Expression of ovarian steroid hormone receptors in tuberoinfundibular dopaminergic neurones during pregnancy and lactation.
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.
Steyn
F J
FJ
Centre for Neuroendocrinology and Department of Anatomy and Structural Biology, University of Otago School of Medical Sciences, Dunedin, New Zealand.
Anderson
G M
GM
Grattan
D R
DR
D000222:Adaptation, Physiological; D000818:Animals; D001111:Arcuate Nucleus of Hypothalamus / Q000166:cytology / Q000378:metabolism; D004031:Diestrus / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism*; D047628:Estrogen Receptor alpha / Q000378:metabolism*; D005246:Feedback; D005260:Female; D007030:Hypothalamo-Hypophyseal System / Q000166:cytology / Q000378:metabolism; D007774:Lactation / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000378:metabolism*; D036801:Parturition / Q000378:metabolism; D011247:Pregnancy; D011388:Prolactin / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011980:Receptors, Progesterone / Q000378:metabolism*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D047628:Estrogen Receptor alpha; D011980:Receptors, Progesterone; D011388:Prolactin; D014446:Tyrosine 3-Monooxygenase; D004298:Dopamine