Effect of selective serotonin agonists on basal, corticotrophin-releasing hormone- and vasopressin-induced ACTH release in vitro from rat pituitary cells

1993 ◽  
Vol 136 (3) ◽  
pp. 381-387 ◽  
Author(s):  
A. E. Calogero ◽  
G. Bagdy ◽  
M. L. Moncada ◽  
R. D'Agata

ABSTRACT The present study was undertaken to evaluate the serotonin (5-HT) receptor subtype(s) by which 5-HT acts on the pituitary to stimulate ACTH secretion. We tested the effects of the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), the 5-HT1C receptor agonist metachloro-phenylpiperazine (m-CPP), which also binds to other 5-HT receptors with lower affinity, and the 5-HT2/1C receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on basal, corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP)-stimulated ACTH release from primary rat anterior pituitary cell cultures. 5-HT, 8-OH-DPAT and DOI significantly increased basal ACTH release, an effect which was antagonized by 5-HT receptor antagonists. 5-HT and DOI were effective at nanomolar concentrations whereas 8-OH-DPAT was effective at higher concentrations. 5-HT, 8-OH-DPAT (both at 10 nmol/l) and DOI (at higher concentrations) blunted the stimulatory effect of CRH. The suppressive effects of 8-OH-DPAT and DOI on CRH-stimulated ACTH release were antagonized by (−)propranolol, a β-adrenergic receptor antagonist which binds the 5-HT1A receptor with elevated affinity, and ketanserin, a 5-HT2 receptor antagonist respectively. 5-HT, 8-OH-DPAT and DOI showed additive stimulatory effects with AVP but only at the highest concentration tested, whereas m-CPP potentiated AVP-induced ACTH release at concentrations of 1 nmol/l or more. This effect was antagonized by metergoline, a non-selective 5-HT receptor antagonist and mianserin, an antagonist which binds the 5-HT1C receptor with elevated affinity. Thus (1) 5-HT and selective 5-HT agonists such as 8-OH-DPAT, m-CPP and DOI modulate ACTH release by acting directly at the pituitary level; (2) serotonergic stimulation of basal ACTH release is mediated by both 5-HT2 and 5-HT1A receptors; (3) serotonergic inhibition of CRH-stimulated ACTH release is mediated by 5-HT1A and 5-HT2 receptors; whereas (4) serotonergic potentiation of AVP-stimulated ACTH release is mediated mainly by 5-HT1C receptors. Journal of Endocrinology (1993) 136, 381–387

1990 ◽  
Vol 127 (1) ◽  
pp. R1-R4 ◽  
Author(s):  
P. Navarra ◽  
S. Tsagarakis ◽  
D. H. Coy ◽  
L.H. Rees ◽  
G. M. Besser ◽  
...  

ABSTRACT It has been suggested that melanin concentrating hormone (MCH) possesses potent corticotrophin (ACTH) inhibitory activity, on the basis of the inhibitory effects displayed by salmon MCH on ACTH release from either trout or rat isolated pituitary fragments. Recently, rat MCH has been characterised, and this prompted us to investigate the putative inhibitory activity of synthetic rat MCH on basal and stimulated ACTH secretion from freshly-dispersed rat pituitary cells or incubated rat pituitary fragments, as well on KCl (28 mmol/l) or noradrenaline-evoked release of corticotrophin releasing hormone-41 (CRH-41) from rat hypothalamic explants in vitro. There were no effects of rat MCH on either CRH-41 or ACTH release in vitro.


1986 ◽  
Vol 111 (1) ◽  
pp. R1-R2 ◽  
Author(s):  
J.A. Franklyn ◽  
M. Wilson ◽  
J.R. Davis ◽  
D.B. Ramsden ◽  
K. Docherty ◽  
...  

ABSTRACT We have reported previously the effect of thyroid status in vivo on pituitary cytoplasmic concentrations of messenger RNA (mRNA) encoding the thyrotrophin (TSH) β-subunit (Franklyn, Lynam, Docherty et al, 1985). Studies in vitro of the regulation of TSH β gene transcription have been confined to thyrotrophic tumour cells. We now report the demonstration of TSH β-subunit mRNA in non-tumorous rat pituitary cells in primary culture. Treatment of cells with thyrotrophin-releasing hormone (TRH) and with forskolin resulted in a marked increase in cellular concentration of TSH β-mRNA. These results suggest that TRH exerts a direct effect on the pretranslational events involved in TSH synthesis and further that the adenylate cyclase system may be involved in the regulation of synthesis. We have thus described a novel system for the study of TSH β-subunit gene expression in normal rat pituitary cells in vitro.


1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S188-S189
Author(s):  
L. KIESEL ◽  
T. RABE ◽  
D. SCHOLZ ◽  
V. KIRSCHNER ◽  
B. RUNNEBAUM

1980 ◽  
Vol 87 (1) ◽  
pp. 95-103 ◽  
Author(s):  
G. DELITALA ◽  
T. YEO ◽  
ASHLEY GROSSMAN ◽  
N. R. HATHWAY ◽  
G. M. BESSER

The inhibitory effects of dopamine and various ergot alkaloids on prolactin secretion were studied using continuously perfused columns of dispersed rat anterior pituitary cells. Bromocriptine (5 nmol/l) and lisuride hydrogen maleate (5 nmol/l) both inhibited prolactin secretion, the effects persisting for more than 3 h after the end of the administration of the drugs. A similar although less long-lasting effect was observed with lergotrile (50 nmol/l) and the new ergoline derivative, pergolide (5 nmol/l). These effects contrasted with the rapid disappearance of the action of dopamine. The potency estimates of the ergots relative to that of dopamine were: lergotrile, 2·3; bromocriptine, 13; lisuride, 15; pergolide, 23. The dopamine-receptor blocking drugs, metoclopramide and haloperidol, antagonized the prolactin release-inhibiting activity of the compounds; bromocriptine and lisuride showed the highest resistance to this dopaminergic blockade. The results suggested that the direct effect of the ergot derivatives on dispersed pituitary cells was mediated through dopamine receptors and emphasized the long-lasting action of bromocriptine and lisuride in vitro.


1995 ◽  
Vol 184 (2) ◽  
pp. 109-112 ◽  
Author(s):  
Atsuhiko Hattori ◽  
Damon C. Herbert ◽  
Mary K. Vaughan ◽  
Ken Yaga ◽  
Russel J. Reiter

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