Serotonin induces excitatory postsynaptic potentials in apical dendrites of neocortical pyramidal cells
Serotonin induces excitatory postsynaptic potentials in apical dendrites of neocortical pyramidal cells
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DOI：
10.1016/s0028-3908(97)00051-8
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发表时间：
1997-04-01
影响因子：
4.7
通讯作者：
Marek, GJ
中科院分区：
文献类型：
--
作者：
Aghajanian, GK;Marek, GJ
通过大鼠脑切片中的细胞内和全细胞记录，发现沐浴式的5-羟色胺（5-HT）在层V层V层V层V型细胞中自发兴奋性突触后/电流（EPSPS/EPSC）的频率和振幅增加新皮层和过渡性皮层（例如内侧前额叶，扣带和额叶）。 EPSC被LY293558抑制，这是一种针对兴奋性氨基酸受体AMPA亚型的拮抗剂，以及两个选择性的5-HT2A受体拮抗剂MDL 100907和SR 46349b。另外，EPSC被快速钠通道阻滞剂四毒素（TTX）抑制，并取决于外部钙。然而，尽管对TTX敏感和钙的依赖性，但没有证据表明EPSP是由于兴奋性神经元传入中脉冲流的增加而导致的，从而层层V锥体细胞。 EPSC可以通过5-HT的微离子电池迅速诱导至“热点”（但不是基底）树突状神经元内的“热点”，表明兴奋性氨基酸可以通过TTX敏感的局灶性作用释放该区域中谷氨酸能末端的子集的5-HT。与这种突触前作用一致，抑制性代谢型谷氨酸受体激动剂（1s，3s） - 氨基细胞烷-1,3-二羧酸盐可显着降低EPSP的诱导5-HT。突触后5-HT增强了亚阈值TTX敏感的钠电流，可能导致EPSC振幅的扩增。这些数据表明5-HT通过5-HT2A受体增强了新皮层层V锥体细胞中自发性EPSP/EPSC，通过TTX敏感的树突状场中的TTX敏感局灶性作用，这可能涉及前和突触后机制。 （c）1997 Elsevier Science Ltd.
By intracellular and whole cell recording in rat brain slices, it was found that bath-applied serotonin (5-HT) produces an increase in the frequency and amplitude of spontaneous excitatory postsynaptic potentials/currents (EPSPs/EPSCs) in layer V pyramidal cells of neocortex and transitional cortex (e.g. medial prefrontal, cingulate and frontoparietal). The EPSCs were suppressed by LY293558, an antagonist selective for the AMPA subtype of excitatory amino acid receptor, and by two selective 5-HT2A receptor antagonists, MDL 100907 and SR 46349B. In addition, the EPSCs were suppressed by the fast sodium channel blocker tetrodotoxin (TTX) and were dependent upon external calcium. However, despite being TTX-sensitive and calcium dependent, there was no evidence that the EPSPs resulted from an increase in impulse flow in excitatory neuronal afferents to layer V pyramidal cells. The EPSCs could be induced rapidly by the microiontophoresis of 5-HT directly to ''hot spots'' within the apical (but not basilar) dendritic field of recorded neurons, indicating that excitatory amino acids may be released by a TTX-sensitive focal action of 5-HT on a subset of glutamatergic terminals in this region. Consistent with such a presynaptic action, the inhibitory metabotropic glutamate receptor agonist (1S,3S)-aminocyclopentane-1,3-dicarboxylate markedly reduced the induction of EPSPs by 5-HT. Postsynaptically, 5-HT enhanced a subthreshold TTX-sensitive sodium current, potentially contributing to an amplification of EPSC amplitudes. These data suggest 5-HT, via 5-HT2A receptors, enhances spontaneous EPSPs/EPSCs in neocortical layer V pyramidal cells through a TTX-sensitive focal action in the apical dendritic field which may involve both pre- and postsynaptic mechanisms. (C) 1997 Elsevier Science Ltd.