Mizoguchi H, Narita M, Nagase H, Suzuki T, Quock R M, Tseng L F
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226, USA.
Life Sci. 1996;59(4):PL69-73. doi: 10.1016/0024-3205(96)00307-4.
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.
脑室内（i.c.v.）注射[D-Ala2]强啡肽II（20微克）可使雄性ICR小鼠产生明显的运动性活动亢进。腹腔注射纳曲苄（NTB，10微克）可抑制因脑室内注射[D-Ala2]强啡肽II（20微克）诱导的运动性活动亢进，但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纳克）则无此作用。研究了δ-阿片受体mRNA反义寡脱氧核苷酸（δ-AS寡核苷酸）或错配寡脱氧核苷酸（MM寡核苷酸）对[D-Ala2]强啡肽II诱导的运动性活动亢进的影响。将小鼠分为几组，每天一次脑室内注射δ-AS寡核苷酸（1微克）、MM寡核苷酸（1微克）或生理盐水（4微升），连续3天，然后脑室内注射[D-Ala2]强啡肽II（10或20微克），并测量对[D-Ala2]强啡肽II的运动反应。脑室内注射δ-AS寡核苷酸预处理可显著抑制脑室内注射[D-Ala2]强啡肽II（10或20微克）诱导的运动性活动亢进，而MM寡核苷酸则无此作用。目前的结果表明，δ-AS寡核苷酸预处理可抑制脑内δ2-阿片受体刺激产生的小鼠运动性活动亢进。
