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大鼠中P13中潜伏期听觉诱发电位的神经化学调制

Neurochemical modulation of the P13 midlatency auditory evoked potential in the rat.

作者信息

Miyazato H, Skinner R D, Garcia-Rill E

机构信息

Department of Anatomy, University of Arkansas for Medical Sciences, Little Rock 72205, USA.

出版信息

Neuroscience. 1999;92(3):911-20. doi: 10.1016/s0306-4522(98)00762-3.

DOI:10.1016/s0306-4522(98)00762-3
PMID:10426532
Abstract

Previous studies have shown that the vertex-recorded P13 auditory evoked potential in the rat appears to be the rodent equivalent of the human P1 (or P50) potential. This sleep state-dependent potential appears to be generated, at least in part, by cholinergic pedunculopontine nucleus projections. The present studies used localized microinjections of neuroactive compounds into the region of the pedunculopontine nucleus in order to modulate the vertex-recorded P13 potential. Both the GABAergic agonist, muscimol, and the noradrenergic alpha2 receptor agonist, clonidine, were found to reduce the amplitude of the P13 potential in a dose-dependent manner. The suppressive effect of clonidine on P13 potential amplitude was blocked by pretreatment with the noradrenergic alpha2 receptor antagonist, yohimbine. In addition, habituation of the P13 potential, measured using a paired stimulus paradigm, was increased by micro-injection of a dose of muscimol or clonidine which did not change the amplitude of the P13 potential induced by the first stimulus of a pair. In contrast, microinjection of yohimbine decreased habituation of the P13 potential. These results show that the vertex-recorded P13 potential and its habituation can be modulated by activation of known inhibitory synapses, both GABAergic and noradrenergic, at the level of the pedunculopontine nucleus. This provides further evidence that the P13 potential is generated, at least in part, by pedunculopontine nucleus outputs.

摘要

先前的研究表明,大鼠顶点记录的P13听觉诱发电位似乎相当于人类的P1(或P50)电位。这种睡眠状态依赖性电位似乎至少部分是由胆碱能脑桥脚核投射产生的。本研究通过将神经活性化合物局部微量注射到脑桥脚核区域,以调节顶点记录的P13电位。发现GABA能激动剂蝇蕈醇和去甲肾上腺素能α2受体激动剂可乐定均以剂量依赖性方式降低P13电位的幅度。可乐定对P13电位幅度的抑制作用可被去甲肾上腺素能α2受体拮抗剂育亨宾预处理所阻断。此外,使用配对刺激范式测量的P13电位的习惯化,通过微量注射一定剂量的蝇蕈醇或可乐定而增加,这两种药物不会改变一对刺激中第一个刺激诱发的P13电位的幅度。相反,微量注射育亨宾会降低P13电位的习惯化。这些结果表明,在脑桥脚核水平,已知的抑制性突触(GABA能和去甲肾上腺素能)的激活可调节顶点记录的P13电位及其习惯化。这进一步证明P13电位至少部分是由脑桥脚核输出产生的。

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