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Effect on Growth of Prolactin Deficiency Induced in Infant Mice^*

Lutcher Brown Center for Diabetes and Endocrinology, Scripps Clinic and Research Foundation, La Jolla, California 92037

Address requests for reprints to: Dr. Y. N. Sinha, Whittier Institute for Diabetes and Endocrinology, Scripps Memorial Hospital, 9894 Genesee Avenue, La Jolla, California 92037.

Abstract

The effect of lowering PRL levels in blood during early infancy on subsequent growth and development was studied in mice. PRL was reduced by injecting either an antiserum raised against homologous PRL or a PRL-inhibiting drug, 2- chloro-6-methylergoline-8β-acetonitrile methanesulfonate (ergoline), into 4-day-old mice for a period of 4 or 5 days. Both the anti-PRL serum and ergoline rapidly killed some of the injected animals, but the effect of anti-PRL serum was much more severe than that of ergoline (39% vs. 8.7% mortality during the period of injection). Similar administration of an antiserum against mouse GH or the GH-inhibiting peptide somatostatin did not cause a significant number of deaths. The deaths from the anti-PRL serum largely ceased when the antiserum was neutralized with rat PRL (NIH-RP-1) before injection. The gain in body weight of baby mice was markedly retarded within 24 h of injecting anti-PRL serum and ergoline, in contrast to the anti-GH serum and somatostatin injections, which took 3–4 days to inhibit growth perceptibly. The anti-PRL serum, despite having only one eighth the titer of anti-GH serum, was by far the most effective of the two antisera in diminishing tibial epiphyseal cartilage width as well as weights of pituitary glands, testes, and adrenals and retarding sexual maturity. The more severe and generalized developmental abnormalities and the incidence of mortality as a result of anti-PRL serum administration suggest that PRL in mice may be involved in the maintenance of some vital function during infancy.

Footnotes

^* his work was supported by Grants CA-18664 and AM-5249 from the NIH, DHEW. Portions of these data were presented at the 53rd Annual Meeting of The Endocrine Society, San Francisco, CA, June 24–26, 1971 (Abstract 166). This is publication 51 from the Lutcher Brown Center for Diabetes and Endocrinology.

Received November 23, 1981.

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