自引率: 1.6%
被引量: 51658
通过率: 暂无数据
审稿周期: 1.92
版面费用: 暂无数据
国人发稿量: 70
投稿须知/期刊简介:
Brain Research provides a medium for prompt publication of articles in the fields of neuroanatomy, neurochemistry, neurophysiology, neuroendocrinology, neuropharmacology, neurotoxicology, neurocommunications, behavioural sciences, molecular neurology and biocybernetics. Clinical studies that are of fundamental importance and have a direct bearing on the knowledge of the structure and function of the brain, the spinal cord, and the peripheral nerves are also published.
期刊描述简介:
Brain Research provides a medium for prompt publication of articles in the fields of neuroanatomy, neurochemistry, neurophysiology, neuroendocrinology, neuropharmacology, neurotoxicology, neurocommunications, behavioural sciences, molecular neurology and biocybernetics. Clinical studies that are of fundamental importance and have a direct bearing on the knowledge of the structure and function of the brain, the spinal cord, and the peripheral nerves are also published.
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Chemical modulation of Akt signaling enhances spinal cord regeneration in zebrafish.
被引量：- 发表：1970
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Decreased SREBP2 of the striatal cell relates to disrupted protein degradation in Huntington's disease.
被引量：- 发表：1970
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Darts fast-learning reduces theta power but is not affected by Hf-tRNS: A behavioral and electrophysiological investigation.
被引量：- 发表：1970
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Novel insights into the role of TREM2 in cerebrovascular diseases.
被引量：- 发表：1970
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Upregulation of NADPH-oxidase, inducible nitric oxide synthase and apoptosis in the hippocampus following impaired insulin signaling in the rats: Development of sporadic Alzheimer's disease.
NADPH-oxidase (NOX) is a multi-subunit enzyme complex. The upregulation of NOX causes massive production of superoxide (O2¯), which avidly reacts with nitric oxide (NO) and increases cellular reactive oxygen/nitrogen species (ROS/RNS). Increased ROS/RNS plays pivotal role in the sporadic Alzheimer's disease (sAD) development and brain damage following impaired insulin signaling. Hence, this study aimed to examine early-time course of changes in NOX and NOS expression, and apoptotic proteins in the rats hippocampi following insulin signaling impairment [induced by STZ injection; intraperitoneal (IP) or in cerebral ventricles (ICV)]. Early effects (1, 3, or 6 weeks) on the NOX activity, translocation of NOX subunits from cytosol to the membrane, NO-synthases [neuronal-, inducible- and endothelial-NOS; nNOS, iNOS and eNOS], The Rac-1 protein expression, levels of NO and O2¯, cytochrome c release, caspase-3 and 9 activations (cleavage) were studied. STZ injection (in both models) increased NOX activity, O2¯ production, and enhanced cytosolic subunits translocation into membrane. The iNOS but not nNOS and eNOS expression and NO levels were increased in STZ treated rats. Finally, STZ injection increased cytochrome c release, caspase-3 and 9 activations in a manner that was significantly associated with levels of O2¯ and NO in the hippocampus. ICV-STZ administration resulted in significant profound changes over the IP route. In conclusion, impairment in insulin function induces early changes in ROS/RNS contents through NOX and iNOS upregulation and neuronal apoptosis in the hippocampus. Our results could mechanistically explain the role of impaired insulin function in the development of sAD.
被引量：- 发表：1970
