Preparation and characterization of an antibody specific to the rat dopamine D2 receptor

1992 ◽  
Vol 134 (2) ◽  
pp. 227-233 ◽  
Author(s):  
J. M. Johnston ◽  
D. F. Wood ◽  
J. D. James ◽  
D. G. Johnston
Keyword(s):  
Dopamine D2 Receptor ◽  
D2 Receptor ◽  
Cross Reactivity ◽  
Receptor Protein ◽  
Pituitary Cells ◽  
Dopamine D2 ◽  
Rat Pituitary ◽  
Normal Rat ◽  
Faint Band ◽  
Rat Pituitary Cells

ABSTRACT Antibodies specific to the dopamine D2 receptor have been raised in rabbits using synthetic peptides. The resulting antiserum was sensitive to picogram quantities of peptide as measured by enzyme-linked immunoassay and was shown to have a 33% cross-reactivity with partially purified D2 receptor protein. No detectable cross-reactivity with similarly prepared fungal membranes was observed. D2 receptor preparations from normal rat pituitary cells were used in Western blot analysis. Bands of Mr = 95 000 and 34 000 were detected in these preparations with a third faint band at 120 000. These correspond to the pituitary D2 receptor. Journal of Endocrinology (1992) 134, 227–233

The dopamine D2 receptor is expressed in GH3 cells

1991 ◽  
Vol 7 (2) ◽  
pp. 131-136 ◽  
Author(s):  
J. M. Johnston ◽  
D. F. Wood ◽  
E. A. Bolaji ◽  
D. G. Johnston
Keyword(s):  
Gene Expression ◽  
Dopamine D2 Receptor ◽  
Receptor Gene ◽  
D2 Receptor ◽  
Receptor Protein ◽  
Gh3 Cells ◽  
Pituitary Cells ◽  
Dopamine D2 ◽  
Receptor Gene Expression ◽  
Gh3 Cell

ABSTRACT Some pituitary tumours respond to dopamine by decreasing the release of prolactin and/or GH and by inhibition of tumour growth. Certain tumours are unresponsive. Dopamine D2 receptor high-affinity binding is impaired in these tumours, and the rat GH3 cell line behaves in a similar way. The hypothesis that the dopamine-binding defect results from impaired D2 receptor gene expression has been tested in the present study. On Northern blots, D2 receptor mRNA was present in both normal rat pituitary cells and in GH3 cells. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis identified a putative D2 receptor protein in normal and GH3 cell membranes. The lack of effect of dopamine in GH3 cells does not reflect the absence of D2 receptor gene expression.

scholarly journals Benzene and 2-ethyl-phthalate induce proliferation in normal rat pituitary cells

Pituitary ◽  
2016 ◽  
Vol 20 (3) ◽  
pp. 311-318 ◽  
Author(s):  
Laura Tapella ◽  
Antonella Sesta ◽  
Maria Francesca Cassarino ◽  
Valentina Zunino ◽  
Maria Graziella Catalano ◽  
...  
Keyword(s):  
Pituitary Cells ◽  
Rat Pituitary ◽  
Normal Rat ◽  
Rat Pituitary Cells

Dopamine D2 receptor stimulation alters G-protein expression in rat pituitary intermediate lobe melanotropes

Endocrine ◽  
1997 ◽  
Vol 6 (3) ◽  
pp. 325-333 ◽  
Author(s):  
Scott A. Sands ◽  
Daniel S. Dickerson ◽  
Stephen J. Morris ◽  
Bibie M. Chronwall
Keyword(s):  
Protein Expression ◽  
G Protein ◽  
Dopamine D2 Receptor ◽  
D2 Receptor ◽  
Intermediate Lobe ◽  
Receptor Stimulation ◽  
Dopamine D2 ◽  
Rat Pituitary ◽  
Pituitary Intermediate Lobe

Dihydropyridine Ca2+ antagonists: potent inhibitors of secretion from normal and transformed pituitary cells

1985 ◽  
Vol 248 (5) ◽  
pp. C510-C519 ◽  
Author(s):  
J. J. Enyeart ◽  
T. Aizawa ◽  
P. M. Hinkle
Keyword(s):  
Endocrine Cells ◽  
Hormone Secretion ◽  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Excitable Cells ◽  
Rat Pituitary ◽  
Ic50 Values ◽  
Normal Rat ◽  
Rat Pituitary Cells ◽  
Ca2 Channels

Three dihydropyridine (DHP) Ca2+ antagonists were compared with several other organic Ca2+ antagonists with respect to their ability to inhibit depolarization-dependent hormone secretion from the GH4C1 pituitary cell line and from normal rat pituitary cells. The three DHP, nimodipine, nisoldipine, and nifedipine, potently and specifically inhibited KCl-stimulated prolactin secretion from GH4C1 cells (estimated IC50 values: 1.8, 1.8, and 6.0 nM, respectively). Both basal and thyrotropin-releasing hormone-stimulated secretion from GH4C1 cells were much less sensitive to inhibition by the DHP. The inhibition by the DHP was reversible, and their potency was independent of depolarizing concentrations of KCl between 18.8 and 53.8 mM. Other organic antagonists, including verapamil, cinnarizine, and diltiazem, blocked secretion from GH4C1 cells but at much higher concentrations. The estimated IC50 values for these three were 1,000, 1,100, and 3,500 nM, respectively. Depolarization-stimulated prolactin secretion from normal pituitaries was inhibited by the DHP and verapamil at the same concentrations found effective in GH4C1 cells. KCl-stimulated 45Ca2+ uptake by GH4C1 cells was also blocked by DHP at concentrations that inhibited secretion. Since depolarization-stimulated secretion and 45Ca2+ uptake are probably triggered by Ca2+ entering through voltage-sensitive channels, the above results suggest that DHP antagonists potently block these channels in both normal and transformed pituitary cells. These Ca2+ channels appear to be identical in this respect. These findings further suggest a similarity between the Ca2+ channels of endocrine cells and those of smooth muscle and other excitable cells.

Flunarizine, a calcium influx blocker, inhibits TRH- but not potassium-stimulated prolactin secretion

1984 ◽  
Vol 107 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Janet E. Merritt ◽  
Stephen Tomlinson ◽  
Barry L. Brown
Keyword(s):  
Calcium Influx ◽  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Monolayer Cultures ◽  
High K ◽  
Rat Pituitary ◽  
Normal Rat ◽  
Rat Pituitary Cells

Abstract. The effect of flunarizine on the secretion of prolactin from monolayer cultures of normal rat pituitary cells has been determined. Both basal and TRHstimulated secretion were found to be significantly inhibited by micromolar concentrations of flunarizine, whereas depolarization (high K+)-stimulated secretion was virtually unaffected. These results indicate that TRH-stimulated prolactin secretion probably involves calcium influx and that flunarizine may be useful as a probe for particular Ca2+ channels.

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