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皮质酮减少体外培养的大鼠海马和新皮层神经元的突触抑制。

Corticosterone Reduces Synaptic Inhibition in Rat Hippocampal and Neocortical Neurons in vitro.

机构信息

Max-Planck-lnstitute for Psychiatry, Clinical Neuropharmacology, Munich, FRG.

出版信息

J Neuroendocrinol. 1992 Feb;4(1):107-12. doi: 10.1111/j.1365-2826.1992.tb00352.x.

Abstract

We examined the effect of corticosterone (10(-7) to 10(-5) M) on membrane properties and postsynaptic potentials, by means of intracellular recordings from neocortical and hippocampal CA1 pyramidal neurons of the intact adult rat in vitro. Corticosterone reduced both the early and the late components of the orthodromically-evoked inhibitory postsynaptic potential in both structures. The glucocorticoid receptor antagonist RU 38486 (10(-6) M) prevented this effect in the hippocampus. In hippocampal, but not in neocortical pyramidal neurons, corticosterone reduced a depolarizing membrane transient evoked by a depolarizing current step and increased the threshold for eliciting action potentials evoked by depolarizing current pulses. Corticosterone did not detectably alter the afterhyperpolarization following repetitive neuronal discharges evoked by current injection, in either the neocortex or in the hippocampus. Excitatory postsynaptic potentials, action potentials, membrane potential and membrane input resistance were also unchanged. The decrease in synaptic inhibition together with the reduction of electrical excitability in the hippocampus, would imply a modulation of response characteristics in pyramidal neurons such that repeated synaptic inputs become more efficient and low frequency input is blunted.

摘要

我们通过对完整成年大鼠体外新皮质和海马 CA1 锥体神经元的细胞内记录,研究了皮质酮(10(-7) 到 10(-5) M)对膜特性和突触后电位的影响。皮质酮降低了这两种结构中传入性诱发抑制性突触后电位的早期和晚期成分。糖皮质激素受体拮抗剂 RU 38486(10(-6) M)在海马体中阻止了这种作用。在海马体而不是新皮质锥体神经元中,皮质酮降低了由去极化电流阶跃引起的去极化膜瞬变,并增加了由去极化电流脉冲引起的动作电位引发的阈值。皮质酮在新皮质或海马体中,均未明显改变重复电流注入引起的神经元放电后的超极化后电位。兴奋性突触后电位、动作电位、膜电位和膜输入电阻也没有变化。海马体中突触抑制的减少以及电兴奋性的降低,意味着锥体神经元的反应特性发生了调制,从而使重复的突触输入变得更加有效,低频输入变钝。

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