| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2002: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2001: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2000: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Research Abstract |
We previously reported that nociceptin and dynorphin A (1-13) improved impairment of learning and/or memory in several animal models. Furthermore, κ-opioid receptor agonists and (-)-nicotine prevented neurodegenerative damage induced by ischemia or β-amyloid peptide (25-35). In this study, we tested whether a κ-opioid receptor agonist, U-50,488H prevents delayed memory impairment induced by β-amyloid peptide (25-35) and changes of prepronociceptin mRNA, prodynorphin mRNA and α7 type nicotinic acetylcholine receptor mRNA. Seven days after β-amyloid peptide (25-35) treatment, memory impairment was prevented, and 10 days after β-amyloid peptide (25-35), there was no change in prepronociceptin mRNA, prodynorphin mRNA or α7 type nicotinic acetylcholine receptor mRNA expression in the hippocampus. These mRNA expressions were significantly decreased when U-50,488H was administered 1 hr before, but not 1 hr after β-amyloid peptide (25-35) treatment. In conclusion, activation of the κ-opioid system may produce neuroprotective effects on β-amyloid peptide (25-35)-induced toxicity, and may be involved in the long-lasting changes of these mRNA expressions.
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