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Camila Calvino, Luana L Souza, Ricardo H Costa-e-Sousa, Norma A S Almeida, Isis H Trevenzoli, and Carmen C Pazos-Moura

, Ahima & Antwi 2008 ). In addition, leptin modulates the activity of several neuroendocrine axes, including the hypothalamus–pituitary–thyroid (HPT) axis. Similar to leptin, thyroid hormones (THs) are essential for the maintenance of basal metabolism and

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K. I. J. Shennan and 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.

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Hanna E Auvinen, Johannes A Romijn, Nienke R Biermasz, Hanno Pijl, Louis M Havekes, Johannes W A Smit, Patrick C N Rensen, and Alberto M Pereira

Introduction Glucocorticoids (GCs; cortisol in humans and corticosterone in rodents) are secreted by the adrenals in response to stimulation of the hypothalamus–pituitary–adrenal (HPA) axis by a stressor, and induce behavioral and metabolic

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Hiroki Otsubo, Susumu Hyodo, Hirofumi Hashimoto, Makoto Kawasaki, Hitoshi Suzuki, Takeshi Saito, Toyoaki Ohbuchi, Toru Yokoyama, Hiroaki Fujihara, Tetsuro Matsumoto, Yoshio Takei, and Yoichi Ueta

/l saline) followed by 4% paraformaldehyde and 0.2% picric acid in 0.1 M PB. Then the brains were removed, coronally cut, and divided into three blocks (forebrain, hypothalamus, and brainstem). The blocks were postfixed with 4% paraformaldehyde and 0

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Yan Zhou, Jacob Bendor, Lauren Hofmann, Matthew Randesi, Ann Ho, and Mary Jeanne Kreek

al. 1998 ) and rodents ( Eisenberg 1980 , Zhou et al. 2005 ). β-Endorphin immuno-reactive (ir) fibers and corticotropin-releasing hormone (CRH)-ir perikarya are colocalized in the paraventricular nucleus (PVN) of the hypothalamus (e.g. Pilcher

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*Joint Academic Unit of Obstetrics, Gynaecology and Reproduction Physiology, The Medical Colleges of St Bartholomew's and The London Hospital, 51–53 Bartholomew Close, London, EC1A 7BE and ‡Department of Physiology, Institute of Physiology, The University, Glasgow, G2 0NA

(Received 17 December 1976)

It is generally accepted that the secretion of prolactin from the mammalian pituitary gland is under inhibitory control from the hypothalamus (Meites, 1973). During studies on the development of gonadotrophin secretion in the early human foetus (Gilmore, Dobbie, McNeilly & Mortimer, 1977) it became apparent that up to week 16, the hypothalamus may exert a stimulatory influence over prolactin release which switches to the adult situation as the foetus develops towards term. This communication describes these findings in more detail.

Pituitary glands, hypothalami, and cortices were collected from foetuses delivered by hysterotomy between 10 and 19 weeks of pregnancy. The tissues were immediately frozen on solid C02 and stored

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The basal hypothalamus of Coturnix quail contains gonadotrophin releasing factor (GRF) activity (Follett, 1970) but the precise location of the neurons producing the neurohormone(s) is unknown. Lesioning studies show that the destruction of either of two sites blocks photo-inducible testicular growth. One of these lies in the dorsal basal hypothalamus around the paraventricular organ and the other directly above the median eminence (Sharp & Follett, 1969). These two areas are morphologically distinct when considered either in terms of the distribution of monoamines (Sharp & Follett, 1968) or of tanycyte processes (Sharp, 1972).

