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本研究观察了神经节苷脂ＧＭ１和缩胆囊肽（ＣＣＫ）拮抗剂ＣＲ１５０５对正常和脑缺血时神经肽Ｙ（ＮＰＹ）体内的体外释放的影响。结果表明，脑缺血１小时后，ＮＰＹ释放明显增高，其后，逐步减小。而缺血６小时后是到释放再次增高。揭示ＮＰＹ参与脑缺血的病理生理过程。ＧＭ１不影响脑缺血时ＮＰＹ的释放，表明含ＮＰＹ的突触释放ＮＰＹ时不受ＧＭ１的调节。ＣＲ１５０５能明显抑制脑缺血时ＮＰＹ的释放，表明脑缺血时ＣＣＫ和ＮＰＹ有协同的相互作用，抑制ＮＰＹ释放是ＣＣＫ拮抗剂保护缺血大脑的机制之一。
This study looked at the effects of ganglioside GM1 and the cholecystokinin (CCK) antagonist CR1505 on in vitro release of neuropeptide Y (NPY) in normal and cerebral ischemia. The results showed that 1 hour after cerebral ischemia, NPY release was significantly increased, then gradually reduced. And 6 hours after ischemia to release again increased. Reveal NPY involved in the pathophysiology of cerebral ischemia. GM1 did not affect the release of NPY during cerebral ischemia, suggesting that NPY-containing synapses are not regulated by GM1 when NPY is released. CR1505 can significantly inhibit the release of NPY during cerebral ischemia, suggesting that CCK and NPY have a synergistic interaction during cerebral ischemia. Inhibition of NPY release is one of the mechanisms by which CCK antagonists protect the ischemic brain.