摘要
对原代培养 7～ 9d的海马神经元给予谷氨酸处理 ,2 4h后 ,神经元的存活率降低。预先给予垂体腺苷酸环化酶激活肽 (PACAP)能显著减少谷氨酸引起的海马神经元死亡。谷氨酸呈剂量依赖性增加海马神经元细胞内钙离子含量 ,PACAP能抑制谷氨酸引起的海马神经元细胞内钙离子浓度的升高 ,特异性PACAPⅠ型受体拮抗剂PACAP 6 38能完全阻断PACAP减轻谷氨酸所致海马神经元损伤及降低谷氨酸所致神经元细胞内钙离子浓度升高的作用。提示PACAP能减轻谷氨酸引起的培养海马神经元的损伤 ,该作用与PACAP抑制谷氨酸引起的海马神经元细胞内钙离子浓度升高有关 。
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.[WT5HZ]
出处
《生理学报》
CAS
CSCD
北大核心
2000年第5期402-406,共5页
Acta Physiologica Sinica
关键词
谷氨酸
PACAP
神经元损伤
保护机制
钙浓度
glutamate
pituitary adenylate cyclase activating polypeptide (PACAP)
neuron
