Effects of bromocriptine and naloxone on plasma levels of prolactin, LH and FSH during suckling in the female rat: responses to gonadotrophin releasing hormone

in Journal of Endocrinology
Authors:
D. J. S. Sirinathsinghji
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L. Martini
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ABSTRACT

The roles of dopamine and the endogenous opiate peptides in the mediation of the inverse relationship between prolactin and gonadotrophin secretion during lactation were studied by comparing the effects of bromocriptine and naloxone on plasma levels of prolactin, LH and FSH during suckling in the female rat. The effects of exogenous gonadotrophin releasing hormone (GnRH) on the LH and FSH responses to bromocriptine and naloxone were also assessed. In control animals (saline), there was a marked fall in LH levels and a large increase in prolactin levels within 15 min of suckling. In response to GnRH (25 ng) there was a small progressive increase in LH levels reaching a maximum at 45 min. Both bromocriptine (500 μg) and naloxone (500 μg) markedly suppressed the suckling-induced prolactin surge when administered in two separate groups of animals. However, despite the bromocriptine-induced suppression of prolactin levels, there was no increase in LH levels which remained low throughout the suckling period. Naloxone (500 μg), however, induced a twofold increase in LH levels within 15 min suggesting that an enhanced opiate rather than dopaminergic activity may be responsible for the suppression of GnRH and hence gonadotrophin secretion during suckling. This is supported by the finding that whereas combined bromocriptine (500 μg) and GnRH (25 ng) treatment suppressed the suckling-induced prolactin rise and also induced only a small progressive increase in LH (similar to GnRH alone), combined naloxone (500 μg) and GnRH (25 ng) treatment induced a sharp sixfold increase in LH levels within 15 min while at the same time markedly suppressing prolactin levels. None of these drug treatments affected the levels of FSH.

The results of this study may thus indicate that (1) the suckling stimulus itself rather than the high prolactin levels may be responsible for the suppression of gonadotrophin secretion during lactation, (2) although dopamine may be an important physiological factor controlling prolactin secretion, it may not be involved in the regulation of LH during lactation and (3) the suckling stimulus may enhance the release of endogenous opiates within the central nervous system which could then stimulate prolactin and at the same time inhibit gonadotrophin secretion by inhibiting GnRH release. This opiate-mediated mechanism may explain the reciprocal nature of prolactin and LH secretion during lactation.

J. Endocr. (1984) 100, 175–182

 

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