To explore this problem further, pituitaries were taken from sexually mature quail and fragments of the cephalic lobes were implanted into the hypothalami of gonadectomized birds. By removing the negative feedback effect of gonadal steroids it was hoped to stimulate GRF activity. It was anticipated that, as in rats (Halász, Pupp & Uhlarik, 1962), implanted pituitary cells would

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Jacob C Garza, Chung Sub Kim, Jing Liu, Wei Zhang, and Xin-Yun Lu

). One of the brain regions that highly express MC4R is the paraventricular nucleus of the hypothalamus (PVN) ( Mountjoy et al . 1994 , Kishi et al . 2003 , Lu et al . 2003 ). Studies suggest that the PVN is one of the key neuroanatomical substrates

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The uptake of [6,7-3H]oestradiol in vivo and in vitro by cell fractions from regions of rat brain and the anterior pituitary gland has been studied. Cytoplasmic and nuclear receptors were detected in anterior and posterior hypothalamus but not in brain cortex.

After labelling in vivo, tissues took up [6,7-3H]oestradiol in the following order of magnitude: anterior pituitary > anterior hypothalamus > posterior hypothalamus > cortex. With the exception of the cortex, all extracts from mature tissues had a higher uptake/mg protein than did extracts from immature animals. In the in-vitro system, oestradiol-17β competed with [6,7-3H]oestradiol-17β in the hypothalamus whereas progesterone, testosterone and oestradiol-17α did not. In the pituitary, oestradiol-17α and 17β competed for binding sites.

A single injection of testosterone propionate on the second day of life affected [6,7-3H]oestradiol binding in later life. By 28 days of age, the androgenized animals had a lower nuclear and higher cytoplasmic uptake of [6,7-3H]oestradiol in anterior hypothalamus. This effect was not seen in the posterior hypothalamus or cortex. Binding was decreased in all fractions from the pituitary. In mature animals (60 days old), binding fell in both nuclear and cytoplasmic fractions from anterior hypothalamus and pituitary. The nuclei from posterior hypothalamus also took up less [6,7-3H]oestradiol after androgenization. Androgenization affected specific binding in uteri at both 28 and 60 days of age.

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Experimental analysis of the rat's hypothalamic-hypophysial-thyroid system, utilizing stereotaxic, radiometric, histochemical, and bioassay procedures, indicated that electrolytic lesions in the anterior and tuberal portions of the hypothalamus altered thyrotrophic hormone (TSH) secretion in the adenohypophysis and reduced thyroid function (histology and 131I release from the gland). Inhibition of thyroidal radio-iodine release was found within 2 weeks after hypothalamic destruction and was greater in rats which became obese. Significant reduction in titres of circulating TSH also occurred. TSH concentration in the smaller pituitaries of animals in which lesions had been made remained normal, but total hormonal stores decreased.

Thyroxine and triiodothyronine suppressed markedly and equally TSH secretion in the adenohypophyses of operated and intact rats; triiodothyronine was more potent (about 5:1). Hypothalamic damage did not prevent the re-accumulation of TSH in pituitaries previously depleted of their hormone by propylthiouracil; pituitary TSH concentrations rebounded to supranormal levels, but titres in blood decreased to subnormal values. The physiological and histochemical changes induced in the adenohypophyses of rats with lesions strongly implicated the basophils (β cells) in the genesis of TSH. All anterior pituitary cell types were affected in hypothalamic deficiency, but only the β basophils persisted when TSH stores were high, or disappeared when the pituitary was depleted of TSH with exogenous thyroid hormone.

The experimental results indicated that the hypothalamus modulates the activity of the pituitary-thyroid system by influencing production and release of TSH by the pituitary. Hypothalamic regulation of TSH secretion exists for normal conditions as well as for those situations in which enhanced TSH secretion is required. The maintenance of abundant TSH reserves in the adenohypophysis, their depletion after thyroid hormone, and their re-accumulation after goitrogen withdrawal, nevertheless revealed: (1) that the 'isolated' rat pituitary possesses a good measure of autonomous TSH function; (2) that thyroid hormone can act directly on the adenohypophysis independently of the hypothalamus; and (3) that the basic thyroid-pituitary servomechanism is systemically controlled by circulatory levels of thyroid hormone and is not under neural domination.