"Short" Loop Feedback Regulation of Hypothalamic and Brain Thyrotropin-Releasing Hormone Content in the Rat and Dwarf Mouse*

Roti, Elio; Christianson, Dana; Harris, Arthur R. C.; Braverman, Lewis E.; Vagenakis, Apostolos G.

doi:10.1210/endo-103-5-1662

Cited by 52 publications

(21 citation statements)

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“…We found reduced CRF activity at 1 week after adrenalectomy. Al though this reduced CRF activity is not compatible with many other reports, it is likely because is has already been shown by sensitive RIA that gonadectomy induces a reduc tion in hypothalamic LH-RH [12], and that thyroidectomy causes a reduction in TRH [14].…”

Section: Discussioncontrasting

confidence: 75%

Vasopressin and CRF-ACTH in Adrenalectomized and Dexamethasone-Treated Rats

Hashimoto¹,

Yunoki²,

Kageyama³

et al. 1981

Neuroendocrinology

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Median eminence corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) and pituitary and peripheral plasma adrenocorticotropin (ACTH) and AVP were measured in male Wistar rats 1 and 2 weeks after bilateral adrenalectomy (ADX), sham operation (SHAM) or dexamethasone-treatment (DEX). Median eminence AVP content was unchanged 1 week after ADX but was significantly elevated 2 weeks after ADX, whereas CRF activity was reduced at 1 week after ADX and returned to control range at 2 weeks. Anterior pituitary ACTH content was elevated but posterior pituitary AVP content was reduced at 1 and 2 weeks after ADX. Plasma ACTH was greatly elevated in ADX rats and reduced in DEX rats, whereas plasma AVP did not differ significantly between these two groups or the control group. When ADX and SHAM rats were laparotomized under ether, plasma ACTH increased greatly, but this elevation was prevented by DEX treatment. The plasma AVP level was elevated in all three groups 2.5 min after onset of stress but returned to the basal range at 20 min. Median eminence CRF and AVP and pituitary ACTH and AVP were not significantly changed after onset of stress. These results indicate that the vasopressin and CRF-ACTH responses were not consistent in the median eminence, pituitary and peripheral plasma and suggest that vasopression is not involved in the feedback and acute stress mechanism of CRF-ACTH secretion. However, we have to measure CRF activity and AVP concentration in the hypophysial portal blood to confirm this conclusion.

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Section: Discussioncontrasting

confidence: 75%

Vasopressin and CRF-ACTH in Adrenalectomized and Dexamethasone-Treated Rats

Hashimoto¹,

Yunoki²,

Kageyama³

et al. 1981

Neuroendocrinology

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“…It has been reported, however, by Bartke (1965) and also observed by Howe and Pollard (unpublished work) that pituitary thyrotrophs are few in number and not in a very active state in dwarf mice. Measurements of TSH also have been extremely low in dwarf mice and TSH secretion did not occur when dwarf mice were administered TRH (Roti et al 1978). Hence it seemed that the observed thyrotroph hypoactivity was not of hypothalamic origin.…”

Section: Discussionmentioning

confidence: 98%

“…The primary cause of this dwarfism has for some time been attributed to an adenohypophyseal deficiency (Carsner and Rennels 1960). Recent work by Roti et al (1978) indicates that this may be the case as the dwarf mouse does not respond to administration of thyrotrophin releasing hormone (TRH) with secretion of thyroid stimulating hormone (TSH). Pituitary basophils (thyrotrophs and gonadotrophs) have been found in the dwarf mouse (Ortman 1956;Peterson 1959) although the thyrotrophs were few in number (Bartke 1964).…”

Section: Introductionmentioning

confidence: 99%

Estimation of Thyroid Gland Activity in the Snell Dwarf Mouse by Ultrastructural Observation of the Thyroid Gland, Measurement of Plasma Thyroxine Concentration and Thyroid Hormone Binding Capacity

Howe¹,

Howe²,

Pollard³

1980

Aust. Jnl. Of Bio. Sci.

