GONADOTROPHS BUT NOT SOMATOTROPHS CARRY GONADOTROPIN-RELEASING-HORMONE RECEPTORS - RECEPTOR LOCALIZATION, INTRACELLULAR CALCIUM, AND GONADOTROPIN AND GH RELEASE
Pt. Bosma et al., GONADOTROPHS BUT NOT SOMATOTROPHS CARRY GONADOTROPIN-RELEASING-HORMONE RECEPTORS - RECEPTOR LOCALIZATION, INTRACELLULAR CALCIUM, AND GONADOTROPIN AND GH RELEASE, Journal of Endocrinology, 152(3), 1997, pp. 437-446
Gonadotrophs are the primary target cells for GnRH in the pituitary. H
owever, during a limited period of neonatal life in the rat, lactotrop
hs and somatotrophs respond to GnRH as well. Also, in the adults of a
number of teleost fishes (e.g. carp, goldfish, and tilapia but not tro
ut), GnRH is a potent GH secretagogue. In studying hypophysiotrophic a
ctions of the two forms of GnRH present in the African catfish (Claria
s gariepinus), chicken GnRH-II ([His(5), Trp(7), Tyr(8)] GnRH; cGnRH-I
I) and catfish GnRH ([His(5), Asn(8)]GnRH; cfGnRH), we have investigat
ed the effects of GnRH on catfish gonadotrophs and somatotrophs. GnRH
binding was examined by incubating dispersed pituitary cells attached
to coverslips with I-125-labelled [D-Arg(6), Trp(7), Leu(8), Pro(9)-Ne
t]GnRH (sGnRHa), a salmon GnRH analogue with high affinity for the GnR
H receptor. Following fixation and immunohistochemistry using antisera
against catfish LH and GH, I-125-labelled sGnRHa was localised autora
diographically and silver grains were quantified on gonadotrophs and s
omatotrophs. Specific binding of I-125-labelled sGnRHa was restricted
to gonadotrophs. Both cfGnRH and cGnRH-II dose-dependently inhibited I
-125-labelled sGnRHa binding to gonadotrophs. To substantiate the loca
lisation of functional GnRH receptors, the effects of cfGnRH and cGnRH
-II on the cytosolic free calcium concentration ([Ca2+](i)) were exami
ned in Fura-2-loaded somatotrophs and gonadotrophs. GnRH-induced incre
ases in [Ca2+](i) appeared to be confined to gonadotrophs, in which bo
th endogenous GnRHs caused a single and transient increase in [Ca2+](i
). The amplitude of this [Ca2+](i) transient depended on the GnRH dose
and correlated well with the GnRHs' effect on LH release. In vivo exp
eriments demonstrated that GnRH treatments which markedly elevated pla
sma LH levels had no effect on plasma GH levels, while a dopamine agon
ist (apomorphine) significantly elevated plasma GH levels. We conclude
that the two endogenous forms of GnRH in the African catfish are not
directly involved in the regulation of the release of GH, suggesting t
hat GnRHs cannot be considered as GH secretagogues in teleosts in gene
ral.