Gonadal steroids regulate the number and activational state of mast cells in the medial habenula

Marta Wilhelm, Blythe King, Ann Judith Silverman, Rae Silver

Research output: Contribution to journalArticle

52 Citations (Scopus)


While mast cells in connective tissues have long been associated with allergic reactions, it is now clear that they are also present within the central nervous system under normal physiological conditions. The mast cell population increases 10-fold in the medial habenular region of the brain within 2 h after pairing in doves. The first study explored whether this increase was due to exposure to gonadal steroids. Light microscopic immunocytochemistry indicates an increased number of brain MC following exposure to either testosterone (T) or dihydrotestosterone (DHT) in the male, or 17 β estradiol (E) in the female, but not in cholesterol-treated controls. Thus, the increased habenular MC population is produced by gonadal hormones in the absence of sexual behavior, is not sexually dimorphic, and does not require aromatization of androgen. In the next study, MC activational state was determined using electron microscopy. Cells were categorized into five states: (I) resting; (II) initiation of degranulation; (III) fully degranulated; (IV) piecemeal secretion; and (V) resynthesizing. Hormone treatment (T, DHT, or E) resulted in a significant increase in the percent of cells in activated states. MC granules contain a wide range of biologically active molecules. The release of these granule contents into the neuropil of the central nervous system is likely to have wide ranging effects at multiple levels including vascular permeability and neuronal excitability. In that steroid treatment is known to result in such effects, the present demonstration of a hormonally induced shift in MC secretory state is one avenue by which these effects are mediated.

Original languageEnglish
Pages (from-to)1178-1186
Number of pages9
Issue number3
Publication statusPublished - Jan 1 2000


ASJC Scopus subject areas

  • Endocrinology

Cite this