CANNABINOIDS AND NEUROPROTECTION IN CEREBRAL ISCHEMIA

描述：（来自申请人摘要的逐字记录） 这一建议是大麻素是脑内内源性神经保护剂， 缺血这一假设是基于几个不同的观察， 包括在脑缺血期间发生的生理事件 将有望提高内源性的合成和释放 大麻素外源施用的合成大麻素类似物可 保护神经元培养物免受缺血样条件的影响， 短暂性全脑缺血后神经元丢失，并可减少梗死体积 大脑中动脉永久闭塞后。此外，这些神经保护 大麻素的作用与其减少 电压门控钙电流，增强内向整流钾电流， 并抑制谷氨酸释放。

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.