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Picrotoxin induces both hypertension and dopamine release in the rat amygdala.

机译:微小毒素在大鼠杏仁核中同时诱发高血压和多巴胺释放。

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摘要

The effects of the epileptogenic agent, picrotoxin, on both the cardiovascular responses and the dopamine (DA) release in the amygdala were studied in anesthetized rats. In vivo voltammetry was used to measure change in extracellular concentrations of DA and its metabolites in the amygdala. Intravenous administration of picrotoxin produced hypertension, increased amygdaloid DA release and behavioral syndromes (such as increased masticatory movements, salivation, and forepaw tremors). Direct administration of picrotoxin into the amygdala also induced the same effects. The picrotoxin-induced effects were suppressed by activation of gamma-aminobutyric acid (GABA) receptors with diazepam or depleting brain DA with 6-hydroxydopamine. Blockade of central DA receptors with haloperidol also attenuated the picrotoxin-induced hypertension. These results indicate that picrotoxin affects interactions between GABA neurons and DA system in rat brain to induce hypertension during an epileptic attack.
机译:在麻醉的大鼠中研究了致癫痫药微毒素对杏仁核中心血管反应和多巴胺(DA)释放的影响。体内伏安法用于测量杏仁核中DA及其代谢产物的细胞外浓度变化。静脉注射微毒素会导致高血压,杏仁核DA释放增加和行为综合症(例如咀嚼运动,唾液增多和前臂震颤增加)。将微毒素直接施用到杏仁核中也引起相同的作用。通过用地西epa激活γ-氨基丁酸(GABA)受体或用6-羟基多巴胺消耗脑DA,抑制了微毒素诱导的作用。氟哌啶醇对中枢DA受体的阻滞也减轻了微毒素诱导的高血压。这些结果表明,微毒素影响癫痫发作期间大鼠大脑中GABA神经元与DA系统之间的相互作用,从而诱发高血压。

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