Fagin K D, Neill J D
Endocrinology. 1981 Dec;109(6):1835-40. doi: 10.1210/endo-109-6-1835.
The direct effects on PRL release of acute changes in dopamine (DA) and TRH concentrations were measured in an in vitro perifusion system. Hemisected anterior pituitaries of lactating rats were perifused with medium that received a coinfusion of DA at 20 ng/ml. These tissues released PRL at 35% of the release rate of controls in the absence of DA. Interruption of the DA coinfusion for 9 min caused a 2-fold increase in PRL release, which was resuppressed when the DA treatment was resumed. During continuous Da exposure, TRH administration (10 ng/ml for 12 min) induced a gradual but slight increase in PRL release. However, when this TRH treatment was administered immediately after the end of the DA interruption, it evoked an immediate 2-fold increase in PRL release to 4 times the initial release rate in the presence of DA. This pronounced effect of TRH after the brief DA interruption was also observed when an 18 min interval was imposed between the two manipulations. During continuous coinfusion of DA at 100 ng/ml, TRH was totally ineffective in eliciting PRL release. However, even after this DA treatment had been interrupted briefly and an increase in PRL release had been evoked, TRH still was not an effective stimulus for PRL release. T was imposed between the two manipulations. During continuous coinfusion of DA at 100 ng/ml, TRH was totally ineffective in eliciting PRL release. However, even after this DA treatment had been interrupted briefly and an increase in PRL release had been evoked, TRH still was not an effective stimulus for PRL release. T was imposed between the two manipulations. During continuous coinfusion of DA at 100 ng/ml, TRH was totally ineffective in eliciting PRL release. However, even after this DA treatment had been interrupted briefly and an increase in PRL release had been evoked, TRH still was not an effective stimulus for PRL release. These data indicate that DA not only can serve as a PRL-inhibiting factor for tonic release of PRL but also may determine by its presence or brief absence, and concentration whether acute release occurs in the presence of a PRL-releasing factor. The direct effect of DA on PRL release and its interference with the action of a PRL-releasing factor appear to be independent of each other.
在体外灌流系统中测定了多巴胺(DA)和促甲状腺激素释放激素(TRH)浓度的急性变化对催乳素(PRL)释放的直接影响。将泌乳大鼠的半切垂体前叶用含有20 ng/ml DA共同灌流的培养基进行灌流。在无DA的情况下,这些组织释放PRL的速率是对照释放速率的35%。中断DA共同灌流9分钟导致PRL释放增加2倍,当恢复DA处理时,PRL释放再次受到抑制。在持续暴露于DA期间,给予TRH(10 ng/ml,持续12分钟)可诱导PRL释放逐渐但轻微增加。然而,当在DA中断结束后立即给予这种TRH处理时,它会使PRL释放立即增加2倍,达到在有DA存在时初始释放速率的4倍。当在两种操作之间设置18分钟的间隔时,也观察到了在短暂DA中断后TRH的这种显著作用。在以100 ng/ml持续共同灌流DA期间,TRH在引发PRL释放方面完全无效。然而,即使在这种DA处理被短暂中断并引发PRL释放增加之后,TRH仍然不是PRL释放的有效刺激物。在两种操作之间设置了时间间隔。在以100 ng/ml持续共同灌流DA期间,TRH在引发PRL释放方面完全无效。然而,即使在这种DA处理被短暂中断并引发PRL释放增加之后,TRH仍然不是PRL释放的有效刺激物。在两种操作之间设置了时间间隔。在以100 ng/ml持续共同灌流DA期间,TRH在引发PRL释放方面完全无效。然而,即使在这种DA处理被短暂中断并引发PRL释放增加之后,TRH仍然不是PRL释放的有效刺激物。这些数据表明,DA不仅可以作为PRL紧张性释放的PRL抑制因子,而且其存在或短暂缺失以及浓度可能决定在有PRL释放因子存在时是否发生急性释放。DA对PRL释放的直接作用及其对PRL释放因子作用的干扰似乎是相互独立的。