Méndez M, Morán J, Wilk S, Joseph-Bravo P, Charli J L
Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos.
Brain Res Bull. 1993;31(5):621-5. doi: 10.1016/0361-9230(93)90131-t.
We have studied [3H]-dopamine ([3H]-DA) release from rat nucleus accumbens lateral septum slices in response to various paradigms aimed at increasing endogenous or exogenous thyrotropin releasing hormone (TRH) concentrations in the extracellular space. High KCl concentrations significantly enhanced [3H]-DA release by fourfold. TRH (10(-4) or 5 x 10(-4) M) did not affect [3H]-DA release. The release of [3H]-DA was not stimulated by TRH either in the presence of N-1-carboxy-2-phenylethyl (N(im)benzyl)-histidyl-beta naphthylamide, a specific pyroglutamyl peptidase II inhibitor, or that of specific inhibitors of prolyl endopeptidase and pyroglutamyl peptidase I. None of the peptidase inhibitors modified the [3H]-DA release by themselves. These results suggest that the TRH stimulation of [3H]-DA release in vitro observed in previous studies is not due to peptide inactivation but may be due to a nonspecific effect. TRH enhancement of DA release in nucleus accumbens in vivo may not be the result of a direct effect of TRH on DA terminals.
我们研究了大鼠伏隔核外侧隔切片中[3H] - 多巴胺（[3H] - DA）的释放情况，该释放是对各种旨在增加细胞外空间内源性或外源性促甲状腺激素释放激素（TRH）浓度的实验范式所做出的反应。高浓度氯化钾显著增强了[3H] - DA的释放，使其增加了四倍。TRH（10^(-4)或5×10^(-4) M）对[3H] - DA的释放没有影响。在存在特异性焦谷氨酸肽酶II抑制剂N - 1 - 羧基 - 2 - 苯乙基（N(im)苄基） - 组氨酰 - β - 萘酰胺，或脯氨酰内肽酶和焦谷氨酸肽酶I的特异性抑制剂的情况下，TRH也不会刺激[3H] - DA的释放。这些肽酶抑制剂自身均不会改变[3H] - DA的释放。这些结果表明，先前研究中观察到的体外TRH对[3H] - DA释放的刺激作用并非由于肽失活，而可能是由于非特异性效应。TRH在体内对伏隔核中多巴胺释放的增强作用可能不是TRH对多巴胺终末直接作用的结果。
