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Microiontophoretically Applied PACAP Blocks Excitatory Effects of Kainic Acid in Vivo

机译:微观诊断施加的PACAP阻断KainiC酸在体内的兴奋性效果

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Pituitary adenylate cyclase-activating polypeptide (PACAP) has been shown to be neuroprotective in animal models of different brain pathologies, including focal and global cerebral ischemia. The application of glutaminergic excitotoxin kainic acid (KA), similar to ischemic events, may lead to neurodegeneration. In the present article, we investigated the effects of microiontophoretic application of PACAP on the excitatory effects of KA. During recording-maintained spontaneous activity of single neurons, we microiontophoretized KA, which was followed by the application of PACAP-38. We found that PACAP could block the excitatory effects of KA in several brain areas (cortex: 89%, hippocampus: 36%, and thalamus: 50%). Moreover, we detected a lower level excitatory effect of PACAP alone (41%). The present results may explain the neuroprotective effects of PACAP observed in experimental models of glutamate (GLU)—receptor-mediated degenerative processes.
机译:垂体腺苷酸环酶活化多肽(PACAP)已被证明是在不同脑病的动物模型中是神经保护的,包括局灶性和全球脑缺血。谷氨酰胺能卓越毒素Kainic acid(Ka)类似于缺血事件,可能导致神经变性。在本文中,我们研究了PACAP微观细胞施用对KA兴奋性效果的影响。在记录 - 维持单一神经元的自发性活性期间,我们的微型诊断化Ka,其次是施用PacaP-38。我们发现PACAP可以阻断KA在几个脑区域(皮质:89%,海马:36%和丘脑:50%)的兴奋性效果。此外,我们检测到单独的PACAP的较低水平兴奋性效果(41%)。目前的结果可以解释在谷氨酸(Glu)-Receptor介导的退行方法的实验模型中观察到PACAP的神经保护作用。

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