Distribution of glucocorticoid receptors in the brain of rainbow trout (Oncorhynchus mykiss): Possible relationships with the neuroendocrine systems controlling reproduction.
Ca. Teitsma et al., Distribution of glucocorticoid receptors in the brain of rainbow trout (Oncorhynchus mykiss): Possible relationships with the neuroendocrine systems controlling reproduction., B FR PECHE, (350-51), 1998, pp. 597-607
Citations number
41
Categorie Soggetti
Aquatic Sciences
Journal title
BULLETIN FRANCAIS DE LA PECHE ET DE LA PISCICULTURE
The distribution of the glucocorticoid receptor (GR) within the forebrain o
f rainbow trout has been studied by means of in situ hybridization (ISH) an
d immunohistochemistry (ICC) using probes and antibodies directed against t
he AB-domain of the rainbow trout GR (rtGR).
Both rtGR mRNA and protein exhibited the same pattern of distribution. A st
rong labelling was observed in all subdivisions of the preoptic nucleus, in
the thalamic region and in the mediobasal hypothalamus (nucleus recessus l
ateralis, nucleus lateralis tuberis). It was notably found that all magnoce
llular neurons of the nucleus preopticus pars magnocellularis (NPOmc) were
positive with both ISH and ICC. Furthermore, numerous cells of the anterior
lobe of the pituitary were positively stained.
Double staining studies allowed to identify part of the rtGR expressing cel
ls. At the telencephalic level, it was found that GnRH neurons frequently e
xpress rtGR in vitellogenic females. Virtually all tyrosine hydroxylase (TH
) cells in the anteroventral part of the preoptic nucleus (NPOav) were rtGR
-positive. In this same area, a colocalization between rainbow trout estrad
iol receptor (rtER) and TH has already been documented, indirectly demonstr
ating that rtER and rtGR are colocalized. The same holds true for the GTH-I
I cells of the anterior pituitary which express both types of receptors.
These results provide information on the potential sites of cortisol action
on the reproductive axis directly at the pituitary level or indirectly on
neuroendocrine systems controlling GTH-II secretion, possibly via GR-ER int
eractions.