CANNABINOIDS AND NEUROPROTECTION IN CEREBRAL ISCHEMIA

描述：(逐字摘自申请者的摘要)潜在的假设 这一观点认为，大麻素是大脑中的内源性神经保护剂。 缺血症。这一假设是基于几个不同的观察结果，其中 包括在脑缺血期间发生的生理事件 有望促进内源性激素的合成和释放 大麻素。外源性给予合成大麻素类似物可以 保护培养的神经元免受缺血样条件的影响，可以减少海马区 短暂性全脑缺血后神经元丢失，并可缩小梗死体积 大鼠大脑中动脉永久性闭塞后。此外，这些神经保护措施 大麻素的作用与它们减少 电压门控钙电流，增强内向整流钾电流， 并抑制谷氨酸的释放。

DESCRIPTION: (Verbatim from the Applicant's Abstract) The hypothesis underlying this proposal is that cannabinoids are endogenous neuroprotectants in cerebral ischemia. This hypothesis is based on several distinct observations, which include the fact that physiological events that occur during cerebral ischemia would be expected to enhance the synthesis and release of endogenous cannabinoids. Exogenously administered synthetic cannabinoid analogs can protect neuronal cultures from ischemia-like conditions, can reduce hippocampal neuronal loss after transient global ischemia, and can reduce infarct volume after permanent MCA occlusion in rat brain. Furthermore these neuroprotective actions of cannabinoids are in keeping with their ability to reduce voltage-gated calcium currents, enhance inwardly rectifying potassium currents, and inhibit glutamate release.