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Keller, J.N., Schmitt, F.A., Scheff, S.W., Ding, Q., Chen, Q., Butterfield, D.A. and Markesbery, W.R. (2005) Evidence of increased oxidative damage in subjects with mild cognitive impairment. Neurology, 64, 1152-1156. doi:10.1212/01.WNL.0000156156.13641.BA

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• TITLE: Changes in the levels of CAM kinase II and synapsin I caused by oxidative stress in the rat brain, and its prevention by vitamin E

  AUTHORS: Nozomi Kaneai, Koji Fukui, Taisuke Koike, Shiro Urano

  KEYWORDS: Oxidative Stress; CAM Kinase II; Synapsin I; Neurotransmission; Vitamin E

  JOURNAL NAME: Advances in Bioscience and Biotechnology, Vol.3 No.8, December 27, 2012

  ABSTRACT: To define whether oxidative stress and aging induce abnormal dissociation of neurotransmitter-enclosing synaptic vesicles in rat brain nerve terminals, we assessed the activation of Ca+/calmodulin dependent protein kinase II (CAM kinase II) and changes in the levels of synapsin I, which is a synaptic vesicle-associated protein involved in the modulation of neurotransmitter release. Assessment of young rats subjected to hyperoxia-induced oxidative stress and normal aged rats revealed that synaptic CAM kinase II in the rat brain was markedly activated through oxidative stress and aging. In accordance with the activation of CAM kinase II, the levels of phosphorylated synapsin I increased significantly in nerve terminals. Furthermore, it was found that vitamin E prevents these oxidative stress-induced abnormal processes in rat nerve terminals. These results suggest that oxidative stress and aging facilitate the mobilization of neurotransmitter-enclosing synaptic vesicles from the reserve pool in the nerve terminal, thereby inducing abnormal accumulation of synaptic vesicles in the synapse, and that vitamin E inhibits this process in the brain through its antioxidative action.