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首页> 外文期刊>Life sciences >Use of antisense oligodeoxynucleotide to determine delta-opioid receptor involvement in (D-Ala2)deltorphin II-induced locomotor hyperactivity.
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Use of antisense oligodeoxynucleotide to determine delta-opioid receptor involvement in (D-Ala2)deltorphin II-induced locomotor hyperactivity.

机译：使用反义寡聚脱氧核苷酸确定δ-阿片受体参与（D-Ala2）deltorphin II诱导的运动亢进。

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Intracerebroventricularly (i.c.v.)-administered [D-Ala2]deltorphin II (20 micrograms) produced a marked locomotor hyperactivity in male ICR mice. The locomotor hyperactivity induced in response to i.c.v. [D-Ala2]deltorphin II (20 micrograms) was suppressed by pretreatment with naltriben (NTB, 10 micrograms) but not 7-benzylidene naltrexone (BNTX, 1 microgram) and D-Phe-Cys-Tyr-D-Try-Orn-Thr-Phe-Thr-NH2 (CTOP, 100 ng). The influence of antisense oligodeoxynucleotide to delta-opioid receptor mRNA (delta-AS oligo) or a mismatch oligodeoxynucleotide (MM oligo) on the locomotor hyperactivity induced by [D-Ala2]deltorphin II was determined. Groups of mice pretreated i.c.v. with delta-AS oligo (1 microgram), MM oligo (1 microgram) or saline (4 microliters) once a day for 3 days, were injected i.c.v. [D-Ala2]deltorphin II (10 or 20 micrograms) and the locomotor response to [D-Ala2]deltorphin II was measured. The locomotor hyperactivity of i.c.v. [D-Ala2]deltorphin II (10 or 20 micrograms) were significantly suppressed by i.c.v. pretreatment with delta-AS oligo but not MM oligo. The present results indicate that pretreatment with delta-AS oligo suppresses mouse locomotor hyperactivity produced by stimulation of delta 2-opioid receptors in the brain.
机译：脑室内（i.c.v.）给药的[D-Ala2] deltorphin II（20微克）在雄性ICR小鼠中产生明显的运动过度活跃。运动性机能亢进是对i.c.v. [D-Ala2] deltorphin II（20微克）通过用纳曲本（NTB，10微克）而不是7-亚苄基纳曲酮（BNTX，1微克）和D-Phe-Cys-Tyr-D-Try-Orn- Thr-Phe-Thr-NH2（CTOP，100 ng）。确定了反义寡聚脱氧核苷酸对δ-阿片样物质受体mRNA（δ-AS寡聚）或错配寡聚脱氧核苷酸（MM寡聚）对由[D-Ala2] deltorphin II诱导的运动过度活跃的影响。成组的小鼠经静脉内预处理每天一次静脉内注射含delta-AS oligo（1微克），MM oligo（1微克）或生理盐水（4微升）的药物，共3天。测量[D-Ala2] deltorphin II（10或20微克）和对[D-Ala2] deltorphin II的运动反应。 i.c.v.的运动过度活跃[D-Ala2] deltorphin II（10或20微克）被i.c.v显着抑制。用delta-AS寡核苷酸而不是MM寡核苷酸进行预处理。目前的结果表明，用delta-AS寡核苷酸进行的预处理可抑制由于刺激大脑中的delta 2-阿片样物质受体而产生的小鼠运动亢进。

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