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首页> 外文期刊>Journal of neuroendocrinology >Reduced dopaminergic tone during lactation is permissive to the hypothalamic stimulus for suckling-induced prolactin release
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Reduced dopaminergic tone during lactation is permissive to the hypothalamic stimulus for suckling-induced prolactin release

机译：减少的多巴胺能音调在哺乳期间允许乳酸诱导的脯氨酸释放的下丘脑刺激

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Dopamine from tuberoinfundibular dopaminergic (TIDA) neurones tonically inhibits prolactin (PRL) secretion. Lactational hyperprolactinaemia is associated with a reduced activity of TIDA neurones. However, it remains controversial whether the suckling-induced PRL surge is driven by an additional decrease in dopamine release or by stimulation from a PRL-releasing factor. In the present study, we further investigated the role of dopamine in the PRL response to suckling. Non-lactating (N-Lac), lactating 4 hour apart from pups (Lac), Lac with pups return and suckling (Lac+S), and post-lactating (P-Lac) rats were evaluated. PRL levels were elevated in Lac rats and increased linearly within 30 minutes of suckling in Lac+S rats. During the rise in PRL levels, dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) levels in the median eminence (ME) and neurointermediate lobe of the pituitary did not differ between Lac+S and Lac rats. However, dopamine and DOPAC were equally decreased in Lac and Lac+S compared to N-Lac and P-Lac rats. Suckling, in turn, reduced phosphorylation of tyrosine hydroxylase in the ME of Lac+S. Domperidone and bromocriptine were used to block and activate pituitary dopamine D2 receptors, respectively. Domperidone increased PRL secretion in both N-Lac and Lac rats, and suckling elicited a robust surge of PRL over the high basal levels in domperidone-treated Lac+S rats. Conversely, bromocriptine blocked the PRL response to suckling. The findings obtained in the present study provide evidence that dopamine synthesis and release are tonically reduced during lactation, whereas dopamine is still functional with respect to inhibiting PRL secretion. However, there appears to be no further reduction in dopamine release associated with the suckling-induced rise in PRL. Instead, the lower dopaminergic tone during lactation appears to be required to sensitise the pituitary to a suckling-induced PRL-releasing factor.
机译：来自结节-漏斗多巴胺能神经元（TIDA）的多巴胺张力性抑制催乳素（PRL）分泌。哺乳期高泌乳素血症与TIDA神经元活性降低有关。然而，哺乳诱导的PRL激增是由多巴胺释放的额外减少还是由PRL释放因子的刺激引起的，目前仍存在争议。在本研究中，我们进一步研究了多巴胺在泌乳时PRL反应中的作用。对非哺乳期（N-Lac）、离幼崽4小时哺乳期（Lac）、幼崽返回哺乳期（Lac+S）和哺乳后（P-Lac）大鼠进行评估。Lac大鼠的PRL水平升高，Lac+S大鼠在哺乳30分钟内呈线性增加。在PRL水平升高期间，Lac+S和Lac大鼠垂体正中隆起（ME）和神经中间叶的多巴胺和3,4-二羟基苯乙酸（DOPAC）水平没有差异。然而，与N-Lac和P-Lac大鼠相比，Lac和Lac+S大鼠的多巴胺和DOPAC同样减少。反过来，哺乳降低了Lac+S的ME中酪氨酸羟化酶的磷酸化。多潘立酮和溴隐亭分别用于阻断和激活垂体多巴胺D2受体。多潘立酮增加了N-Lac和Lac大鼠的PRL分泌，在多潘立酮治疗的Lac+S大鼠中，哺乳引起PRL在高基础水平上激增。相反，溴隐亭阻断了PRL对哺乳的反应。本研究中获得的结果提供了证据，证明在哺乳期多巴胺的合成和释放张力降低，而多巴胺在抑制PRL分泌方面仍有功能。然而，与哺乳诱导的PRL升高相关的多巴胺释放似乎没有进一步减少。相反，哺乳期较低的多巴胺能张力似乎是使垂体对哺乳诱导的PRL释放因子敏感所必需的。

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