Ovarian Steroids Modulate the Release of Dopamine into Hypophysial Portal Blood and the Density of Anterior Pituitary [3H]Spiperone-Binding Sites in Ovariectomized Rats*

Endocrinology ◽  
1984 ◽  
Vol 114 (6) ◽  
pp. 2306-2311 ◽  
Author(s):  
NANCY S. PILOTTE ◽  
DAVID R. BURT ◽  
CHARLES A. BARRACLOUGH
2015 ◽  
Vol 226 (2) ◽  
pp. T13-T24 ◽  
Author(s):  
George Fink

Geoffrey Harris, while still a medical student at Cambridge, was the first researcher (1937) to provide experimental proof for the then tentative view that the anterior pituitary gland was controlled by the CNS. The elegant studies carried out by Harris in the 1940s and early 1950s, alone and in collaboration with John Green and Dora Jacobsohn, established that this control was mediated by a neurohumoral mechanism that involved the transport by hypophysial portal vessel blood of chemical substances from the hypothalamus to the anterior pituitary gland. The neurohumoral control of anterior pituitary secretion was proved by the isolation and characterisation of the ‘chemical substances’ (mainly neuropeptides) and the finding that these substances were released into hypophysial portal blood in a manner consistent with their physiological functions. The new discipline of neuroendocrinology – the way that the brain controls endocrine glands andvice versa– revolutionised the treatment of endocrine disorders such as growth and pubertal abnormalities, infertility and hormone-dependent tumours, and it underpins our understanding of the sexual differentiation of the brain and key aspects of behaviour and mental disorder. Neuroendocrine principles are illustrated in this Thematic Review by way of Harris' major interest: hypothalamic–pituitary–gonadal control. Attention is focussed on the measurement of GnRH in hypophysial portal blood and the role played by the self-priming effect of GnRH in promoting the onset of puberty and enabling the oestrogen-induced surge or pulses of GnRH to trigger the ovulatory gonadotrophin surge in humans and other spontaneously ovulating mammals.


1996 ◽  
Vol 149 (1) ◽  
pp. 19-27 ◽  
Author(s):  
A De ◽  
T E Morgan ◽  
R C Speth ◽  
N Boyadjieva ◽  
D K Sarkar

Abstract Transforming growth factor β1 (TGFβ1) has recently been shown to be produced in the prolactin (PRL)-secreting lactotropes of the pituitary gland. TGFβ1 inhibits lactotropic secretion and proliferation, and the production of TGFβ1 in lactotropes is reduced during lactotropic growth following estrogen treatment in ovariectomized rats. In many estrogen-responsive tissues, TGFβ1 has been shown to exert its effect by binding to TGFβ1 type II receptors (TβR II) at the cell surface. In this study, we sought to ascertain whether TβR II is involved in TGFβ1 action on lactotropes by determining the changes of TβR II mRNA and protein levels and specific 125I-TGFβ1 binding sites on the lactotropes during estrogen-induced proliferation of lactotropes in Fischer 344 rats. Double immunohistochemical procedures were employed to identify immunoreactive TβR II in PRL-reactive cells. The majority of TβR II-reactive cells in the anterior pituitary were observed to be lactotropes. Dual immunohistochemistry and in situ hybridization procedures also indicated that lactotropes were the major cell types containing TβR II mRNA hybrids. Both the levels of immunoreactive TβR II protein and in situ TβR II mRNA hybrids in the pituitary were significantly decreased in ovariectomized rats after 15 days of estrogen treatment. Determination of 125I-TGFβ1 binding sites in lactotropes by double immunohistochemistry and receptor autoradiography also revealed specific binding sites of 125I-TGFβ1 in lactotropes in the anterior pituitary. 125I-TGFβ1 binding in the anterior pituitary was also reduced following estrogen treatment in ovariectomized rats. These data suggest that down-regulation of TβR II may be an important mechanism of estrogen action on lactotropic cell growth and PRL secretion, and further support the notion that TGFβ1 controls lactotropic function by autocrine/paracrine mechanisms. Journal of Endocrinology (1996) 149, 19–27


Author(s):  
Burton B. Silver ◽  
Ronald S. Nelson

Some investigators feel that insulin does not enter cells but exerts its influence in some manner on the cell surface. Ferritin labeling of insulin and insulin antibody was used to determine if binding sites of insulin to specific target organs could be seen with electron microscopy.Alloxanized rats were considered diabetic if blood sugar levels were in excess of 300 mg %. Test reagents included ferritin, ferritin labeled insulin, and ferritin labeled insulin antibody. Target organs examined were were diaphragm, kidney, gastrocnemius, fat pad, liver and anterior pituitary. Reagents were administered through the left common carotid. Survival time was at least one hour in test animals. Tissue incubation studies were also done in normal as well as diabetic rats. Specimens were fixed in gluteraldehyde and osmium followed by staining with lead and uranium salts. Some tissues were not stained.


Science ◽  
1972 ◽  
Vol 176 (4040) ◽  
pp. 1252-1254 ◽  
Author(s):  
A. R. Schadlow ◽  
M. I. Surks ◽  
H. L. Schwartz ◽  
J. H. Oppenheimer

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