET-5-HT可以修饰76.9％的受试神经元中的MFA，在61.5％的情况下可降低MFA，在其余的23.1％的情况下可以提高。通过应用5-HT1A受体拮抗剂N- [2-[-（2-甲氧基苯基）-1-哌嗪基]乙基] -N-2-吡啶基环己烷羧酰胺马来酸盐（5-HT1A受体拮抗剂）来拮抗8-OH-DPAT诱导的MFA降低。 WAY100635），而使用5-HT2受体拮抗剂酒石酸ketanserine（KET）则只能拮抗由a-MET-5-HT诱导的MFA升高。这些结果表明5-HT能够通过5-HT1A和5-HT2受体调节GN神经元的背景激发活性。使用a-MET-5-HT可以修饰76.9％的受试神经元中的MFA，在61.5％的情况下可降低MFA，在其余的23.1％的情况下可以提高。通过应用5-HT1A受体拮抗剂N- [2-[-（2-甲氧基苯基）-1-哌嗪基]乙基] -N-2-吡啶基环己烷甲酰胺盐（ WAY100635），而使用5-HT2受体拮抗剂酒石酸ketanserine（KET）则只能拮抗由a-MET-5-HT诱导的MFA升高。这些结果表明5-HT能够通过5-HT1A和5-HT2受体调节GN神经元的背景激发活性。通过应用5-HT1A受体拮抗剂N- [2-[-（2-甲氧基苯基）-1-哌嗪基]乙基] -N-2-吡啶基环己烷甲酰胺马来酸盐（5-HT1A受体拮抗剂）来拮抗8-OH-DPAT诱导的MFA降低。 WAY100635），而使用5-HT2受体拮抗剂酒石酸ketanserine（KET）则只能拮抗由a-MET-5-HT诱导的MFA升高。这些结果表明5-HT能够通过5-HT1A和5-HT2受体调节GN神经元的背景激发活性。通过应用5-HT1A受体拮抗剂N- [2-[-（2-甲氧基苯基）-1-哌嗪基]乙基] -N-2-吡啶基环己烷甲酰胺马来酸盐（5-HT1A受体拮抗剂）来拮抗8-OH-DPAT诱导的MFA降低。 WAY100635），而使用5-HT2受体拮抗剂酒石酸ketanserine（KET）则只能拮抗由a-MET-5-HT诱导的MFA升高。这些结果表明5-HT能够通过5-HT1A和5-HT2受体调节GN神经元的背景激发活性。