Dong Y, Tang T S, Lu C L, He C, Dong J B, Huang X Y, Sun F Z, Bao X
Department of Neurobiology, Second Military Medical University, Shanghai 200433, China.
Sheng Li Xue Bao. 2000 Oct;52(5):402-6.
Hippocampal neurons cultured from 7 to 9 d in vitro were used to observe the effect of glutamate. Treatment of glutamate for 24 h greatly decreased neuronal survival and pretreatment with pituitary adenylate cyclase activating polypeptide (PACAP) significantly attenuated hippocampal neuron death induced by glutamate. Moreover, glutamate dose-dependently increased the intracellular calcium concentration in cultured hippocampal neurons, while PACAP inhibited the increase of intracellular calcium concentration induced by glutamate. PACAP 6-38, a specific PACAP type I receptor antagonist, completely inhibited the amelioration of glutamate induced death and the decrease of intracellular calcium concentration induced by PACAP in cultured hippocampal neurons. The data suggest that PACAP has a neuroprotective effect on the hippocampal neuronal damage induced by glutamate, which is related to an inhibition of glutamate-induced increase of intracellular calcium concentration and mediated by PACAP type I receptor.
使用体外培养7至9天的海马神经元来观察谷氨酸的作用。用谷氨酸处理24小时可显著降低神经元存活率，而用垂体腺苷酸环化酶激活多肽（PACAP）预处理可显著减轻谷氨酸诱导的海马神经元死亡。此外，谷氨酸可剂量依赖性地增加培养的海马神经元内的钙浓度，而PACAP可抑制谷氨酸诱导的细胞内钙浓度升高。PACAP 6-38是一种特异性的PACAP I型受体拮抗剂，它完全抑制了培养的海马神经元中谷氨酸诱导的死亡改善以及PACAP诱导的细胞内钙浓度降低。这些数据表明，PACAP对谷氨酸诱导的海马神经元损伤具有神经保护作用，这与抑制谷氨酸诱导的细胞内钙浓度升高有关，并由PACAP I型受体介导。
