Characteristics of spontaneous and evoked EPSPs recorded from dentate spiny hilar cells in rat hippocampal slices.
Characteristics of spontaneous and evoked EPSPs recorded from dentate spiny hilar cells in rat hippocampal slices.
复制标题
大鼠海马切片齿状棘肺门细胞记录的自发和诱发 EPSP 的特征。
DOI：
10.1152/jn.1993.70.2.742
复制
发表时间：
1993
影响因子：
2.5
通讯作者：
Scharfman,HE
中科院分区：
文献类型：
--
作者：
Scharfman,HE
1. 海马叶门细胞的细胞内记录表征了齿状筋膜叶门神经元棘亚型的兴奋。通过刺激外层分子层来激活射孔通道。诱发反应被检查，以及大的自发兴奋电位，这是脊髓门细胞的一个显著特征。2. 自发产生的兴奋电位，以及响应外分子层刺激产生的兴奋电位，在被取样的细胞中是相似的，无论形态变化，如有无带刺的赘生物。自发和诱发兴奋性突触后电位（EPSPs）是复杂的去极化，通常有几个离散的峰。自发EPSPs振幅随超极化轻微增加，诱发EPSPs振幅随超极化明显增加。3. 应用兴奋性氨基酸受体的选择性拮抗剂来确定哪些兴奋性氨基酸受体介导这些细胞的EPSPs。使用6-氰基-7-硝基喹啉-2,3-二酮（CNQX）选择性阻断受体亚型，以激动剂α -氨基-3-羟基-5-甲基-4-异恶唑烯丙酸（AMPA）和kainic酸（“AMPA/kainate”受体）。使用2-氨基-5-磷酸戊酸（APV）阻断激动剂n -甲基- d -天冬氨酸（NMDA；“NMDA”受体）特异性受体。灌注CNQX（5-25微米）完全阻断了所有自发和诱发的兴奋，即使在相对去极化的膜电位下检测活性和使用低浓度的细胞外镁（0.5 mM）时也是如此。在这些条件下，APV（25-50微米）对自发活动没有可检测到的影响，但确实增加了引起外部分子层刺激反应所需的刺激强度。4. 当细胞外镁降低到0 mM（名义上）时，有强有力的证据表明NMDA受体对自发和诱发的epsp有贡献。因此，当细胞灌注0 mM的胞外镁和5微米的CNQX时，细胞出现自发去极化，epsp可以通过刺激外分子层而被触发。自发epsp和诱发epsp均被25微米APV阻断。5. 由于γ -氨基丁酸（GABA）A受体可引起海马神经元的去极化，因此使用GABAA受体拮抗剂双丘碱来确定某些epsp是否由GABA能神经元介导，而GABA能神经元通常通过自发释放兴奋性氨基酸而激活。Bicuculline（5-25微米）对自发去极化没有影响，但会导致诱发去极化增强。因此，GABAA受体介导的去极化并不会导致门状细胞的去极化。（摘要删节为400字）
1. Excitation of the spiny subtype of hilar neurons in the fascia dentata was characterized by intracellular recording from hilar cells in hippocampal slices. Stimulation of the outer molecular layer was used to activate the perforant path. Evoked responses were examined, as well as the large spontaneous excitatory potentials that are a distinctive characteristic of spiny hilar cells. 2. Excitatory potentials that occurred spontaneously, as well as those that occurred in response to outer molecular layer stimulation, were similar among the cells that were sampled, regardless of morphological variations such as the presence or absence of thorny excrescences. Spontaneous and evoked excitatory postsynaptic potentials (EPSPs) were complex depolarizations that often had several discrete peaks. Spontaneous EPSPs increased in amplitude slightly with hyperpolarization, and evoked EPSPs clearly increased with hyperpolarization. 3. Applications of selective antagonists of excitatory amino acid receptors were used to determine which excitatory amino acid receptor mediates EPSPs of these cells. 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) was used to block the receptor subtype selective for the agonists alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainic acid (the "AMPA/kainate" receptor). 2-amino-5-phosphonovaleric acid (APV) was used to block receptors specific for the agonist N-methyl-D-aspartate (NMDA; the "NMDA" receptor). Perfusion with CNQX (5-25 microM) completely blocked all spontaneous and evoked excitation, even when activity was examined at relatively depolarized membrane potentials and a low concentration of extracellular magnesium (0.5 mM) was used. Under these conditions, APV (25-50 microM) had no detectable effect on spontaneous activity but did increase the stimulus strength required to elicit responses to outer molecular layer stimulation. 4. When extracellular magnesium was lowered to 0 mM (nominally), there was strong evidence for a contribution of NMDA receptors to spontaneous and evoked EPSPs. Thus, when cells were perfused with 0 mM extracellular magnesium and 5 microM CNQX, spontaneous depolarizations were present and EPSPs could be triggered by stimulation of the outer molecular layer. Both the spontaneous and evoked EPSPs were blocked by 25 microM APV. 5. Because gamma-aminobutyric acid (GABA)A receptors can cause depolarizations in hippocampal neurons, the GABAA receptor antagonist bicuculline was used to determine whether some of the EPSPs were mediated by GABAergic neurons that are normally activated by spontaneous release of excitatory amino acids. Bicuculline (5-25 microM) had no effect on spontaneous depolarizations, and led to an enhancement of evoked depolarizations. Therefore it does not appear that GABAA receptor-mediated depolarizations contribute to hilar cell depolarizations.(ABSTRACT TRUNCATED AT 400 WORDS)