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Volume 16, Number 16, Issue of August 15, 1996 pp. 4823-4834
Copyright ©1996 Society for Neuroscience

Dopaminergic Regulation of Progesterone Receptors: Brain D5 Dopamine Receptors Mediate Induction of Lordosis by D1-Like Agonists in Rats

Received Dec. 27, 1995; revised May 8, 1996; accepted May 13, 1996.

Ede Marie Apostolakis1, Janos Garai2, Charles Fox3, Carolyn L. Smith1, Stanley J. Watson4, James H. Clark1, and Bert W. O'Malley1

1 Department of Cell Biology, Baylor College of Medicine, Houston, Texas 77030, 2 Department of Pathophysiology, University Medical School of Pécs, Pécs, Hungary, 3 Engineering Animation Inc., Ames, Iowa 50010, and 4 Mental Health Research Institute, University of Michigan, Ann Arbor, Michigan 48109

To characterize the signaling pathway by which the neurotransmitter dopamine modulates progesterone receptor (PR) activation, the steroid-dependent behavior lordosis was used in estrogen-primed ovariectomized Sprague-Dawley rats with stereotaxic implanted third ventricle cannulas. Lordosis was observed in response to solicitous males in females after central administration of the D1-like agonist SKF38393 and three of its analogs (SKF77434, SKF75640, and SKF85174). In contrast, D1-like antagonist SCH23390 and D1-like/D2 repopulation inhibitor EEDQ blocked behavior inducible by the D1-like agonists. Further, antisense oligonucleotides to D5, but not D1, dopamine receptor mRNA suppressed reproductive behavior associated with D1-like stimulation. This finding provides strong evidence that dopaminergic modulation of lordosis is mediated by the novel D5 dopamine receptor. Although D1, but not D5, dopamine receptor mRNAs were detected in the ventromedial nucleus (VMN) by in situ hybridization, agonists microinjected into the VMN, but not into the arcuate nucleus or preoptic area, induced lordosis, suggesting the functional presence of D5 dopamine receptors in the VMN. Also in support, D5 receptor mRNA antisense microinjected into the VMN blocked the subsequent induction of lordosis by D1-like agonists. Finally, facilitation of sex behavior by D1-like agonists was blocked by the antiprogestin RU38486 and PR antisense oligonucleotide. Collectively, the data provide strong evidence for dopaminergic modulation of reproductive behavior through D5 dopamine receptor-mediated modulation of PR-dependent behavior in rat CNS.

Key words: steroid receptors; D5 dopamine receptors; lordosis; antisense oligonucleotides; progesterone; estrogen




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