Codd E E, Scholtens H, Wolterink G, Verhoef J C, Van Ree J M, Witter A
Eur J Pharmacol. 1983 Apr 8;88(4):365-70. doi: 10.1016/0014-2999(83)90587-3.
The beta-endorphin (beta E) fragment des-Tyr1-gamma-endorphin (DT gamma E, beta E-(2-17)) has been reported to interact with neuroleptic binding in vivo but not in vitro. We have attempted to replicate the in vivo experiments and extended the work to include conditions in which des-enkephalin-gamma-endorphin (DE gamma E, beta E-(6-17)) exhibited behavioral activity. Systemically administered haloperidol significantly elevated plasma and decreased striatal [3H]spiperone. DE gamma E significantly elevated plasma [3H]apomorphine when both substances were injected directly into the nucleus accumbens. gamma-type endorphins consistently but non significantly decreased brain spiperone or apomorphine binding. It is concluded that the interaction between gamma-type endorphins and dopaminergic binding sites may be either indirect or limited to a subset of these sites.
据报道，β-内啡肽（βE）片段去酪氨酸1-γ-内啡肽（DTγE，βE-(2-17)）在体内而非体外与抗精神病药物结合相互作用。我们试图重复体内实验，并将工作扩展至包括去脑啡肽-γ-内啡肽（DEγE，βE-(6-17)）表现出行为活性的条件。全身给予氟哌啶醇显著升高血浆并降低纹状体[3H]螺哌隆。当两种物质都直接注射到伏隔核时，DEγE显著升高血浆[3H]阿扑吗啡。γ型内啡肽持续但不显著地降低脑内螺哌隆或阿扑吗啡结合。结论是γ型内啡肽与多巴胺能结合位点之间的相互作用可能是间接的，或仅限于这些位点的一个子集。