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An ultrastructural study of the thyroid gland of the Snell dwarf mouse showed cellular activity to be very low. Follicle cell diameters were significantly lower than in controls whilst the nucleocytoplasmic ratio was significantly higher.The observed cellular activity of the thyroid cells was associated with the circulating levels of thyroxine which were found to be significantly lower than in controls. Measurement of the free thyroxine index showed very little free hormone available for tissue uptake. No differences in thyroid function due to age or sex in the dwarf mice were seen.Possible endocrine imbalances contributing to the low thyroid activity in the Snell dwarf mouse are discussed.

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“…The deficient TSH status of the Snell mutant has been based largely on the failure to detect thyrotrophs in the anterior pituitary (Roux et al 1982), the failure of thyrotrophichormone-releasing hormone (TRH) to elicit a rise in plasma TSH (Roti, Christianson, Harris, Braverman & Vagenakis, 1978) and estimations of thyroid activity both physiologically and ultrastructurally (Howe, Howe & Pollard, 1980;Van Buul-Offers, Hackeng The exact aetiology of the condition remains unknown. Although a hypothalamic defect controlling growth-hormone production seems ruled out by the experiment of Garsner & Rennels (1960), a deficiency in hypothalamic dopamine may explain the prolactin deficiency (Morgan, Bartke & Pfeil, 1981).…”

Section: The Snell Dwarf Mousementioning

confidence: 99%

Mouse Mutants as Models in Endocrine Research

Charlton

1984

Exp Physiol

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Although Shire (1979) has listed some forty‐eight mouse mutants of interest to the endocrinologist, this short review has concentrated upon eleven mutations which have resulted in a significant number of scientific publications over the last 4 or 5 years. The selection of references has had to be limited, but it should be possible easily to expand the list given in this review. Although the proximate cause of none of the eleven mutations has been identified with certainty, the abnormalities of function have included hormone deficiencies and receptor and post‐receptor malfunctions. It is perhaps a reflexion on our society in the 1980s, that the bulk of research has concentrated on the obese mouse. However, we still do not know the initial cause of this syndrome. The major disadvantage of the mouse to the hormone assayist lies in the small blood volume and the extreme difficulty in taking serial blood samples over a short period of time. With increased sophistication of assay techniques this may prove less daunting, but is an area where a review of the literature reveals discrepancies between laboratories, and even between data generated by the same laboratory at different times. With regard to the hormone content of endocrine tissues, the way forward for peptide‐secreting glands may be in the measurement of mRNA levels for particular hormones. Certainly the methods of recombinant‐DNA technology will yield positive information upon the aetiology and expression of some of the syndromes considered above. Organ transplantation is an area in which mutant mice have proved useful, for example gonadal, pituitary and pancreatic tissue transplantation. The grafting of neural tissue in the hpg mouse has added a further dimension to this field of research. The great infrastructure of genetical research in mice has enabled us to breed mutant genes onto different genetic backgrounds. This area of research is one which deserves to expand. The techniues of in vitro fertilization, chimera formation and embryo transfer have been used, in part, in studies on mouse mutants, and should provide technical means for further investigating gene expression. The family of dwarf mutants are ideally suited for research into the expression of genes micro‐injected into the fertilized egg (see Charlton & Cox, 1983). As new hormones are isolated and become available for study these mouse mutants may well be useful in delineating physiological functions for natural and pharmacological products. Again, the dwarf mutants would seem ideally suited for research into the synthesis and action of GRF. Mouse mutants have proved of use to biochemists and embryologists and provide fertile ground for endocrine investigations ranging from molecular genetics to membrane biophysics.

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"Short" Loop Feedback Regulation of Hypothalamic and Brain Thyrotropin-Releasing Hormone Content in the Rat and Dwarf Mouse*

Cited by 52 publications

References 0 publications

Vasopressin and CRF-ACTH in Adrenalectomized and Dexamethasone-Treated Rats

Vasopressin and CRF-ACTH in Adrenalectomized and Dexamethasone-Treated Rats

Estimation of Thyroid Gland Activity in the Snell Dwarf Mouse by Ultrastructural Observation of the Thyroid Gland, Measurement of Plasma Thyroxine Concentration and Thyroid Hormone Binding Capacity

Mouse Mutants as Models in Endocrine Research

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