Van Ree J M, Caffé A R, Wolterink G
Neuropharmacology. 1982 Nov;21(11):1111-7. doi: 10.1016/0028-3908(82)90168-x.
The hypoactivity in rats induced by small doses of apomorphine, injected bilaterally into the nucleus accumbens area of the brain, could be antagonized by pretreatment with the neuroleptic-like neuropeptide des-enkephalin-gamma-endorphin (DE gamma E, beta-endorphin 6-17) as well as with the neuroleptic drugs haloperidol, sulpiride and clozapine injected into the accumbens. Dose-response studies revealed that a dose of 100 pg DE gamma E completely inhibited the apomorphine-induced hypomotility. The influence of DE gamma E appeared to be specific for gamma-type endorphins, since alpha-type endorphins were inactive in this respect. Treatment with DE gamma E injected into the accumbens for 4 days resulted in an enhancement of apomorphine-induced hypoactivity. It is concluded that gamma-type endorphins may control the activity of dopaminergic transmission in the nucleus accumbens, a suggestion which may be of significance for the purported neuroleptic-like and antipsychotic action of gamma-type endorphins.
双侧注射小剂量阿扑吗啡至大鼠脑伏隔核区域所诱导的活动减退,可被神经安定样神经肽去甲脑啡肽-γ-内啡肽(DEγE,β-内啡肽6-17)预处理拮抗,也可被注射至伏隔核的神经安定药物氟哌啶醇、舒必利和氯氮平拮抗。剂量反应研究显示,100 pg DEγE的剂量可完全抑制阿扑吗啡诱导的运动减少。DEγE的影响似乎对γ型内啡肽具有特异性,因为α型内啡肽在这方面无活性。向伏隔核注射DEγE治疗4天导致阿扑吗啡诱导的活动减退增强。结论是γ型内啡肽可能控制伏隔核中多巴胺能传递的活性,这一观点可能对γ型内啡肽所谓的神经安定样和抗精神病作用具有重要意义。