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      Permanent link:
      https://www.ias.ac.in/article/fulltext/jbsc/007/02/0095-0103

    • Keywords

       

      Lactational amennorrhea; hyperprolactinemia; ovary; luteinizing hormone; lactogenic hormone

    • Abstract

       

      Lactating bonnet monkeys were used as a model to understand the mechanism of ovarian quiescence during lactation. The ovary of the bonnet monkey in the 3rd month of lactation responds well to exogenous pregnant mare serum gonadotropin stimulation with serum estrogen values reaching maximal levels by day 3 of the gonadotropin injection. The adminstration of ovine prolactin to such monkeys significantly inhibited the ovarian responsiveness to exogenous gonadotropin. The responsiveness of the pituitary of the lactating monkey (in the 3rd month of lactation) to luteinizing hormone releasing hormone injection was suppressed and supplementation with exogenous prolactin further accentuating this effect. The relative ability of chlorpromazine given intravenously/intramuscularly/intranasally to enhance endogenous prolactin levels was assessed. During the first 5 months of lactation when the basal prolactin levels were high, the luteinizing hormone levels were low. As the suckling stimulus reduces and prolactin levels fall, luteinizing hormone levels increase, the first post-parturient mensus occurring by 218 ± 4 days. This event was postponed by 3 months on increasing endogenous prolactin levels by administering chlorpromazine (250 μg/day by intranasal mode) over a 5 day period every month starting from the 3rd month of lactation.

    • Author Affiliations

       

      N R Moudgal1 R Maneckjee1 B R Srinath1 K Ramasharma1

      1. Center for Advanced Research in Reproductive Biology, Department of Biochemistry, Indian Institute of Science, Bangalore - 560 012, India
    • Dates

       
  • Journal of Biosciences | News

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