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Involvement of genes required for synaptic function in aging control in C.elegans
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作者 沈露露 汪洋 王大勇 《Neuroscience Bulletin》 SCIE CAS CSCD 2007年第1期21-29,共9页
Objective To identify new genes required for neurosecretory control of aging in C. elegans. Methods In view of the importance of nervous system in aging regulation, we performed the screen for genes involved in the ag... Objective To identify new genes required for neurosecretory control of aging in C. elegans. Methods In view of the importance of nervous system in aging regulation, we performed the screen for genes involved in the aging regulation from genetic loci encoding synaptic proteins by lifespan assay and accumulation of lipofuscin autofluorescence. We further investigated the dauer formation phenotypes of their corresponding mutants and whether they were possibly up-regulated by the insulin-like signaling pathway. Results The genetic loci of unc-10, syd-2, hlb-1, dlk-1, mkk-4, scd- 2, snb-1, ric-4, nrx-1, unc-13, sbt-1 and unc-64 might be involved in the aging control. In addition, functions of unc-10, syd-2, hlb-1, dlk-1, mkk-4, scd-2, snb-1, ric-4 and nrx-1 in regulating aging may be opposite to those of unc-13, sbt-1 and unc-64. The intestinal autofluorescence assay further indicated that the identified long-lived and short-lived mutants were actually due to the suppressed or accelerated aging. Among the identified genes, syd-2, hlb-1, mkk-4, scd-2, snb-1, ric-4 and unc-64 were also involved in the control of dauer formation. Moreover, daf-2 mutation positively regulated the expression of syd-2 and hlb-1, and negatively regulated the expression of mkk-4, nrx-1, ric-4, sbt-1, rpm-1, unc-10, dlk- 1 and unc-13. The daf-16 mutation positively regulated the expression of syd-2 and hlb-1, and negatively regulated the expression of mkk-4, nrx-1, sbt-1, rpm-1, unc-10, dlk-1 and unc-13. Conclusion These data suggest the possibly important status of the synaptic transmission to the animal' s life-span control machinery, as well as the dauer formation control. 展开更多
关键词 AGING NEUROTRANSMISSION SYNAPSE dauer formation insulin pathway C. elegans
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Physiologic role for“inducible”nitric oxide synthase:A new form of astrocytic-neuronal interface
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作者 Yael Amitai 《神经损伤与功能重建》 2011年第1期52-58,共7页
长期以来,一氧化氮(NO)都被看作是影响兴奋性突触传递的非典型神经信使分子,其细胞来源尚不清楚。许多脑区中的神经元型一氧化氮合酶(nNOS)只在少量抑制性神经元中表达。众所周知,胶质细胞诱导型一氧化氮合酶(iNOS)不在正常大脑中表达,... 长期以来,一氧化氮(NO)都被看作是影响兴奋性突触传递的非典型神经信使分子,其细胞来源尚不清楚。许多脑区中的神经元型一氧化氮合酶(nNOS)只在少量抑制性神经元中表达。众所周知,胶质细胞诱导型一氧化氮合酶(iNOS)不在正常大脑中表达,其在免疫刺激后可经转录介导上调。因此,iNOS调节正常神经功能的作用常被忽视。许多研究表明,有功能的iNOS存在于哺乳动物的正常脑区,包括星形胶质细胞。NO可通过iN-OS调节突触前膜的递质释放。据以上研究结果推测,正常脑组织中,星形胶质细胞表达基础水平的iNOS,被激活后,星形胶质细胞可释放NO并影响突触释放。 展开更多
关键词 兴奋突触 DAF-2DA 突触性释放 LTP 一氧化氮
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