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运用逆转录 多聚酶联反应 (RT PCR)、鞘内注射和反义技术 ,研究脊髓水平一氧化氮 (NO)对大鼠吗啡戒断反应和脊髓及脑干NMDA1A受体mRNA (NMDA1ARmRNA)表达的影响。结果表明 ,鞘内注射NOS反义寡核苷酸能明显减轻吗啡戒断反应 ,且脑型NOS (nNOS)反义寡核苷酸的作用强于内皮型NOS (eNOS)反义寡核苷酸。吗啡依赖大鼠脊髓和脑干NMDA1ARmRNA表达增加 ,纳洛酮催促戒断 ,使其进一步增加 ;鞘内注射nNOS反义寡核苷酸 ,能明显抑制吗啡戒断大鼠脊髓和脑干NMDA1ARmRNA表达的增加 ;eNOS反义寡核苷酸也可抑制吗啡戒断大鼠脊髓NM DA1ARmRNA表达的增加 ,但作用弱于nNOS反义寡核苷酸 ,对脑干NMDA1ARmRNA表达无明显影响。上述结果提示 :脊髓水平NO参与介导吗啡戒断反应和NMDA受体表达的调控
The effects of nitric oxide (NO) at spinal level on the morphine withdrawal response and NMDA1AR mRNA expression in the spinal cord and brainstem were investigated by reverse transcription-polymerase chain reaction (RT PCR), intrathecal injection and antisense technique . The results showed that intrathecal injection of NOS antisense oligonucleotide significantly reduced morphine withdrawal response, and the effect of nNOS antisense oligonucleotide was stronger than that of endothelial NOS (eNOS) antisense oligonucleotide . NMDA1AR mRNA expression increased in the spinal cord and brainstem of morphine dependent rats, and naloxone induced withdrawal, which further increased. Intrathecal injection of nNOS antisense oligonucleotide significantly inhibited NMDA1AR mRNA expression in spinal cord and brainstem of morphine withdrawal rats The eNOS antisense oligonucleotides also inhibited the increase of NMDA1AR mRNA expression in the spinal cord of morphine withdrawal rats, but the effect was weaker than that of nNOS antisense oligonucleotides, and had no significant effect on the expression of NMDA1AR mRNA. The above results suggest that spinal cord level NO is involved in the regulation of morphine withdrawal response and NMDA receptor expression