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Research Article Free access | 10.1172/JCI118153

Lactation as a model for naturally reversible hypercorticalism plasticity in the mechanisms governing hypothalamo-pituitary- adrenocortical activity in rats.

D Fischer, V K Patchev, S Hellbach, A H Hassan, and O F Almeida

Department of Neuroendocrinology, Max Planck Institute of Psychiatry (Clinical Institute), Munich, Germany.

Find articles by Fischer, D. in: PubMed | Google Scholar

Department of Neuroendocrinology, Max Planck Institute of Psychiatry (Clinical Institute), Munich, Germany.

Find articles by Patchev, V. in: PubMed | Google Scholar

Department of Neuroendocrinology, Max Planck Institute of Psychiatry (Clinical Institute), Munich, Germany.

Find articles by Hellbach, S. in: PubMed | Google Scholar

Department of Neuroendocrinology, Max Planck Institute of Psychiatry (Clinical Institute), Munich, Germany.

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Department of Neuroendocrinology, Max Planck Institute of Psychiatry (Clinical Institute), Munich, Germany.

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Published September 1, 1995 - More info

Published in Volume 96, Issue 3 on September 1, 1995
J Clin Invest. 1995;96(3):1208–1215. https://doi.org/10.1172/JCI118153.
© 1995 The American Society for Clinical Investigation
Published September 1, 1995 - Version history
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Abstract

Steady state levels of hypothalamic expression of the genes encoding corticotropin-releasing hormone (CRH), proopiomelanocortin (POMC), arginine vasopressin (AVP), and oxytocin (OT) were studied in rats to investigate the mechanisms underlying the transitions between hypercorticalism during lactation and normocorticalism upon weaning. During lactation, CRH mRNA levels and blood titers of adrenocorticotropin (ACTH) were found to be significantly reduced, although POMC mRNA levels in the anterior pituitary were not significantly different from those found in cycling virgin (control) rats; during all phases of lactation, an inverse relationship was observed between the blood levels of ACTH and corticosterone (CORT). Plasma prolactin (PRL) concentrations were elevated approximately 30-fold during lactation. Whereas steady state levels of OT mRNA were markedly increased throughout lactation, those of AVP mRNA were only transiently (initially) elevated, and the blood levels of these hormones were not significantly altered in lactating as compared with cycling virgin and postlactating rats. CRH and POMC gene expression and blood levels of ACTH, CORT, and PRL were normalized within 1-3 d of removal of suckling pups. The temporal relationships between the biosynthetic profiles of the various peptide hormones and the patterns of ACTH and CORT secretion during the two physiological states suggest that lactation-associated hypercorticalism does not merely result from increased ACTH secretion; although still not well substantiated at this time, the evidence points to contributory roles of PRL, OT, and AVP in the hypercorticalismic state found during lactation.

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