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Posterior Pituitary Lobectomy: Differential Elevation of Plasma Prolactin and Luteinizing Hormone in Estrous and Lactating Rats^*

NIRA BEN-JONATHAN and LUANNE L. PETERS

Department of Physiology, Indiana University School of Medicine, Indianapolis, Indiana 46223

Address requests for reprints to: Nira Ben-Jonathan, Department of Physiology, Indiana University School of Medicine, 1100 West Michigan Street, Indianapolis, Indiana 46223.

Abstract

The effects of posterior pituitary lobectomy on PRL and LH secretion in estrous and lactating rats were examined. Blood was collected from a femoral artery immediately before and at various times after the removal of the posterior lobe from anesthetized rats. Rats in estrus were also subjected to chronic posterior lobectomy, and their water consumption and vaginal cytology were determined for 3 weeks.

Within 5–10 min after posterior lobectomy in estrous rats, plasma PRL increased 3-fold, but declined to near control levels by 1–2 h. Plasma LH increased more gradually, reaching 4 times the control level after 2–3 h. No change was observed in plasma GH. Injection of dopamine to posterior lobectomized estrous rats caused an immediate fall in plasma PRL, but no change in LH. Plasma PRL in lactating rats increased 4-fold after posterior lobectomy, reaching a peak concentration by 30 min and remaining elevated for at least 3 h; plasma LH was unchanged. Eighty percent of chronic posterior lobecomized rats became pseudopregnant and then resumed normal cyclicity. Water consumption increased 3-fold after posterior lobectomy, but declined to 60–70% above the control level after 2–3 weeks.

The data suggest that the posterior lobe participates in the regulation of PRL secretion via a dopaminergic mechanism; such regulation might be more pronounced during lactation than in estrus. In addition, the posterior pituitary appears to contribute to the regulation of LH secretion during estrus. The factor (s) of posterior pituitary origin responsible for inhibiting LH secretion is unknown at the present time.

Footnotes

^* Presented in part at the 62nd Annual Meeting of The Endocrine Society, Washington, D.C., June 1980. This work was supported by NIH Grants NS-13234 and HD-14348.

Recipient of Research Career Development Award NS-219

Received December 7, 1981.

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