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Control of the Estradiol-Induced Prolactin Surge by the Suprachiasmatic Nucleus

Netherlands Institute for Brain Research (I.F.P., J.v.d.V., R.M.B., A.K.), 1105 AZ Amsterdam, The Netherlands; Human and Animal Physiology Group (I.F.P., E.M.v.d.B., H.J.M.S.), Department of Animal Sciences, Wageningen University, Wageningen 6709 PJ, The Netherlands; and Medical Pharmacology Group (V.M.W.), Rudolf Magnus Institute for Neurosciences, University Medical Center Utrecht, Utrecht 3584 CG, The Netherlands

Address all correspondence and requests for reprints to: I. F. Palm, Netherlands Institute for Brain Research, Meibergdreef 33, 1105 AZ Amsterdam, The Netherlands. E-mail: I.Palm{at}nih.knaw.nl

In the present study we investigated how the suprachiasmatic nucleus (SCN) controls the E₂-induced PRL surge in female rats. First, the role of vasopressin (VP), a SCN transmitter present in medial preoptic area (MPO) projections and rhythmically released by SCN neurons, as a circadian signal for the E₂-induced PRL surge was investigated. Using a reverse microdialysis technique, VP was administered in the MPO during the PRL surge, resulting in a suppression of the surge. VP administration before the surge did not affect PRL secretion. Also, administration of a V1a receptor antagonist before the surge was ineffective. Second, lesions of the SCN were made that resulted in constant basal PRL levels, suggesting that with removal of the SCN a stimulatory factor for PRL secretion disappeared. Indeed, the PRL secretory response to blockade of pituitary dopamine receptors was significantly reduced in SCN-lesioned animals. These data suggest that the afternoon decrease of VP release in the MPO by SCN terminals enables the PRL surge to occur, and may thus be a circadian signal for the PRL surge. Simultaneously the SCN is involved in the regulation of the secretory capacity of the pituitary, possibly via specific PRL-releasing factors.

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