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ABSTRACT
The aim of the present study was to use the technique of immunoneutralization with anti-thyrotrophin-releasing hormone (anti-TRH) serum to investigate the role of TRH in mediating the TSH and prolactin responses to electrical stimulation of the hypothalamus and the prolactin response to suckling in lactating rats. Electrical stimulation of either the median eminence or paraventricular nuclei of male or female rats anaesthetized with urethane resulted in significant increases in the plasma concentrations of both TSH and prolactin. Injection of sheep anti-TRH serum blocked the rise in plasma TSH concentration in response to stimulation of either brain area, but did not block the increase in plasma prolactin concentration. In anaesthetized, lactating female rats, the suckling stimulus produced a significant increase in the plasma prolactin concentration, but did not alter the plasma TSH concentration. Injection of anti-TRH serum, but not control non-immune or anti-bovine serum albumin, significantly decreased the basal release of TSH but did not abolish the prolactin response to suckling. These results show that TRH is the principal mediator of the neural control of TSH release in the rat, but is not crucial for the release of prolactin in response to either hypothalamic stimulation or suckling.
J. Endocr. (1985) 106, 113–119
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SUMMARY
Diced quarter anterior pituitaries from mature female Wistar rats were cultured in synthetic medium with or without added serum. Using each culture as its own control, the thyrotrophin-releasing hormone (TRH) dose–thyrotrophin (TSH) response characteristics of both media were similar; significant TSH secretion being stimulated at TRH doses around 1·5 × 10−9 mol/l. During days 1–3 of culture, basal TSH secretion fell significantly but TRH responsiveness was unchanged. Neither tri-iodothyronine (T3) nor thyroxine (T4) influenced basal TSH secretion.
In both culture media inhibition of TRH responsiveness was demonstrated with concentrations of T3 and T4 within the ranges 1·5 × 10−12 to 1·5 × 10−9 mol/l for T3 and 6·5 × 10−10 to 6·5 × 10−7 mol/l for T4. Equivalent inhibition was accompanied by similar T3 concentrations whether T3 or T4 supplements were used, suggesting that T4 itself has no feedback action. The similar concentrations of T3 required to inhibit TRH responsiveness in media either with or without serum suggest that the pituitary is responsive not only to free but also to total thyroid hormone concentrations, since serum-free medium contains no thyroid hormone-binding protein.
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The capacity of the pigeon pituitary gland to release prolactin was investigated in vivo, to evaluate its hypothalamic regulation and to establish the dominant hypothalamic factor for prolactin secretion. After 3 days of systemic administration of some physiological and pharmacological agents, followed by 2 consecutive days of local intradermal injections of prolactin into their crop sacs, the crop mucosa was scraped, dried and weighed. The substances tested were: oestradiol and tamoxifen (antioestrogen), thyrotrophin-releasing hormone (TRH) and anti-TRH serum, perphenazine (releases prolactin in mammals) and bromocriptine (suppresses prolactin in mammals). Prolactin and anti-prolactin serum were tested as controls.
While prolactin markedly proliferated and anti-prolactin serum significantly inhibited the mucosal weight, oestradiol, TRH and perphenazine dramatically depressed proliferation of the mucosa, suggesting that prolactin secretion was inhibited. Tamoxifen, anti-TRH serum and bromocriptine significantly increased the proliferation of the crop mucosa, indicating an increase in the endogenous release of prolactin. Since the effect of these substances on prolactin release in the pigeon is the opposite from their well-established effects in mammals, these results suggest, in a specific and homologous model, that the dominating regulator for prolactin in the pigeon is contrary to that in the mammal, namely prolactin-releasing factor, and that TRH may play a significant role in the physiological regulation of prolactin secretion.
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ABSTRACT
Tri-iodothyronine (T3) had no effect on the basal level of GH release from chicken hemipituitary glands perifused in vitro. The GH response to TRH was, however, markedly suppressed following exposure to T3. Suppression of TRH-stimulated GH secretion was observed after a 2-h preincubation with T3, and was induced, in a dose-related way, by 0·01–10 μmol T3/l. Exposure to T3 also reduced the effectiveness of TRH, at concentrations of 0·001–10 μg/ml, to stimulate GH release.
These results demonstrate that, in addition to a hypothalamic site of action, T3 is likely to suppress GH secretion in vivo by direct effects on pituitary GH release.
Journal of Endocrinology (1990) 126, 75–81
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Introduction
Growth hormone (GH) secretion has traditionally been considered to be under dual hypothalamic control, being stimulated by a GH-releasing factor (GRF) and suppressed by somatostatin (SRIF), an inhibitory releasing factor (Müller, 1987). These hypothalamic peptides are released into hypophysial circulation in response to stimuli in the internal and external environment, and act at receptors on somatotroph cells to regulate GH synthesis and release. Hypophysial portal plasma, however, also transports other hypophysiotrophic factors to the pituitary gland, and somatotrophs are undoubtedly exposed to other putative GRFs.
