Presynaptic regulation of the electrically evoked release of endogenous dopamine from the isolated neurointermediate lobe or isolated neural lobe of the rat pituitary gland in vitro

1988 ◽  
Vol 337 (5) ◽  
Author(s):  
K. Rack� ◽  
A. Gro�hans ◽  
S. Sirrenberg ◽  
K. Ziegler
Keyword(s):  
Pituitary Gland ◽  
Neural Lobe ◽  
Neurointermediate Lobe ◽  
Endogenous Dopamine ◽  
Rat Pituitary ◽  
Presynaptic Regulation

Cyproheptadine and desmethylcyproheptadine directly inhibit the release of adrenocorticotrophin and β-lipotrophin/β-endorphin activity from the neurointermediate lobe of the rat pituitary gland

1983 ◽  
Vol 96 (3) ◽  
pp. 395-400 ◽  
Author(s):  
S. W. J. Lamberts ◽  
E. G. Bons ◽  
P. Uitterlinden ◽  
W. H. Hackeng
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Serotonin Receptor ◽  
Direct Action ◽  
Anterior Pituitary Gland ◽  
Hormone Release ◽  
Neurointermediate Lobe ◽  
Rat Pituitary

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.

DISTRIBUTION OF NEUROSECRETORY GRANULES AMONG THE ANATOMICAL COMPARTMENTS OF THE NEUROSECRETORY PROCESSES OF THE PITUITARY GLAND: A QUANTITATIVE ULTRASTRUCTURAL APPROACH TO HORMONE STORAGE IN THE NEURAL LOBE

1976 ◽  
Vol 68 (2) ◽  
pp. 225-NP ◽  
Author(s):  
J. F. MORRIS
Keyword(s):  
Basement Membrane ◽  
Pituitary Gland ◽  
Neurosecretory Granules ◽  
Neural Lobe ◽  
Releasable Pool ◽  
Readily Releasable Pool ◽  
Rat Pituitary ◽  
Axonal Swellings ◽  
Granule Release

SUMMARY The distribution of neurosecretory granules in various anatomical compartments of neurosecretory axons of the neural lobe of the rat pituitary has been studied. Apart from the most anterior tip of the gland, where granules are largely restricted to undilated axons and a few 'swellings', the proportional compartmental storage of granules is essentially homogeneous for the rest of the gland: 13% of granules are found in undilated axons, 31% in axonal 'endings' (which contain microvesicles and abut the basement membrane) and 55% in axonal 'swellings' (which are devoid of significant numbers of microvesicles). These values indicate that the 'endings' contain a much greater proportion of the total number of granules stored in the neural lobe than would be predicted if the readily releasable pool of hormone were composed of all the granules in the 'endings'. Some further constraint on granule release either physiological or anatomical (e.g. the position of the granule in relation to the plasmalemma of the 'ending') must be operative.

Inhibition by prostaglandin E2of the release of vasopressin and β-endorphin from rat pituitary neurointermediate lobe or medial basal hypothalamus in vitro

1985 ◽  
Vol 106 (2) ◽  
pp. 189-195 ◽  
Author(s):  
W. Knepel ◽  
D. Nutto ◽  
M. Vlaskovska ◽  
Ch. Kittel
Keyword(s):  
Direct Action ◽  
Effective Concentration ◽  
Neurosecretory System ◽  
Intermediate Lobe ◽  
Medial Basal Hypothalamus ◽  
Neurointermediate Lobe ◽  
Rat Pituitary ◽  
Prostaglandin F ◽  
Spontaneous Secretion

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

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