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[垂体腺苷酸环化酶激活多肽改善谷氨酸诱导的培养海马神经元损伤并抑制细胞内钙浓度升高]

[Pituitary adenylate cyclase activating polypeptide ameliorates the damage and inhibits the increase of intracellular calcium concentration in cultured hippocampal neurons induced by glutamate].

作者信息

Dong Y, Tang T S, Lu C L, He C, Dong J B, Huang X Y, Sun F Z, Bao X

机构信息

Department of Neurobiology, Second Military Medical University, Shanghai 200433, China.

出版信息

Sheng Li Xue Bao. 2000 Oct;52(5):402-6.

Abstract

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.

摘要

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。

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