Onoue Satomi, Endo Kosuke, Yajima Takehiko, Kashimoto Kazuhisa
Health Science Division, Itoham Foods Inc., Ibaraki 302-0104, Moriya, Japan.
Regul Pept. 2002 Jul 15;107(1-3):43-7. doi: 10.1016/s0167-0115(02)00065-4.
Both vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) act as neurotransmitters in the central and peripheral nervous systems. Attention has been focused on these neuropeptides because among their numerous biological activities, they have been confirmed to show neuroprotective effects against ischemia and glutamate-induced cytotoxicity. It is well established that glutamate has excitatory effects on neuronal cells, and that excessive glutamate shows potent neurotoxicity, especially in neuronal nitric oxide synthase-containing neurons. Glutamate stimulates the production of nitric oxide (NO) in neurons, and the NO generated is tightly associated with the delayed death of neurons. We examined the effects of these neuropeptides on the glutamate-induced neural actions using PC12 cells, and we confirmed the important activities of PACAP/VIP on the production of NO as well as the delayed cell death stimulated by glutamate.
血管活性肠肽（VIP）和垂体腺苷酸环化酶激活肽（PACAP）在中枢和外周神经系统中均作为神经递质发挥作用。人们一直关注这些神经肽，因为在它们众多的生物学活性中，已证实它们对缺血和谷氨酸诱导的细胞毒性具有神经保护作用。众所周知，谷氨酸对神经元细胞具有兴奋作用，并且过量的谷氨酸会表现出强大的神经毒性，尤其是在含有神经元型一氧化氮合酶的神经元中。谷氨酸刺激神经元中一氧化氮（NO）的产生，并且产生的NO与神经元的延迟死亡密切相关。我们使用PC12细胞研究了这些神经肽对谷氨酸诱导的神经作用的影响，并证实了PACAP/VIP对NO产生以及谷氨酸刺激的细胞延迟死亡具有重要作用。
