Steyn F J, Anderson G M, Grattan D R
Centre for Neuroendocrinology and Department of Anatomy and Structural Biology, University of Otago School of Medical Sciences, Dunedin, New Zealand.
J Neuroendocrinol. 2007 Oct;19(10):788-93. doi: 10.1111/j.1365-2826.2007.01590.x.
During late-pregnancy, tuberoinfundibular dopaminergic (TIDA) neurones, a critical component of the negative-feedback loop regulating prolactin secretion, become unresponsive to the stimulatory effects of prolactin. The change in TIDA responsiveness to prolactin at this time results in a decrease in dopamine secretion and a prolactin surge. As the onset of parturition and the antepartum prolactin surge depend on the withdrawal of progesterone in the presence of oestrogen, it is likely that ovarian steroid hormones mediate this change in TIDA responsiveness. To determine whether ovarian steroids can directly modulate TIDA activity, and whether changes of receptor numbers might contribute to overall steroid-regulation of these neurones, we investigated the level of oestrogen receptor alpha (ERalpha) and progesterone receptor (PR) expression within TIDA neurones during pregnancy and lactation. Animals were sacrificed on dioestrous, days 12, 19 and 21 of pregnancy and day 5 of lactation, and the proportion of TIDA neurones expressing ERalpha or PR, as well as the total number of PR expressing cells within the arcuate nucleus, was determined. Approximately 75% and 55% of tyrosine hydroxylase neurones expressed ERalpha and PR, respectively. Levels of steroid receptor expression within TIDA neurones remained fairly constant, except for an increase in ERalpha on days 12 and 19 of pregnancy compared to dioestrous and lactation day 5. The presence of steroid receptors on TIDA neurones during pregnancy and lactation supports the concept of a direct effect of steroid hormones on these neurones at this time. Thus, steroid hormones may directly act on TIDA neurones to regulate maternal prolactin secretion. The relatively stable level of expression during late pregnancy suggests that a shift in steroid receptor expression during late pregnancy does not contribute to the change in TIDA responsiveness to prolactin at this time.
在妊娠晚期，结节漏斗多巴胺能（TIDA）神经元是调节催乳素分泌的负反馈回路的关键组成部分，对催乳素的刺激作用变得无反应。此时TIDA对催乳素反应性的变化导致多巴胺分泌减少和催乳素激增。由于分娩的开始和产前催乳素激增取决于雌激素存在下孕酮的撤退，卵巢甾体激素很可能介导了TIDA反应性的这种变化。为了确定卵巢甾体激素是否能直接调节TIDA活性，以及受体数量的变化是否可能有助于这些神经元的整体甾体调节，我们研究了妊娠和哺乳期TIDA神经元内雌激素受体α（ERα）和孕酮受体（PR）的表达水平。在动情后期、妊娠第12、19和21天以及哺乳第5天处死动物，确定表达ERα或PR的TIDA神经元的比例，以及弓状核内表达PR的细胞总数。分别约75%和55%的酪氨酸羟化酶神经元表达ERα和PR。TIDA神经元内甾体受体的表达水平保持相当稳定，除了与动情后期和哺乳第5天相比，妊娠第12和19天ERα增加。妊娠和哺乳期TIDA神经元上存在甾体受体支持了此时甾体激素对这些神经元有直接作用的概念。因此，甾体激素可能直接作用于TIDA神经元以调节母体催乳素分泌。妊娠晚期相对稳定的表达水平表明，妊娠晚期甾体受体表达的变化并不导致此时TIDA对催乳素反应性的改变。
