Luteinizing Hormone and Prolactin Responses to Naloxone Vary with Stage of Lactation in the Sow1
Author(s) -
F. De Rensis,
John R. Cosgrove,
G. R. Foxcroft
Publication year - 1993
Publication title -
biology of reproduction
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.366
H-Index - 180
eISSN - 1529-7268
pISSN - 0006-3363
DOI - 10.1095/biolreprod48.5.970
Subject(s) - opioidergic , lactation , prolactin , medicine , endocrinology , biology , (+) naloxone , luteinizing hormone , endogenous opioid , endogeny , opioid , antagonism , hormone , opioid antagonist , pregnancy , receptor , genetics
The principal aim of this study was to investigate the involvement of an opioidergic mechanism in the development of suckling-induced inhibition of LH secretion during early lactation in the sow. A preliminary experiment suggested that 2 mg/kg naloxone given as a single bolus injection was above the threshold for antagonism of endogenous opioid activity in early lactation. In the main experiment, injection of 2 mg/kg naloxone 39 h postpartum, followed by injection of 1 mg/kg naloxone at 3-h intervals from 42 h to 78 h postpartum, was not able to prevent the gradual inhibition of LH secretion observed in untreated lactating sows. In contrast, a single injection of 2 mg/kg naloxone at Day 10 of lactation was effective in increasing LH secretion (p < 0.05). There were no effects of the naloxone treatment at any time on FSH secretion. Naloxone decreased (p < 0.05) plasma prolactin at Day 10 of lactation; but again during the first 78 h after farrowing, chronic naloxone treatment did not affect plasma prolactin. These data suggest that the development of the inhibitory effect of suckling on LH secretion in the sow may not be opioid dependent. In contrast, an opiate-dependent mechanism was confirmed as an important component of the suckling-induced suppression of LH secretion in established lactation.
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