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强直刺激穿通路径对大鼠海马场电位群体锋电位成分的长期增强作用的研究:多巴胺激动剂SKF-38393的影响。

Studies on long-term potentiation of the population spike component of hippocampal field potential by the tetanic stimulation of the perforant path rats: effects of a dopamine agonist, SKF-38393.

作者信息

Yanagihashi R, Ishikawa T

机构信息

Department of Physiology and Biochemistry, School of Nursing, Chiba University, Japan.

出版信息

Brain Res. 1992 May 1;579(1):79-86. doi: 10.1016/0006-8993(92)90744-t.

Abstract

Long-term potentiation of the field potentials recorded in the dentate gyrus of the hippocampus was observed in freely-moving rats by delivering a brief tetanic stimulation to the perforant path, and the effects of the D1 agonist, SKF-38393, on it was investigated. The field potential was divided into two components; excitatory postsynaptic potential (EPSP) and population spike. In Expt. I, synaptic stimulus-response (S-R) relationship, spike S-R relationship, and EPSP-spike (E-S) relationship were plotted. The estimated slope of the regression line in the spike S-R relationship was enhanced after delivery of the tetanic stimulation (10 pulse at 400 Hz), where that in synaptic S-R relationship was not enhanced. The estimated slope of the regression line in the E-S relationship was also enhanced by the tetanic stimulation. In Expt. II, time-dependent change of the field potential after tetanic stimulation was investigated. The population spike was enhanced significantly for about 2 h following tetanic stimulation, while pEPSP did not change significantly. These changes following tetanic stimulation in Expt. I and II were significantly inhibited by previous administration of SKF-38393 (10 mg/kg, i.p.), and the effect of this drug was dose-dependently antagonized by the D1 antagonist, SCH-23390 (0.1, 0.2 and 0.5 mg/kg, i.p.). These results suggest that a brief tetanic stimulation of the perforant path induces long-term potentiation of the population spike without potentiating the synaptic input in the perforant path-dentate synapses, and that potentiation of the population spike is inhibited by the dopaminergic D1 mechanism.

摘要

通过向穿通路径施加短暂的强直刺激,在自由活动的大鼠中观察到海马齿状回记录的场电位的长期增强,并研究了D1激动剂SKF-38393对其的影响。场电位分为两个成分:兴奋性突触后电位(EPSP)和群体峰电位。在实验I中,绘制了突触刺激-反应(S-R)关系、峰电位S-R关系和EPSP-峰电位(E-S)关系。在强直刺激(400Hz,10个脉冲)后,峰电位S-R关系中回归线的估计斜率增加,而突触S-R关系中的斜率未增加。强直刺激也增强了E-S关系中回归线的估计斜率。在实验II中,研究了强直刺激后场电位的时间依赖性变化。强直刺激后群体峰电位显著增强约2小时,而pEPSP没有显著变化。在实验I和II中,强直刺激后的这些变化被预先给予的SKF-38393(10mg/kg,腹腔注射)显著抑制,并且该药物的作用被D1拮抗剂SCH-23390(0.1、0.2和0.5mg/kg,腹腔注射)剂量依赖性地拮抗。这些结果表明,穿通路径的短暂强直刺激可诱导群体峰电位的长期增强,而不增强穿通路径-齿状突触中的突触输入,并且群体峰电位的增强被多巴胺能D1机制抑制。

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