Bandopadhyay R, de Belleroche J
Department of Biochemistry, Charing Cross and Westminster Medical School, London.
Neuropeptides. 1991 Mar;18(3):159-63. doi: 10.1016/0143-4179(91)90108-u.
Cholecystokinin octapeptide (CCK) is an abundant neuropeptide of cerebral cortex but its function in this region is largely unknown. In this study we have examined the effect of glutamate receptor activation on the depolarisation-induced release of CCK-like immunoreactivity from tissue slices of rat cerebral cortex. The K(+)-evoked release of cholecystokinin was found to be significantly increased by the three excitatory amino acid agonists effective against glutamate receptor subtypes. N-methyl-D-aspartate (NMDA), kainic acid and quisqualate. The facilitation of CCK release by NMDA was examined in more detail and shown to be significantly attenuated by Mg2+ (2.5 mM), Zn2+ (50 microM), MK-801 (0.1 and 0.3 microM), aminophosphonovaleric acid (100 microM) and kynurenic acid (100 microM and 300 microM). These results support the conclusion that release of CCK in cerebral cortex is modulated by the NMDA receptor.
胆囊收缩素八肽(CCK)是大脑皮层中一种丰富的神经肽,但其在该区域的功能很大程度上尚不清楚。在本研究中,我们检测了谷氨酸受体激活对大鼠大脑皮层组织切片中去极化诱导的CCK样免疫反应性释放的影响。发现三种对谷氨酸受体亚型有效的兴奋性氨基酸激动剂能显著增加钾离子诱发的胆囊收缩素释放。N-甲基-D-天冬氨酸(NMDA)、 kainic酸和quisqualate。对NMDA促进CCK释放的作用进行了更详细的研究,结果表明,Mg2+(2.5 mM)、Zn2+(50 microM)、MK-801(0.1和0.3 microM)、氨基磷酸戊酸(100 microM)和犬尿氨酸(100 microM和300 microM)能显著减弱这种促进作用。这些结果支持以下结论:大脑皮层中CCK的释放受NMDA受体调节。