The role of cytoplasmic (newly synthesized) dopamine for the spontaneous and electrically evoked release of dopamine and its metabolites from the isolated neurointermediate lobe of the rat pituitary gland in vitro

1987 ◽  
Vol 335 (1) ◽  
pp. 21-27 ◽  
Author(s):  
K. Racke ◽  
E. B�hm ◽  
E. Muscholl
1983 ◽  
Vol 96 (3) ◽  
pp. 395-400 ◽  
Author(s):  
S. W. J. Lamberts ◽  
E. G. Bons ◽  
P. Uitterlinden ◽  
W. H. Hackeng

Cyproheptadine and its metabolite desmethylcyproheptadine were shown to suppress directly the release of adrenocorticotrophin (ACTH) and β-lipotrophin/β-endorphin activity from the neurointermediate lobe of the pituitary gland incubated in vitro. Neither compound affected the release of ACTH from the anterior pituitary gland. Serotonin stimulated the release of ACTH and β-lipotrophin/β-endorphin activity from the neurointermediate lobe, but did not influence the (desmethyl)cyproheptadine-mediated inhibition of hormone release. These results indicate that serotonin and cyproheptadine affect hormone release by the neurointermediate lobe by a direct action. The effect of cyproheptadine, however, might not be exerted by a serotonin receptor.


1985 ◽  
Vol 106 (2) ◽  
pp. 189-195 ◽  
Author(s):  
W. Knepel ◽  
D. Nutto ◽  
M. Vlaskovska ◽  
Ch. Kittel

ABSTRACT The present study was performed to examine the effect of the cyclo-oxygenase inhibitor, indomethacin, and that of various prostaglandins on the release of vasopressin and β-endorphin-like immunoreactivity (β-EI) from the rat neurointermediate lobe of the hypophysis, which was superfused in vitro. Indomethacin (2·8 and 28 μmol/l) changed neither basal secretion of vasopressin nor that evoked by electrical stimulation, whereas the resting release of β-EI was enhanced by indomethacin (28 μmol/l). Prostaglandin (PG) E2 did not influence resting release of vasopressin but markedly inhibited (by about 50%) electrically induced release of vasopressin (least effective concentration: 300 nmol/l) as well as spontaneous secretion of β-EI (least effective concentration: 100 nmol/l) in the presence of indomethacin (28 μmol/l). Prostaglandin F2α (5 μmol/l) also inhibited the evoked release of vasopressin, whereas PGD2 (5 μmol/l) did not. Prostaglandin F2α (5 μmol/l), D2 and I2 (1·5 μmol/l each) produced no effects on β-EI release. As observed in the neurohypophysis, PGE2 inhibited the electrically induced release of vasopressin from the medial basal hypothalamus in vitro. We conclude that prostaglandins (especially PGE2) can inhibit (1) the stimulated release of vasopressin when acting on vasopressin-containing nerve terminals of either neurosecretory system (neurohypophysis, median eminence region), and (2) the secretion of β-EI and, as can be inferred, α-MSH, by a direct action on intermediate lobe cells. J. Endocr. (1985) 106, 189–195


2002 ◽  
Vol 174 (1) ◽  
pp. 121-125 ◽  
Author(s):  
TM Ortiga-Carvalho ◽  
KJ Oliveira ◽  
BA Soares ◽  
CC Pazos-Moura

Leptin has been shown to stimulate the hypothalamus-pituitary-thyroid axis in fasting rodents; however, its role in thyroid axis regulation under physiological conditions is still under investigation. Here it was investigated in freely fed rats whether leptin modulates thyrotroph function in vivo and whether leptin has direct pituitary effects on TSH release. Since leptin is produced in the pituitary, the possibility was also investigated that leptin may be a local regulator of TSH release. TSH was measured by specific RIA. Freely fed adult rats 2 h after being injected with a single s.c. injection of 8 microg leptin/100 g body weight showed a 2-fold increase in serum TSH (P<0.05). Hemi-pituitary explants incubated with 10(-9) and 10(-7) M leptin for 2 h showed a reduced TSH release of 40 and 50% respectively (P<0.05). Conversely, incubation of hemi-pituitary explants with antiserum against leptin, aiming to block the action of locally produced leptin, resulted in higher TSH release (45%, P<0.05). In conclusion, also in the fed state, leptin has an acute stimulatory effect on TSH release in vivo, acting probably at the hypothalamus. However, the direct pituitary effect of leptin is inhibitory and data also provide evidence that in the rat pituitary leptin may act as an autocrine/paracrine inhibitor of TSH release.


Neuroscience ◽  
1985 ◽  
Vol 16 (3) ◽  
pp. 501-510 ◽  
Author(s):  
K. Racke´ ◽  
D. Abel ◽  
E. Muscholl

1981 ◽  
Vol 90 (3) ◽  
pp. 315-322 ◽  
Author(s):  
ELIZABETH A. LINTON ◽  
NICKI WHITE ◽  
OFELIA LIRA DE TINEO ◽  
S. L. JEFFCOATE

The effects of 2-hydroxyoestradiol (2OH-OE2), dopamine, oestradiol-17β and 2OH-OE2 plus dopamine on prolactin and LH release from the male rat pituitary gland were examined in vitro. 2-Hydroxyoestradiol reduced prolactin secretion by 51% at 10−10 mol/l and by 34% at 10−7 mol/l, while oestradiol-17β had no effect at these doses. Dopamine alone (5 × 10−7 mol/l) decreased prolactin released by 58%, 2OH-OE2 plus dopamine produced a similar inhibition of 60%. No significant effect on LH release was observed throughout.


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