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      Impairments in Lactation in the Rat Following Destruction of the Median Raphe Nucleus

      ,

      Neuroendocrinology

      S. Karger AG

      Oxytocin, Lactation, Median raphe lesions, Lactogenic hormones

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          Abstract

          Lesions of the median raphe (MR) nucleus were placed in cycling female rats and their ability to lactate was evaluated following subsequent pregnancies. Pups from MR-lesioned (MRL) animals grew more slowly and had greatly impaired survival rates compared to pups from sham-lesioned animals. Chronic treatment of MRL mothers with oxytocin (Oxy; 1 IU, s.c, once or twice/day) did not increase the growth rates of their litters. Acute responses to exogenous Oxy (1 IU, i.p.) in MRL mothers, measured by the weight gain of litters during ½-h suckling intervals before and after injection, were marginally significant. Milk yield during the total hour suckling period (stomach contents of pups) was clearly less in the MRL animals (p < 0.01). Treatment with either prolactin (Prl; 250 μg, twice/day), Prl + GTC (4 mg/kg growth hormone, 30 μg/kg thyroxine, 0.5 mg/rat cortisol, once/day), or 5-HTP (75 mg 5-hydroxytryptoρhan/kg, twice/day) did not improve the growth rates of litters from MRL animals. However, when milk yield (stomach contents after 1 h) following a 14-h non-suckling interval was measured, lactogenic hormones (Prl or Prl + GTC) restored milk yield in MRL animals to control levels. This response was clearly not dependent upon exogenous Oxy. These results suggest that deficits in the release of lactogenic hormones are involved in the impairments in lactation following lesions of the MR nucleus.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1978
          1978
          26 March 2008
          : 26
          : 6
          : 333-351
          Affiliations
          Department of Pharmacology, Massachusetts College of Pharmacy, Boston, Mass. and Department of Physiology and Biophysics, Howard University College of Medicine, Washington, D.C.
          Article
          122789 Neuroendocrinology 1978;26:333–351
          10.1159/000122789
          692808
          © 1978 S. Karger AG, Basel

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          Page count
          Pages: 19
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