These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Regional differences in estradiol effects on numbers of HSD2-containing neurons in the nucleus of the solitary tract of rats.
    Author: Fan L, Smith CE, Curtis KS.
    Journal: Brain Res; 2010 Oct 28; 1358():89-101. PubMed ID: 20728435.
    Abstract:
    Estrogens affect body fluid balance, including sodium ingestion. Recent findings of a population of neurons in the hindbrain nucleus of the solitary tract (NTS) of rats that are activated during sodium need suggest a possible central substrate for this effect of estrogens. We used immunohistochemistry to label neurons in the NTS that express 11-β-hydroxysteroid dehydrogenase type 2 (HSD2), an enzyme that promotes aldosterone binding, in male rats, and in ovariectomized (OVX) rats given estradiol benzoate (EB) or oil vehicle (OIL). During baseline conditions, the number of HSD2 immunoreactive neurons in the NTS immediately rostral to the area postrema was greater in EB-treated OVX rats compared to those in OIL-treated OVX and male rats. A small number of HSD2 immunoreactive neurons was also labeled for dopamine-β-hydroxylase (DBH), an enzyme involved in norepinephrine biosynthesis. Double-labeled neurons in the NTS were located primarily in the more lateral portion of the HSD2 population, at the level of the area postrema in all three groups, with no sex or estrogen-mediated differences in the number of double-labeled neurons. These results suggest that two subpopulations of HSD2 neurons are present in the NTS. One subpopulation, which does not colocalize with DBH and is increased during conditions of elevated estradiol, may contribute to the effects of estrogens on sodium ingestion. The role of the other, smaller subpopulation, which colocalizes with DBH and is not affected by estradiol, remains to be determined, but one possibility is that these latter neurons are part of a larger network of catecholaminergic input to neuroendocrine neurons in the hypothalamus.
    [Abstract] [Full Text] [Related] [New Search]