Hentschel K, Moore K E, Lookingland K J
Department of Pharmacology and Toxicology, Michigan State University, B-432 Life Sciences Bldg., East Lansing, MI 48824-1317, USA.
Brain Res. 2000 Feb 28;857(1-2):110-8. doi: 10.1016/s0006-8993(99)02362-8.
Dual immunohistochemistry was employed to determine the effects of prolactin on expression of Fos and its related antigens (FRA) in tuberoinfundibular dopamine (TIDA) neurons located in the dorsomedial (DM) and ventrolateral (VL) subdivisions of the arcuate nucleus (ARC) in the male rat. Systemic administration of the DA receptor antagonist haloperidol caused a sustained (up to 12 h) increase in plasma prolactin concentrations that was accompanied by a transient increase (at 3 h) in the percentage of tyrosine hydroxylase (TH)-immunoreactive (IR) neurons containing FRA-IR nuclei in the DM-ARC. In contrast, haloperidol caused a prolonged (1. 5 to 12 h) decrease in the percentage of TH-IR neurons with FRA-IR nuclei in the VL-ARC. Haloperidol had no effect, however, on the overall number of TH-IR neurons in either of these regions. Co-administration of prolactin antisera (PRL-AB) blocked haloperidol-induced increases in both plasma prolactin concentrations and the percentage of TH-IR neurons expressing FRA in the DM-ARC, but had no effect on haloperidol-induced inhibition of FRA expression in TH-IR neurons in the VL-ARC. Intracerebroventricular (i.c.v.) administration of prolactin also increased the percentage of TH-IR neurons containing FRA-IR nuclei in the DM-ARC, but this effect was of longer duration (up to 6 h) than that of haloperidol in all but the most caudal portion of the DM-ARC. In the VL-ARC, prolactin caused a transient increase (at 1.5 h) in the percentage of TH-IR containing FRA-IR nuclei. These results demonstrate that prolactin regulates immediate early gene expression in TIDA neurons in male rats, and reveal that there are temporal differences in the responsiveness of discrete subpopulations of these neurons to prolactin. Prolactin causes a short-lived increase in FRA expression in TIDA neurons in the VL-ARC which is followed by a more prolonged activation of FRA expression in TIDA neurons in the DM-ARC.
采用双重免疫组织化学法，以确定催乳素对雄性大鼠弓状核（ARC）背内侧（DM）和腹外侧（VL）亚区的结节漏斗多巴胺（TIDA）神经元中Fos及其相关抗原（FRA）表达的影响。系统性给予多巴胺受体拮抗剂氟哌啶醇可使血浆催乳素浓度持续升高（长达12小时），同时伴随着DM-ARC中含FRA-免疫反应性（IR）细胞核的酪氨酸羟化酶（TH）免疫反应性（IR）神经元百分比的短暂升高（3小时时）。相比之下，氟哌啶醇可使VL-ARC中含FRA-IR细胞核的TH-IR神经元百分比持续降低（1.5至12小时）。然而，氟哌啶醇对这两个区域中TH-IR神经元的总数没有影响。同时给予催乳素抗血清（PRL-AB）可阻断氟哌啶醇诱导的血浆催乳素浓度升高以及DM-ARC中表达FRA的TH-IR神经元百分比升高，但对氟哌啶醇诱导的VL-ARC中TH-IR神经元FRA表达抑制没有影响。脑室内（i.c.v.）注射催乳素也可增加DM-ARC中含FRA-IR细胞核的TH-IR神经元百分比，但除DM-ARC最尾端部分外，此效应的持续时间（长达6小时）比氟哌啶醇的效应更长。在VL-ARC中，催乳素可使含FRA-IR细胞核的TH-IR神经元百分比短暂升高（1.5小时时）。这些结果表明，催乳素可调节雄性大鼠TIDA神经元中即早基因的表达，并揭示这些神经元的不同亚群对催乳素的反应存在时间差异。催乳素可使VL-ARC中TIDA神经元的FRA表达短暂增加，随后DM-ARC中TIDA神经元的FRA表达被更持久地激活。
