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      Oestrogen-dependent suppression of pulsatile luteinising hormone secretion and kiss1 mRNA expression in the arcuate nucleus during late lactation in rats.

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          Abstract

          Follicular development and ovulation are strongly suppressed during lactation in mammals via a profound suppression of gonadotrophin secretion. The present study aimed to examine the role of oestrogen feedback action in suppressing luteinising hormone (LH) secretion and hypothalamic kisspeptin expression during the latter half of lactation. Plasma LH concentrations kept at low levels throughout the lactating period in intact and oestrogen-replaced ovariectomised (OVX) lactating rats, whereas plasma LH concentrations gradually elevated from day 10 postpartum in lactating OVX rats. OVX lactating rats showed frequent LH pulses at late lactation, although the LH pulses were significantly inhibited by an oestrogen replacement, which is much less effective on LH release in nonlactating rats. Oestrogen replacement in lactating OVX rats significantly reduced the number of Kiss1 mRNA-expressing cells in the arcuate nucleus (ARC) at late lactation, although the same oestrogen treatment did not affect the number of Kiss1-expressing cells in nonlactating controls. Exogenous kisspeptin challenge (0.2 nmol) into the third cerebroventricle significantly increased LH secretion in lactating OVX, lactating OVX + subcutaneous 17β-oestradiol and intact lactating rats at day 16 postpartum. These results suggest that LH pulse suppression during late lactation could be a result of the enhanced oestrogen-dependent suppression of ARC kisspeptin expression.

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          Author and article information

          Journal
          J Neuroendocrinol
          Journal of neuroendocrinology
          Wiley
          1365-2826
          0953-8194
          Sep 2012
          : 24
          : 9
          Affiliations
          [1 ] Laboratory of Reproductive Science, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
          Article
          10.1111/j.1365-2826.2012.02330.x
          22536815
          e8036de7-a510-42b2-b367-54bf9b665b37
          © 2012 The Authors. Journal of Neuroendocrinology © 2012 British Society for Neuroendocrinology.
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