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ABSTRACT
Young, growing rats which had been chronically (2 weeks) adrenalectomized or parathyroidectomized were used to define the roles of the adrenal and parathyroid glands on the maintenance of normal circadian rhythms of DNA, collagen and non-collagen protein synthesis in the skeleton. The animals were conditioned to food being available ad libitum and to 12 h light: 12 h darkness (lights on from 08.00 to 20.00 h). The pace of DNA, collagen and non-collagen protein synthesis in different regions of the tibia (tibial growth cartilage, metaphysial bone and diaphysial bone) was measured by the in-vivo incorporation of tritiated thymidine (1 h) and radioactive proline (48 h). In intact rats there were no regional differences in the phasing of the circadian profiles; peak DNA and non-collagen protein synthesis occurred at the onset of the dark period while peak collagen synthesis occurred during the middle of the period of light. Adrenalectomy selectively abolished the regional DNA synthesis rhythms without altering the phases of the serum Ca and phosphorus (P) rhythms, which peak at mid-day and at the onset of darkness respectively. Parathyroidectomy abolished the regional rhythms for collagen and non-collagen protein synthesis and serum Ca rhythms, without altering the phase of the serum P and corticosterone rhythms. Dietary Ca-lactate supplements, which raised serum Ca levels towards normal in parathyroidectomized rats, were able to correct serum corticosterone values but did not normalize bone collagen and non-collagen protein synthesis values. These data indicate that the adrenal rhythm governs the proliferative activities of bone and cartilage cells, and that parathyroid hormone is essential to maintain normal collagen and non-collagen protein synthesis rhythms.
J. Endocr. (1984) 103, 49–57
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North Carolina Sea Grant, Institute of Biology, Department of Zoology
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North Carolina Sea Grant, Institute of Biology, Department of Zoology
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Compensatory growth (CG) is a period of growth acceleration that exceeds normal rates after animals are alleviated of certain growth-stunting conditions. In hybrid striped bass (HSB, Morone chrysops×Morone saxatilis), 3 weeks of complete feed restriction results in a catabolic state that, when relieved, renders a subsequent phase of CG. The catabolic state was characterized by depressed levels of hepatic Type I and II GH receptor (ghr1, ghr2) and igf1 mRNA, along with considerable decreases in plasma Igf1. The state of catabolism also resulted in significant declines in hepatic igf2 mRNA and in circulating 40 kDa Igf-binding protein (Igfbp). Skeletal muscle expression of ghr2 mRNA was significantly increased. Upon realimentation, specific growth rates (SGRs) were significantly higher than sized-matched controls, indicating a period of CG. Hepatic ghr1, ghr2, igf1 and igf2 mRNA levels along with plasma Igf1 and 40 kDa Igfbp increased rapidly during realimentation. Plasma Igf1 and total hepatic igf2 mRNA were significantly correlated to SGR throughout the study. Skeletal muscle igf1 mRNA also increased tenfold during CG. These data suggest that endocrine and paracrine/autocrine components of the GH–Igf axis, namely igf1, igf2, and ghr1 and ghr2, may be involved in CG responses in HSB, with several of the gene expression variables exceeding normal levels during CG. We also demonstrate that normalization of hepatic mRNA as a function of total liver production, rather than as a fraction of total RNA, may be a more biologically appropriate method of quantifying hepatic gene expression when using real-time PCR.
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ABSTRACT
The effects of morphine dependence and abrupt opiate withdrawal on the release of oxytocin and corticotrophin-releasing factor-41 (CRF-41) into hypophysial portal vessel blood in rats anaesthetized with urethane were investigated. Adult female Sprague–Dawley rats were made dependent upon morphine by intracerebroventricular infusion of morphine for 5 days; abrupt opiate withdrawal was induced by injection of the opiate antagonist naloxone. The basal concentrations of oxytocin in portal or peripheral plasma from morphine-dependent rats did not differ significantly from those in control, vehicle-infused rats. In rats in which the pituitary gland was not removed after stalk section, the i.v. injection of naloxone hydrochloride (5 mg/kg) resulted in a large and sustained increase in the concentration of oxytocin in both portal and peripheral plasma in control and morphine-dependent rats. The i.v. injection of naloxone resulted in a threefold increase in the secretion of oxytocin into portal blood in acutely hypophysectomized rats infused with morphine, but did not alter oxytocin secretion in vehicle-infused hypophysectomized rats. The concentration of oxytocin in peripheral plasma in both vehicle- and morphine-infused hypophysectomized rats was at the limit of detection of the assay and was unchanged by the administration of naloxone. There were no significant differences in the secretion of CRF-41 into portal blood in vehicle- or morphine-infused hypophysectomized rats either before or after the administration of naloxone. These data show that, as for oxytocin release from the neurohypophysis into the systemic circulation, the mechanisms which regulate oxytocin release into the portal vessel blood can also be made morphine dependent. The lack of effect of morphine or naloxone on the release of CRF-41 or other stress neurohormones suggests that the effect of opiate dependence and withdrawal is selective for oxytocin and is not simply a non-specific response to 'stress'.
