Protein oxidation inhibits NO-mediated signaling pathway for synaptic plasticity.
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概要
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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
- 横光利一と自然科学--「形式主義文学論争」前後を中心に
- 超高強度(圧縮強度100N/mm^2以上)コンクリート
- 高耐久性鉄筋コンクリート構造と高耐久性住宅
- 線維性骨異形成症とホルモン (第55回中部日本整形外科災害外科学会) -- (骨,軟部腫瘍-1-)
- いのち (子孫に伝えたい生き方の美徳--「古き良き日本」を知る最後の世代からのメッセージ)