Some Catecholamine Inhibitors Do Not Cause Accumulation of Nuclear Estrogen Receptors in Rat Hypothalamus and Anterior Pituitary Gland

1986 ◽  
Vol 43 (2) ◽  
pp. 143-149 ◽  
Author(s):  
Jeffrey D. Blaustein ◽  
Theodore J. Brown ◽  
John F. McElroy
1988 ◽  
Vol 155 (1-2) ◽  
pp. 163-166 ◽  
Author(s):  
Mercedes Lasaga ◽  
Beatriz H. Duvilanski ◽  
Adriana Seilicovich ◽  
Sandra Afione ◽  
Luciano Debeljuk

1982 ◽  
Vol 93 (2) ◽  
pp. 151-160 ◽  
Author(s):  
M. C. Holmes ◽  
G. Di Renzo ◽  
U. Beckford ◽  
B. Gillham ◽  
M. T. Jones

The status of serotonin as a putative neurotransmitter involved in the control of the secretion of corticotrophin-releasing activity from the rat hypothalamus has been further investigated. The experimental model used for the investigation was the rat hypothalamus incubated in vitro. It was confirmed that serotonin causes a dose-related release of corticotrophin-releasing activity from the tissue and it was shown that this effect was mimicked by the addition to the tissue of chlorimipramine or d-fenfluramine, two drugs expected to cause an increase in the concentration of serotonin in the synaptic cleft. The effect of the latter drug was greatly reduced by the simultaneous addition of either methysergide or metergoline. Destruction of serotonin-containing nerve terminals in the hypothalamus was caused by the intraventricular administration of the neurotoxic drug 5,7-dihydroxytryptamine. This treatment resulted in an 84% reduction of the serotonin concentration in the hypothalamus 12 days later. Hypothalami taken from animals 12 days after treatment with the drug secreted corticotrophin-releasing activity in basal amounts equal to those found in tissues taken from control rats, but showed supersensitivity in response to added serotonin. No such supersensitivity was seen in response to d-fenfluramine and a diminished response to chlorimipramine was noted. Despite its intraventricular route of administration, 5,7dihydroxytryptamine was found to increase the sensitivity of segments of anterior pituitary gland in vitro to low doses of preparations containing corticotrophin releasing factor. These results are consistent with the view that endogenous serotonin can act as a stimulator of the secretion of corticotrophin-releasing activity from the rat hypothalamus. They also suggest that conclusions about the control of the release of this trophic material inferred from measurements of corticotrophin or corticosterone in the circulation must be viewed with caution when the drug 5,7-dihydroxytryptamine has been used, because of the development of supersensitivity both in the hypothalamus and in the anterior pituitary gland.


1983 ◽  
Vol 97 (1) ◽  
pp. 105-111 ◽  
Author(s):  
K. I. J. Shennan ◽  
M. C. Sheppard

Neurotensin is a hypothalamic peptide which inhibits secretion of TSH in the rat in vivo. We have demonstrated a calcium-dependent release of neurotensin from incubated rat hypothalamus in response to depolarizing stimuli, as well as a dose-dependent stimulatory effect of tri-iodothyronine (T3) on neurotensin secretion. We suggest that part of the neuroendocrine control of TSH secretion involves the interaction of T3, neurotensin and TSH; the presence of neurotensin in extracts of anterior pituitary gland is further evidence for its hypophysiotrophic role.


1979 ◽  
Vol 16 (2) ◽  
pp. 99-112 ◽  
Author(s):  
Thérèse Di Paolo ◽  
Réjean Carmichael ◽  
Fernand Labrie ◽  
Jean-Pierre Raynaud

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