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以谷氨酸、ＮＭＤＡ作用原代培养的大鼠大脑皮层神经元，随药物浓度递增，作用时间延长，细胞存活率逐渐下降。八肽胆囊收缩素对谷氨酸、ＮＭＤＡ诱导的神经元死亡具有明显的拮抗作用，在其浓度为１×１０－７ｍｏｌ／Ｌ时其拮抗率为７７８±４４％和７５４±６７％。ＣＣＫＢ受体拮抗剂Ｌ－３６５２６０可完全阻断八肽胆囊收缩素的保护作用，而ＣＣＫＡ受体拮抗剂Ｌ－３６４７１８无此作用。应用Ｆｕｒａ－２荧光技术测定新生大鼠大脑皮层神经元细胞内游离钙浓度（［Ｃａ２＋］ｉ），八肽胆囊收缩素可明显抑制ＮＭＤＡ诱导的神经元［Ｃａ２＋］ｉ升高，在浓度为１×１０－７ｍｏｌ／Ｌ时其抑制率为９５７％。结果显示：八肽胆囊收缩素可能通过其Ｂ受体产生拮抗谷氨酸神经兴奋毒性作用，抑制Ｃａ２＋内流是其产生拮抗作用的机制之一。
The primary cultured rat cerebral cortical neurons with glutamate and NMDA function increased with the increase of drug concentration, prolonged action time, and the cell survival rate decreased gradually. Cholecystokinin octapeptide had a significant antagonistic effect on glutamate and NMDA-induced neuronal death. The antagonistic rates were 778 ± 44% and 754 at the concentration of 1 × 10-7mol / L ± 6.7%. The CCKB receptor antagonist L-365260 completely blocked the octopeptide cholecystokinin protective effect, while the CCKA receptor antagonist L-364718 did not. Fura-2 fluorescence was used to determine intracellular free calcium concentration ([Ca2 +] i) in neonate rat cortical neurons. Cholecystokinin octapeptide significantly inhibited NMDA-induced [Ca2 +] i elevation in neurons. × 10-7mol / L, the inhibition rate was 957%. The results showed that octapeptide cholecystokinin may antagonize the excitotoxicity of glutamate through its receptor B, and inhibition of Ca2 + influx may be one of the mechanisms of its antagonism.