Evidence that members of the TGF beta superfamily play a role in regulation of the GnRH neuroendocrine axis: Expression of a type I serine-threonine kinase receptor for TGR beta and activin in GnRH neurones and hypothalamic areas of the female rat

Citation
V. Prevot et al., Evidence that members of the TGF beta superfamily play a role in regulation of the GnRH neuroendocrine axis: Expression of a type I serine-threonine kinase receptor for TGR beta and activin in GnRH neurones and hypothalamic areas of the female rat, J NEUROENDO, 12(7), 2000, pp. 665-670
Citations number
30
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROENDOCRINOLOGY
ISSN journal
09538194 → ACNP
Volume
12
Issue
7
Year of publication
2000
Pages
665 - 670
Database
ISI
SICI code
0953-8194(200007)12:7<665:ETMOTT>2.0.ZU;2-0
Abstract
The present study was designed to determine whether transforming growth fac tor (TGF)beta and/or activin participate in the regulation of the gonadotro pin releasing hormone (GnRH) neuroendocrine axis in vivo. Single-label in s itu hybridization histochemistry was used to determine the anatomical distr ibution of a TGF beta and activin type I receptor (B1) mRNA, in the adult f emale rat hypothalamic areas that are known to be important sites for the r egulation of reproduction. Dual-label in situ hybridization histochemistry was performed to determine whether B1 mRNA was expressed in GnRH neurones. The results of these studies revealed an extensive distribution of B1 mRNA in the hypothalamic regions, including diagonal bands of Broca, preoptic ar ea, arcuate nucleus and median eminence. In the median eminence, B1 mRNA wa s detected in tanycytes and in the endothelial cells of the pituitary porta l blood capillaries. Dual-label in situ hybridization histochemistry showed that 31 +/- 5% of GnRH neurones expressed B1 mRNA, thus providing evidence that TGF beta and/or activin can act directly on GnRH neurones to modulate their activity. Taken together, these data provide morphological arguments in favour of a participation of TGF beta and/or activin in the regulation of reproduction at the hypothalamic level.