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Oestradiol Decreases Melanin‐Concentrating Hormone (MCH) and MCH Receptor Expression in the Hypothalamus of Female Rats
Author(s) -
Santollo J.,
Eckel L. A.
Publication year - 2013
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/jne.12032
Subject(s) - melanin concentrating hormone , medicine , endocrinology , hypothalamus , orexigenic , receptor , messenger rna , hormone , biology , chemistry , neuropeptide , gene , neuropeptide y receptor , biochemistry
Previous studies have shown that oestradiol (E 2 ) decreases the orexigenic effect of melanin‐concentrating hormone (MCH). In the present study, we examined whether this action of E 2 is mediated by its ability to decrease the expression of MCH or its receptor (MCHR1). Using immunocytochemistry and western blotting, we examined whether E 2 decreases MCH‐immunoreactive neurones or MCHR1 protein content in the hypothalamus of female rats. We found that both MCH and MCHR1 protein expression was decreased by acute E 2 treatment in ovariectomised rats, and by the peri‐ovulatory increase in circulating E 2 in pro‐oestrous rats, relative to rats at other cycle stages. To determine whether these changes in MCH/MCHR1 protein expression may be mediated by E 2 's ability to directly regulate the transcription of MCH and MCHR1 genes, the effect of E 2 treatment on MCH and MCHR1 mRNA expression in a neuronal hypothalamic cell line was examined using real‐time reverse transcriptase‐polymerase chain reaction. We also determined whether MCH and oestrogen receptor (ER)α are co‐expressed in the hypothalamus of female rats. E 2 treatment did not decrease MCH or MCHR1 mRNA expression in vitro , and no hypothalamic neurones were identified that co‐expressed MCH and ERα. We conclude that E 2 ‐dependent decreases in hypothalamic MCH/MCHR1 protein expression mediate the ability of E 2 to decrease MCH‐induced feeding. The current findings suggest, however, that E 2 exerts these actions indirectly, most likely though interactions with other neuronal systems that provide afferent input to MCH and MCHR1 neurones.