Protein oxidation inhibits NO-mediated signaling pathway for synaptic plasticity.
スポンサーリンク
概要
- 論文の詳細を見る
Oxidative stress is a primary factor inducing brain dysfunction in aged animals. However, how oxidation affects brain function is not fully understood. Here we show that oxidation inhibits signaling pathways essential for synaptic plasticities in the cerebellum. We first revealed that nitric oxide (NO)-dependent plasticities at the parallel fiber-Purkinje cell synapse (PF synapse) were impaired in the cerebellar slices from aged mice, suggesting a possible inhibitory action of protein oxidation by endogenous reactive oxygen species. PF-synaptic plasticities were also blocked in the cerebellar slices from young mice preincubated with oxidizing agents or thiol blocker. Because the treatment of the slices with the oxidizing agent did not affect basic electrophysiological properties of excitatory postsynaptic current of PF (PF-EPSC) and did not occlude the synaptic plasticities, oxidation was revealed to specifically inhibit signaling pathways essential for PF-synaptic plasticities. Finally, biochemical analysis confirmed the idea that inhibitory action of protein oxidation on the PF-synaptic plasticities was mediated by impairment of nitric oxide-induced protein S-nitrosylation. Therefore, oxidation was revealed to inhibit the S-nitrosylation-dependent signaling pathway essential for synaptic plasticity in a "competitive" manner.
- 2010-06-24
論文 | ランダム
- 低分化滑膜肉腫 : 組織学的、免疫組織化学的および分子遺伝子学的検討
- 肺転移をきたした骨巨細胞腫 : 7例の臨床病理学的検討
- 座長のことば(シンポジウム4 産科の病診連携〜オープン・セミオープンシステム〜日本での産科オープンシステムは成り立つのか!)
- 看護学生が看護師となっていく道筋をつくる
- チームのチカラで支える助産師の現任教育