Thyrotrophin-releasing hormone (TRH; pGlu-His-Pro-NH2) was the first hypophysiotrophic peptide to be isolated and synthesized chemically and was called TRH because it was found to stimulate thyrotrophin (TSH) release from the pituitary gland (Nelson, 1982). However, since its discovery, TRH has been found to be synthesized in numerous locations throughout the 'diffuse neuroendocrine system', and in addition to its neuroendocrine role in the regulation of
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A.R.C. Institute of Animal Physiology, Babraham, Cambridge, CB2 4AT
(Received 1 November 1977)
Thyrotrophin releasing hormone (TRH) can have a stimulatory effect on the release of both prolactin and thyrotrophin (TSH; Deis & Alonso, 1973), although in the rat, supraphysiological doses of TRH are required to affect the secretion of prolactin (Burnet & Wakerley, 1976). A more important factor in the control of the release of prolactin is considered to be prolactin release inhibiting factor (PIF), which is thought to act through the catecholamine, dopamine (MacLeod, 1976). Stimuli which cause the concomitant release of TSH and prolactin are thought to have a direct effect at the hypothalamic level such that neurones releasing TRH are excited, whereas those releasing PIF are inhibited. In the present work, we have tested this hypothesis using the suckling stimulus to elicit the simultaneous release of prolactin and TSH (Blake, 1974; Burnet & Wakerley, 1976). If
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The change in the plasma concentration of cortisol after the administration of thyrotrophin releasing hormone (TRH) and LH releasing hormone (LH-RH) was studied in normal dogs and in dogs with pituitary-dependent hyperadrenocorticism (PDH). The normal dogs showed a small but significant increase in the plasma concentration of cortisol 15 min after intravenous injection of TRH and LH-RH. In ten of the dogs with PDH the response to TRH was not significantly different from that in the normal dogs, but in 13 the response was significantly greater. In 15 of the dogs with PDH the response to LH-RH administration was within or below the range of responses in the normal dogs and in only one dog was the response to LH-RH greater than that in the normal dogs. These findings are discussed in relation to the pathogenesis of PDH.
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Pharmacological doses of glucocorticoids inhibit thyroid function in man and laboratory animals due to suppression of thyrotrophin (TSH) secretion (Wilber & Utiger, 1969). Administration of prednisolone or dexamethasone for 1–2 days results in a suppression of basal serum TSH levels in normal subjects and in patients with primary hypothyroidism, whilst the pituitary TSH reserve capacity, as assessed by the response to synthetic thyrotrophin releasing hormone (TRH), remains unaltered (Wilber & Utiger, 1969; Besser, Ratcliffe, Kilborn, Ormston & Hall, 1971; Haigler, Pittman & Hershman, 1971). However, impairment of serum TSH response to administered TRH does occur in patients treated with glucocorticoids for 1 or more months (Otsuki, Dakoda & Baba, 1973). These studies suggest that glucocorticoids may inhibit TSH secretion at both hypothalamic and pituitary levels but the main effect of the short-term treatment is suppression of TRH production.
Nicoloff, Fisher & Appleman (1970) found that the circadian rhythm of thyroidal
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Morphine reduced the release of thyroid-stimulating hormone (TSH) which was stimulated by exposure to cold and by thyroidectomy as well as reducing the basal level of TSH in the serum of male rats. The inhibitory effect of morphine was antagonized by naloxone which did not enhance the basal or cold-induced TSH release. Pretreatment with morphine did not reduce the release of TSH induced by exogenous thyrotrophin-releasing hormone (TRH) but enhanced it. This effect of morphine was also antagonized by naloxone. The above results suggested that the effect of morphine in reducing levels of serum TSH was not mediated by blocking the effect of TRH on the anterior pituitary gland, but that it was probably mediated by the inhibition of the release of TRH.
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A radioimmunoassay for canine prolactin has been used to measure prolactin in the ferret. Serial dilutions of extracts of ferret pituitary glands and of ferret plasma yielded curves that were parallel with the canine prolactin standard curve. The sensitivity, accuracy, reproducibility and precision of the assay were within acceptable limits. Plasma prolactin levels increased after the administration of thyrotrophin releasing hormone (TRH) or chlorpromazine, but not after giving luteinizing hormone releasing hormone. Female ferrets, which were anoestrous, oestrous or spayed, and male ferrets had similar basal prolactin levels when sampled under sodium pentobarbitone anaesthesia. These basal levels were higher than in conscious males and the latter also showed a lesser response to TRH. Hypophysectomy significantly reduced basal prolactin levels in female ferrets by 2 h postoperatively and abolished the response to TRH.
