López F J, Dominguez J R, Sánchez-Franco F, Negro-Vilar A
Reproductive Neuroendocrinology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.
Endocrinology. 1989 Jan;124(1):527-35. doi: 10.1210/endo-124-1-527.
The present studies were designed to obtain a detailed characterization of pulsatile PRL secretory patterns under basal conditions and to explore the role of dopamine (DA) and vasoactive intestinal peptide (VIP) in the genesis of PRL pulses. Adult intact male rats received chronic indwelling jugular canula and were bled at 3-min intervals for periods ranging from 90-150 min. Pulse analysis was performed using the algorithm Detect. Blockade of DA receptors with domperidone, pimozide, or haloperidol resulted in a 2-fold increase in PRL pulse frequency, with no change in pulse duration. All quantitative parameters, i.e. peak and trough values, pulse amplitude, and area under the pulse, were significantly increased after dopaminergic blockade. Blockade of endogenous VIP activity was achieved by passive immunization with a potent VIP antiserum. This treatment, by itself, did not modify basal PRL levels or PRL pulsatility parameters. However, when VIP antiserum was administered in combination with domperidone, a reduction in all quantitative pulse parameters was observed. Heterogeneity of PRL pulses was evaluated by frequency distribution analysis, using the area under the pulse divided by basal secretion, to evaluate the mass of hormone secreted per pulse normalized to the basal rate of secretion. Untreated animals presented pulses within a range of different masses. Dopaminergic blockade resulted in a great reduction in big mass pulses, and the distribution of pulses was restricted primarily to small mass pulses. The increased pulse frequency after dopaminergic blockade, therefore, results mainly from an increase in the appearance of small mass pulses. These results indicate that DA exerts a tonic inhibitory action on the frequency as well as the qualitative parameters of PRL pulses. They also suggest that big mass PRL pulses are dopaminergic in origin, i.e. they may result from temporary interruptions in DA activity. Small mass PRL pulses appear to result from other neural stimulatory inputs. Endogenous VIP enhances quantitative PRL pulse parameters, but this activity is only apparent after removal of DA inhibition.
本研究旨在详细描述基础条件下促乳素（PRL）的脉冲式分泌模式，并探讨多巴胺（DA）和血管活性肠肽（VIP）在PRL脉冲产生中的作用。成年未阉割雄性大鼠植入慢性颈静脉插管，每隔3分钟采血一次，采血时间为90 - 150分钟。使用Detect算法进行脉冲分析。用多潘立酮、匹莫齐特或氟哌啶醇阻断DA受体会导致PRL脉冲频率增加2倍，脉冲持续时间无变化。多巴胺能阻断后，所有定量参数，即峰值和谷值、脉冲幅度和脉冲下面积，均显著增加。通过用高效VIP抗血清进行被动免疫来阻断内源性VIP活性。这种处理本身并未改变基础PRL水平或PRL脉冲参数。然而，当VIP抗血清与多潘立酮联合使用时，所有定量脉冲参数均降低。通过频率分布分析评估PRL脉冲的异质性，用脉冲下面积除以基础分泌量来评估每个脉冲分泌的激素量相对于基础分泌率的标准化值。未处理的动物出现一系列不同量的脉冲。多巴胺能阻断导致大量脉冲大幅减少，脉冲分布主要限于小量脉冲。因此，多巴胺能阻断后脉冲频率增加主要是由于小量脉冲出现增加。这些结果表明，DA对PRL脉冲的频率和定性参数发挥着紧张性抑制作用。它们还表明，大量PRL脉冲起源于多巴胺能，即它们可能是由DA活性的暂时中断导致的。小量PRL脉冲似乎是由其他神经刺激输入产生的。内源性VIP增强PRL脉冲的定量参数，但这种活性仅在去除DA抑制后才明显。
