著者

郡山 恵樹

出版者

公益社団法人 日本薬学会

雑誌

YAKUGAKU ZASSHI (ISSN:00316903)

巻号頁・発行日

vol.133, no.8, pp.843-848, 2013 (Released:2013-08-01)

参考文献数

12

被引用文献数

3 4

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The retina has been regarded as 'an approachable part of the brain' for investigating central nervous system (CNS). The optic nerve injury is a well-accepted model to study the mechanisms of neural degeneration and/or axonal regeneration after trauma in the CNS. Nitric oxide (NO) is a gaseous messenger molecule biosynthesized from L-arginine and molecular oxygen by NO synthase. Many reports suggest that excess production of NO plays a crucial role in neuronal cell death including in death of retinal ganglion cells (RGCs). In contrast, several lines of evidence indicate that NO can prevent neuronal death. In general, NO mediates neuroprotection through two main signaling pathways: the NO/cyclic guanosine monophosphate (cGMP) pathway and the S-nitrosylation pathway. Especially, whether S-nitrosylation of proteins promotes RGCs survival and its axonal regeneration after injury is unclear. Thus, we focused on the S-nitrosylation-dependent mechanism of RGCs survival and axonal regeneration by NO after nerve injury.