Septal neurons related with hippocampus increase their firing rate after long-term clomipramine.

M L Marván, M A Guzmán-Sáenz, J Alberto Barradas, C M Contreras
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Abstract

In the rat, long-term clomipramine increases the firing rate in lateral septal neurons. Although the hippocampus is the main afference for septal nuclei, it is unknown whether clomipramine increases the firing rate in most of hippocampal-septal neurons. Therefore, the present study explored the actions of long-term clomipramine in lateral septal neurons identified by their relation to the hippocampus. In most recordings, hippocampal stimulation produced a brief excitatory short-latency response, followed by a period of inhibition of firing. These neurons increased their firing rate after clomipramine treatment. Other septal neurons not respondent to hippocampal stimulation did not respond to clomipramine treatment, either. We concluded that only hippocampal-septal neurons are clomipramine responders too, and the drug-induced enhancement of firing rate is likely to be mediated by an interneuron-mediated disinhibition process.

与海马相关的间隔神经元长期服用氯丙帕明后放电频率增加。
在大鼠中,长期服用氯咪嗪会增加侧隔神经元的放电率。虽然海马体是中隔核的主要传入区,但氯丙帕明是否会增加大多数海马-中隔神经元的放电率尚不清楚。因此,本研究探讨了长期氯丙帕明对侧隔神经元的作用,通过它们与海马的关系来确定。在大多数记录中,海马刺激产生了短暂的兴奋性短潜伏期反应,随后是一段时间的抑制放电。氯丙咪嗪治疗后,这些神经元的放电频率增加。其他对海马刺激无反应的间隔神经元对氯丙咪嗪治疗也无反应。我们得出结论,只有海马-间隔神经元也对氯丙帕明有反应,药物诱导的放电率增强可能是通过神经元间介导的去抑制过程介导的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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