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A Sex-Specific Endogenous Stimulatory Rhythm Regulating Prolactin Secretion^*

BRIAN J. AREY, ROBERT L. W. AVERILL and MARC E. FREEMAN

Department of Biological Sciences, Florida State University Tallahassee, Florida 323

Abstract

In the rat, PRL secretion is under inhibitory control by tuberoinfiindibular dopaminergic neurons. The levels of dopamine (DA) in hypophysial portal blood decline during surges of PRL secretion (e.g. suckling and cervical stimulation). However, this decline alone is not sufficient to account for the amount of PRL released. In this study we investigated the possible existence of an endogenous stimulatory rhythm for PRL secretion that may be masked by the tonic inhibitory tone of DA and unmasked by the DA-lowering effects of cervical stimulation. The PRL secretory response to pharmacological depression of DA-ergic tone was studied in ovariectomized (OVX) female, adult castrated (AC) male, neonatally androgen-sterilized (TP) female, and neonatally castrated (NC) male rats. Since mated rats have serum PRL surges at 0300 and 1700 h, these groups were treated with 200 µg/kg domperidone (DOM), N, at 0300 h, 1700 h, or the intersurge interval, 1200 h. Serial blood samples were collected immediately before and at frequent intervals after DOM injection. OVX female rats had significantly greater serum PRL responses to DOM at 0300 and 1700 h than at 1200 h. AC male rats secreted significantly less PRL in response to DOM compared to OVX rats, and their PRL responses to DOM were similar at all three times. TP female rats had PRL secretory responses similar to those of the OVX rats at 1200 h, and the responses at 0300 and 1700 h were similar. NC male rats had PRL secretory responses similar to those of AC male rats. There was no difference between the PRL secretory profiles at any time after DOM injection in NC rats. These data provide evidence for an endogenous stimulatory rhythm for PRL secretion that is specific to female rats. They further suggest that the neonatal steroid environment is critical for differentiation of some sexually specific characteristics. (Endocrinology 124: 119–123,1989)

Footnotes

^* This work was supported by NIH, NICHHD Grant HD-11669.

Supported by a Fulbright Fellowship. Present address: Zoology Department, Victoria University of New Zealand, Private Bag, Wellington, New Zealand.

To whom requests for reprints should be addressed.

Received June 14, 1988.

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