The role of nitric oxide in the development of cortical spreading depression-induced tolerance to transient focal cerebral ischemia in rats

Takashi Horiguchi, James A. Snipes, Bela Kis, Katsuyoshi Shimizu, David W. Busija

研究成果: Article査読

36 被引用数 (Scopus)

抄録

Cortical spreading depression (CSD) has been documented to confer ischemic tolerance on brain. Although nitric oxide (NO) is a crucial mediator in preconditioning under certain circumstances, the role of NO in CSD-induced neuroprotection is unclear. We examined the effect of L-NAME, an inhibitor of NO synthase, on CSD-induced tolerance against transient focal cerebral ischemia. A solution of 0.5 M KCl was applied for 2 h on the right hemisphere to induce CSD. Animals received either vehicle or L-NAME (4 mg/kg, iv) 30 min before CSD. Temporary occlusion (120 min) of the right middle cerebral artery was induced 4 days after preconditioning and the infarct volume was measured. Additionally, ERK 1/2 activation and cyclooxygenase-2 (COX-2) expression in the cerebral cortex were examined by Western blotting analysis immediately after cessation of CSD, or at 1, 2, 4, 8, and 24 h after CSD. CSD reduced infarct volume from 275 ± 15 mm3 (mean ± SEM) in the non-CSD group to 155 ± 14 mm3 in the CSD group (P < 0.05). L-NAME abolished this protection (281 ± 14 mm3; P < 0.05 vs. CSD group). Elevated ERK activation and COX-2 expression were observed immediately after or 8 h after preconditioning, respectively. Those responses are significantly augmented by L-NAME (3-fold for ERK and 4-fold for COX-2). These results suggest a crucial role of NO in the establishment of preconditioning with CSD.

本文言語English
ページ(範囲)84-89
ページ数6
ジャーナルBrain Research
1039
1-2
DOI
出版ステータスPublished - 2005 3 28
外部発表はい

ASJC Scopus subject areas

  • 神経科学(全般)
  • 分子生物学
  • 臨床神経学
  • 発生生物学

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