CANNABINOIDS AND NEUROPROTECTION IN CEREBRAL ISCHEMIA

大麻素与脑缺血的神经保护

• 批准号: 6704181
• 负责人: David Alan Greenberg
• 金额: $ 45.01万
• 依托单位: BUCK INSTITUTE FOR RESEARCH ON AGING
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-04-15 至 2005-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6704181
• 关键词: G protein; biological signal transduction; calcium channel; cannabinoid receptor; cannabinoids; cerebral ischemia /hypoxia; cytotoxicity; glutamates; laboratory rat; neuropharmacology; neuroprotectants; receptor expression; tissue /cell culture

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.

描述：（逐字摘自申请人摘要）潜在的假设