Alterations in hippocampal GAP-43, BDNF, and L1 following sustained cerebral ischemia

Keiko Miyake, Wataru Yamamoto, Mina Tadokoro, Norio Takagi, Kyoko Sasakawa, Atsumi Nitta, Shoei Furukawa, Satoshi Takeo*

*この論文の責任著者

研究成果: ジャーナルへの寄稿学術論文査読

69 被引用数 (Scopus)

抄録

Alterations in factors involved in the regeneration of the neuronal network in the hippocampus of rats with microsphere embolism (ME) were examined. Nine hundred microspheres (48 μm in diameter) were injected into the right hemisphere, and immunochemical and immunohistochemical studies on the hippocampus were performed on the seventh day thereafter. Hematoxylin-eosin staining showed progressive and severe degeneration of the hippocampus after ME. The protein levels of brain-derived neurotrophic factor (BDNF), 43-kDa growth-associated protein (GAP-43), and adhesion protein L1 (L1) in the ipsilateral hippocampus of the ME animal, determined by Western blot analysis or enzyme immunoassay, were increased, unaltered, and decreased, respectively. In contrast, the immunohistochemical study showed increases in a marker of axonal sprouting GAP-43, and a neurotrophic factor BDNF, and a decrease in an adhesion molecule L1 in some areas of the hippocampal ischemic penumbra of such animals. These results suggest that some factors for regeneration of the neuronal network in the ischemic penumbra responded to sustained cerebral ischemia for a certain period, although functional network of the nerve cells in the microsphere-injected hemisphere would be unlikely established after ME.

本文言語英語
ページ(範囲)24-31
ページ数8
ジャーナルBrain Research
935
1-2
DOI
出版ステータス出版済み - 2002/05/10

ASJC Scopus 主題領域

  • 神経科学一般
  • 分子生物学
  • 臨床神経学
  • 発生生物学

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