Wambebe C
Jpn J Pharmacol. 1987 Feb;43(2):121-8. doi: 10.1254/jjp.43.121.
In this paper, the effects of three antipsychotic agents using the avian species laboratory model are described. d-Amphetamine (2-5 mg/kg, s.c.) dose-dependently antagonized catalepsy induced by haloperidol (0.25 mg/kg, i.p.), YM-09151-2 (0.02-0.04 mg/kg, i.p.) and (-)-sulpiride (20-40 mg/kg, i.p.) in rats. (-)-Sulpiride (10-40 mg/kg, i.p.) dose-dependently antagonized apomorphine (0.125 mg/kg, s.c.)-induced stereotyped behavior in young chicks. Similarly, YM-09151-2 (0.04 mg/kg, i.p.) antagonized apomorphine (0.125 mg/kg, s.c.)-induced stereotyped behavior in young chicks. (-)-Sulpiride (40 mg/kg, i.p.) significantly antagonized apomorphine (0.25 mg/kg, s.c.)-induced stereotyped behavior in 6 week old chicks. Parachlorophenylalanine (PCPA, 300 mg/kg, i.p.) significantly reduced the intensity of stereotyped behavior induced by apomorphine (0.125 mg/kg, s.c.) in young chicks. However, (-)-sulpiride (40 mg/kg, i.p.) did not significantly influence the effect of PCPA on apomorphine-induced stereotyped behavior. Similarly, catalepsy induced by (-)-sulpiride (40 mg/kg, i.p.), haloperidol (0.25 mg/kg, i.p.) and YM-09151-2 (0.04 mg/kg, i.p.) in male rats was profoundly suppressed by PCPA (300 mg/kg, i.p.). The present results indicate that apomorphine-induced stereotyped pecking in young (4-6 day old) chicks may serve as a suitable laboratory model for testing potential antipsychotic drugs. In addition, the data indicates that endogenous 5-hydroxytryptamine mechanisms may be involved in the genesis of drug-induced catalepsy in rats.
本文描述了使用鸟类实验室模型研究三种抗精神病药物的效果。右旋苯丙胺(2 - 5毫克/千克,皮下注射)能剂量依赖性地拮抗氟哌啶醇(0.25毫克/千克,腹腔注射)、YM - 09151 - 2(0.02 - 0.04毫克/千克,腹腔注射)和(-)-舒必利(20 - 40毫克/千克,腹腔注射)诱导的大鼠僵住症。(-)-舒必利(10 - 40毫克/千克,腹腔注射)能剂量依赖性地拮抗阿扑吗啡(0.125毫克/千克,皮下注射)诱导的幼雏刻板行为。同样,YM - 09151 - 2(0.04毫克/千克,腹腔注射)能拮抗阿扑吗啡(0.125毫克/千克,皮下注射)诱导的幼雏刻板行为。(-)-舒必利(40毫克/千克,腹腔注射)能显著拮抗阿扑吗啡(0.25毫克/千克,皮下注射)诱导的6周龄雏鸡刻板行为。对氯苯丙氨酸(PCPA,300毫克/千克,腹腔注射)能显著降低阿扑吗啡(0.125毫克/千克,皮下注射)诱导的幼雏刻板行为强度。然而,(-)-舒必利(40毫克/千克,腹腔注射)对PCPA拮抗阿扑吗啡诱导的刻板行为的效果没有显著影响。同样,PCPA(300毫克/千克,腹腔注射)能显著抑制(-)-舒必利(40毫克/千克,腹腔注射)、氟哌啶醇(0.25毫克/千克,腹腔注射)和YM - 09151 - 2(0.04毫克/千克,腹腔注射)诱导的雄性大鼠僵住症。目前的结果表明,阿扑吗啡诱导的幼雏(4 - 6日龄)刻板啄食行为可作为测试潜在抗精神病药物的合适实验室模型。此外,数据表明内源性5 - 羟色胺机制可能参与了大鼠药物诱导僵住症的发生。