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      Glucoprivation increases estrogen receptor α immunoreactivity in the brain catecholaminergic neurons in ovariectomized rats

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      Neuroscience Letters
      Elsevier BV

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          Abstract

          Estrogen-dependent enhancement of glucoprivic-induced luteinizing hormone (LH) suppression is hypothesized to be due to increased estrogen receptor alpha (ERalpha)-immunoreactive (ir) cells in specific brain nuclei in a manner similar to fasting. ERalpha expression in various brain areas was determined in ovariectomized rats after systemic 2-deoxy-D-glucose (2DG)-induced glucoprivation. Expression of ERalpha in catecholaminergic neurons in the lower brainstem was also examined. ERalpha-ir cells increased in hypothalamic paraventricular and periventricular nuclei, and A1 and A2 regions of the brainstem 1 h after 2DG injection. The percentage of ERalpha in the tyrosine hydroxylase (TH)- and dopamine-beta-hydroxylase (DBH)-ir neurons was higher in A1 and A2 regions of 2DG-treated rats, but the number of TH- and DBH-ir cells did not change. Thus, 2DG induces ERalpha expression in specific brain nuclei and expression of ERalpha in catecholaminergic neurons of the brainstem indicates a role for estrogen in activating those neurons projecting to the hypothalamic paraventricular nucleus to suppress LH secretion during glucoprivation.

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          Author and article information

          Journal
          Neuroscience Letters
          Neuroscience Letters
          Elsevier BV
          03043940
          February 2001
          February 2001
          : 299
          : 1-2
          : 109-112
          Article
          10.1016/S0304-3940(01)01490-2
          11166950
          c247de0f-b722-462f-ab33-9d3b7dcefaca
          © 2001

          https://www.elsevier.com/tdm/userlicense/1.0/

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