Reference : Decreased responsiveness of GH3 cells to the dopaminergic inhibition of prolactin
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/2268/26688
Decreased responsiveness of GH3 cells to the dopaminergic inhibition of prolactin
English
Faure, Nacia [> > > >]
Cronin, Michaël J [> > > >]
Martial, Joseph mailto [Université de Liège - ULg > Département des sciences de la vie > GIGA-R : Biologie et génétique moléculaire >]
Weiner, Richard I [> > > >]
1980
Endocrinology
Endocrine Society
107
4
1022-1026
Yes (verified by ORBi)
0013-7227
Chevy Chase
MD
[en] Animals ; Apomorphine/pharmacology ; Bromocriptine/*pharmacology ; Butaclamol/pharmacology ; Cell Line ; Clone Cells ; Dopamine/*pharmacology ; Dose-Response Relationship, Drug ; Mice ; Pituitary Neoplasms ; Prolactin/*secretion
[en] The inhibitory regulation of PRL secretion by dopamine (DA) or the dopaminergic agonists bromergocryptine (CB-154) and apomorphine was studied in cultured GH3 cells, an established rat anterior pituitary cell line which produces both PRL and GH. The basal release of PRL from GH3 cells was unaffected when incubated for 6 h with DA concentrations as high as 10(-4) M. The inability of DA to suppress PRL secretion could not be explained by the catabolism of DA or the presence of unknown inhibitors (e.g. estradiol) in the fetal calf serum present in the incubation media. Apomorphine and CB-154 were only partially effective in suppressing PRL release at high concentrations of 10(-4) and 10(-5) M, respectively. Various concentrations of the dopaminergic antagonist d-butaclamol did not reverse the inhibitory action of 10(-5) M CB-154, while equal concentrations (10(-5) M) of both d- and l-butaclamol significantly suppressed PRL release. The greatly lowered responsiveness of GH3 cells to dopaminergic inhibition of PRL is suggestive of some impairment of DA receptors. This hypothesis is supported by radioligand binding studies in which high affinity dopaminergic binding sites are absent in the same cell line used in this study.
http://hdl.handle.net/2268/26688
10.1210/endo-107-4-1022
http://endo.endojournals.org/cgi/content/abstract/107/4/1022
1980/10/01

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