Radhakishun F S, Stoof J C, Mulder A H, Versteeg D H, van Ree J M
Department of Neurology, Free University, Amsterdam, The Netherlands.
Brain Res. 1987 Nov 24;426(2):235-42. doi: 10.1016/0006-8993(87)90877-8.
In rats, the non-opioid beta-endorphin (beta E) fragment desenkephalin-gamma-endorphin (DE gamma E, beta E6-17) antagonizes the hypomotility induced by a small dose of dopamine (DA) receptor agonists. It has been suggested that DE gamma E might act in this respect by a direct or indirect blockade of presynaptically located DA receptors in the nucleus accumbens, thereby causing an increase of DA release. Therefore in the present study the effect of DE gamma E was examined on DA receptor agonist-induced inhibition of the electrically evoked release of previously accumulated [3H]DA from rat nucleus accumbens slices in vitro. The DA receptor agonists apomorphine, LY 171555 and n,n-di-n-propyl-7-hydroxy-2-aminotetralin (DP-7-AT) inhibited in a concentration-dependent manner the electrically evoked release of [3H]DA. The selective D2 receptor antagonist (-)-sulpiride blocked the effects of apomorphine, corroborating that the DA receptor involved is of a D2 type. DE gamma E was tested at several concentrations (10(-9)-10(-6) M) and under various experimental conditions. DE gamma E, by itself, did not affect either the electrically stimulated or the basal release of [3H]DA. The inhibiting effect of DA receptor agonists was slightly reduced by DE gamma E, but this effect was present in some experiments only. It is concluded that DE gamma E does not function as an antagonist for the DA receptor mediating DA release and that the interaction observed in behavioural experiments between DA agonists and DE gamma E does not occur at the level of this receptor.
在大鼠中,非阿片类β-内啡肽(βE)片段脱脑啡肽-γ-内啡肽(DEγE,βE6-17)可拮抗小剂量多巴胺(DA)受体激动剂诱导的运动减少。有人提出,DEγE在这方面可能通过直接或间接阻断伏隔核中突触前定位的DA受体起作用,从而导致DA释放增加。因此,在本研究中,检测了DEγE对DA受体激动剂诱导的体外大鼠伏隔核切片中预先积累的[3H]DA电诱发释放的抑制作用。DA受体激动剂阿扑吗啡、LY 171555和n,n-二正丙基-7-羟基-2-氨基四氢萘(DP-7-AT)以浓度依赖性方式抑制[3H]DA的电诱发释放。选择性D2受体拮抗剂(-)-舒必利阻断了阿扑吗啡的作用,证实所涉及的DA受体为D2型。在几种浓度(10(-9)-10(-6)M)下和各种实验条件下对DEγE进行了测试。DEγE本身既不影响[3H]DA的电刺激释放,也不影响其基础释放。DEγE使DA受体激动剂的抑制作用略有降低,但仅在某些实验中出现这种作用。结论是,DEγE不作为介导DA释放的DA受体的拮抗剂起作用,并且在行为实验中观察到的DA激动剂与DEγE之间的相互作用不在该受体水平发生。