Unilateral lesion increases oestrogen receptor α expression in the intact side of the ventromedial hypothalamic nucleus in ovariectomised rats

Y. Shimogawa, F. Maekawa, K. Yamanouchi

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

To determine the relationship between the right and left sides of the ventrolateral ventromedial hypothalamic nucleus (vlVMN) in regulating the expression of oestrogen receptor (ER)α, the unilateral vlVMN was lesioned and the number of ERα-immunoreactive cells and the ERα mRNA level in the intact side of the vlVMN and arcuate nucleus (ARC) were measured in ovariectomised rats. Twenty-four hours after lesioning, brain samples were collected for analysis of ERα expression by immunohistochemistry and the real-time reverse transcriptase-polymerase chain reaction. The number of ERα-immunoreactive cells in the intact side of the vlVMN but not the ARC in the unilateral lesioned group was significantly higher than that in the control or sham-lesioned group. Expression levels of ERα mRNA in the intact side of the vlVMN but not the ARC in unilateral lesioned rats were significantly higher than those in the sham-lesioned group. Of transcript variants with alternative 5′-untranslated regions (0S, 0N, 0, 0T and E1), the ERα 0 transcript level was significantly increased. These results indicate that unilateral damage of vlVMN induces an increase in ERα in the intact side by increasing ERα transcription in a promoter-specific manner. The findings also suggest the existence of new neuroendocrine control system between the right and left sides for the expression of ERα in the vlVMN.

Original languageEnglish
Pages (from-to)258-266
Number of pages9
JournalJournal of Neuroendocrinology
Volume26
Issue number4
DOIs
Publication statusPublished - 2014

Keywords

  • Compensation
  • Oestrogen receptor α
  • Unilateral lesion
  • Ventromedial hypothalamic nucleus

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Endocrine and Autonomic Systems
  • Cellular and Molecular Neuroscience
  • Medicine(all)

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