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Estrogen-dependent post-translational change in the nitric oxide system may mediate the leptin action on LH and prolactin secretion.

Abstract：

:Gonadotrophin-releasing hormone (GnRH) neurons do not express the leptin receptor (OB-R) in the medial preoptic area (MPOA) and the medial basal hypothalamus (MBH). We assessed whether the effect of leptin on the secretion of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) in proestrus could be mediated by nitric oxide (NO) under estrogen modulation. Female rats were treated with an estrogen antagonist (tamoxifen s.c. 3mg/rat) or vehicle during metestrus and diestrus. At proestrus, they received leptin (3 or 10 μg/μl) or intracerebroventricular saline at 11:00 am and were decapitated at 5:00 pm. The following were analyzed in this work: plasma LH, FSH and PRL levels (radioimmunoassay); neuronal NO-synthase (nNOS) and OB-R transcription (RT-PCR); nNOS and phosphorylated nNOS (pnNOS) translation levels (western blotting); and pSTAT3 immunoreactivity. Tamoxifen reduced the plasma LH and PRL levels and decreased the nNOS mRNA and pnNOS expression in the MPOA. Three micrograms of leptin increased the LH secretion and pnNOS protein levels in the MPOA and MBH. Ten micrograms of leptin decreased the transcription, translation and phosphorylation of nNOS in the MPOA. In the MBH, 10 μg of leptin increased the protein expression of nNOS but not the mRNA expression neither pnNOS protein. Tamoxifen did not change either the mRNA or protein expression of nNOS or the phosphorylation of nNOS but decreased the number of cells that contained pSTAT3 immunoreactivity in both areas. In conclusion, the stimulatory effect of leptin on the secretion of LH and PRL on the afternoon of proestrus may be mediated by estrogen-dependent post-translational changes in the nNOS in the MPOA and MBH.

journal_name

Brain Res

journal_title

Brain research

authors

Del Bianco-Borges B,Franci CR

doi

10.1016/j.brainres.2015.02.001

subject

Has Abstract

pub_date

2015-04-16 00:00:00

pages

62-73

eissn

0006-8993

issn

1872-6240

pii

S0006-8993(15)00080-3

journal_volume

1604

pub_type

杂志文章

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