Ukponmwan O E, Murugaiah K D
Department of Physiological Sciences, Obafemi Awolowo University, Ile-Ife Oyo State, Nigeria.
Pharmacol Res. 1990 Nov-Dec;22(6):691-9. doi: 10.1016/s1043-6618(05)80095-7.
Intracerebroventricular administration of the enkephalinase inhibitor, phosphoramidon (PHA, 3.7 X 10(-7) moles, i.c.v.) induced distinct wet-dog-shakes (WDS) behaviour. Naltrexone (NX) given in a low dose (0.25 mg/kg, i.p.) did not antagonize the WDS induced by PHA. A higher dose of NX (2.5 mg/kg i.p.) decreased WDS behaviour. Morphine (25 mg/kg, i.p.) induced marked catalepsy. Ketocyclazocine (0.01-1.0 mg/kg, i.p.) induced a dose related decrease in spontaneous locomotor activity. Chronic (20 mg/kg, i.p. daily for 10 days and withdrawn, 24 h prior, C.CLO) and acute (20 mg/kg, i.p., 60 min prior, A.CLO) clomipramine treatments decreased PHA-induced WDS compared to saline pretreatments. However, C.CLO treatments antagonized the morphine-induced catalepsy and ketocyclazocine-induced sedation whereas A.CLO did not alter the opiate-induced cataleptic/sedative behaviours. It is suggested that chronic clomipramine treatment induced a functional deficiency of central mu and kappa opioid receptor systems without altering the delta opioid mechanisms.
脑室内注射脑啡肽酶抑制剂福斯屈胺（PHA，3.7×10⁻⁷摩尔，脑室内注射）可诱发明显的湿狗样抖动（WDS）行为。腹腔注射低剂量纳曲酮（NX，0.25毫克/千克）不能拮抗PHA诱导的WDS。较高剂量的NX（腹腔注射2.5毫克/千克）可减少WDS行为。吗啡（腹腔注射25毫克/千克）可诱发明显的僵住症。酮环唑辛（腹腔注射0.01 - 1.0毫克/千克）可使自发运动活性呈剂量依赖性降低。与生理盐水预处理相比，慢性氯米帕明治疗（腹腔注射20毫克/千克，每日一次，共10天，在实验前24小时停药，C.CLO）和急性氯米帕明治疗（腹腔注射20毫克/千克，在实验前60分钟，A.CLO）可减少PHA诱导的WDS。然而，C.CLO治疗可拮抗吗啡诱导的僵住症和酮环唑辛诱导的镇静作用，而A.CLO对阿片类药物诱导的僵住症/镇静行为无影响。提示慢性氯米帕明治疗可导致中枢μ和κ阿片受体系统功能缺陷，而不改变δ阿片机制。
