Accelerated kindling development in μ-opioid receptor deficient mice
Accelerated kindling development in μ-opioid receptor deficient mice
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DOI：
10.1007/s00210-004-0870-4
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发表时间：
2004-03-01
影响因子：
3.6
通讯作者：
Höllt, V
中科院分区：
文献类型：
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作者：
Grecksch, G;Becker, A;Höllt, V
使用μ阿片受体敲除小鼠的研究强调了μ阿片系统与中枢兴奋性和点燃相关的学习障碍表现的相关性。缺乏μ-阿片受体的小鼠表现出由惊厥药物戊四氮诱导的加速点燃发展。通过纳曲吲哚阻断δ-阿片受体抑制野生型动物的点燃发展，导致敲除小鼠点燃癫痫发作发展的进一步加速。缺乏μ-阿片受体的小鼠在穿梭箱中表现出如此低的学习性能，以至于未检测到在野生型小鼠中观察到的点燃诱导的学习缺陷。结果进行了讨论的基础上的受体结合的研究亚型的阿片受体，δ-阿片受体和生长抑素受体。谷氨酸和生长抑素结合的增加可能有助于增强μ阿片受体敲除小鼠的兴奋性。
The relevance of mu-opioid systems for central excitability and kindling related disturbed learning performance was underlined by investigations using mu-opioid receptor knockout mice. Mice lacking mu-opioid receptors showed an accelerated kindling development induced by the convulsant drug pentylenetetrazol. Blockade of delta-opioid receptors by naltrindole suppressing kindling development in wild-type animals led to a further acceleration of kindled seizure development in the knockout mice. Mice lacking mu-opioid receptors showed such a low learning performance in the shuttle box, that the kindling induced learning deficit as seen in wild-type mice was not detected. The results were discussed on the basis of receptor binding studies with regard to subtypes of glutamatergic receptors, delta-opioid and somatostatin receptors. An increase in glutamate and somatostatin binding could contribute to the enhanced excitability in the-mu-opioid receptor knockout mice.