Journal of Endocrinology (1990) 124, 141–150
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ABSTRACT
The involvement of the region anterior and ventral to the third ventricle (AV3V region) in the control of oxytocin release was investigated using electrical stimulation and electrolytic lesioning techniques in the rat. Electrical stimulation (0·5 mA, 50 Hz, 15–25 s) of the AV3V region of lactating rats evoked a reproducible rise in intramammary pressure equivalent to that induced by 0·25–0·5 mu. oxytocin (i.v.). Increases in circulating concentrations of oxytocin, as determined by specific radioimmunoassay, confirmed that AV3V stimulation released oxytocin in both lactating and non-lactating rats. The increases in plasma oxytocin concentration evoked by electrical stimulation of the AV3V region were dependent upon intensity and frequency of stimulation, and electrode position. A significant (P<0·05) increase followed stimulation at 25 Hz and 0·1 mA, and a maximal response was obtained with 50 Hz and 1·0 mA. Stimulation of the area in and around the nucleus medianus produced the greatest rise in oxytocin secretion.
The milk-ejection reflex was not abolished after acute electrolytic ablation of the AV3V region in urethane-anaesthetized lactating rats, but electrolytic lesion of the AV3V region prevented the increase in plasma oxytocin concentration which normally followed an osmotic stimulus (1 ml 1·5 mol NaCl/l, i.p.),
These studies provide evidence that the AV3V region is a major source of excitatory afferents to oxytocin neurones; this input is essential for the osmoresponsiveness of these neurones but plays little role in the control of such neurones during reflex milk ejection.
J. Endocr. (1987) 114, 253–261
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ABSTRACT
The region anterior and ventral to the third ventricle (AV3V) region is a major source of excitatory afferents to the magnocellular neuroendocrine system, and is essential for the osmotically regulated release of oxytocin. We investigated whether this input has a similarly essential role in parturition. Rats were implanted with a guide cannula in the AV3V region on days 9–18 of pregnancy. Following the birth of the third pup, rats were anaesthetized briefly with ether and either given an electrolytic AV3V lesion or a sham procedure was carried out. In eight AV3V-lesioned rats the mean (± s.e.m.) median interbirth interval following the lesion was 6·3 ± 1·2 min compared with 5·2 ± 0·6 min in 11 sham-lesioned rats. All rats completed delivery of their litters. The mean plasma concentration of oxytocin was unchanged following the sham procedure (pre-sham 17·1±2·8 pmol/l, n = 8; 15 min post-sham 18·1±2·7 pmol/l, n = 8; 30 min post-sham 19·2 ± 3·5 pmol/l, n = 8). In AV3V-lesioned rats, plasma oxytocin was significantly raised following the lesion (pre-lesion 14·6±1·3 pmol/l, n = 7; post-lesion 58·3 ± 9·8 pmol/l, n = 7) and was still higher than the sham-treated group after 30 min (55·8 ± 9·9 pmol/l). Thus there was no significant difference in the time-course of parturition between AV3V-lesioned rats and sham-lesioned rats, and no evidence that the lesion impaired the release of oxytocin. Furthermore, in rats given an AV3V lesion on the morning of the expected day of delivery, parturition was neither delayed nor disrupted, suggesting that the AV3V region does not contribute to the mechanisms controlling the onset of parturition.
Journal of Endocrinology (1989) 121, 109–115
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ABSTRACT
Oxytocin secretion is inhibited by opioids, and oxytocin is important in parturition. The effects on parturition of morphine, a relatively selective μ-opioid receptor agonist, were studied in the rat. Morphine or vehicle with or without the opiate antagonist naloxone were administered immediately after the birth of the second pup and the subsequent course of parturition was recorded in a total of 80 rats. Both s.c. morphine (10 mg/kg) and intracerebroventricular (i.c.v.) morphine (18 μg through a previously implanted cannula) interrupted parturition, delaying the birth of the sixth pup after treatment to 187·3 ± 35·9 (s.e.m.) min and 195·4 ± 19·5 min respectively, compared with 46·4 ± 3·7 and 66·1 ± 17·5 min after vehicle alone. The dose of morphine given i.c.v. had no effect when given s.c. Naloxone given concurrently prevented the effects of morphine. Eventually the rate of parturition in the morphine-treated groups recovered. Perinatal pup mortality rate was not increased when morphine was given to the mothers, but it did inhibit the expression of normal intrapartum maternal behaviour.
Pup mortality was increased 48 h post partum by morphine given during parturition, and it reduced the proportion of rats with normal maternal behaviour 24 h post partum. Morphine did not affect spontaneous or oxytocin-stimulated contractile activity of the parturient uterus in vitro. The concentration of oxytocin in trunk blood plasma was decreased 40 min after i.c.v. morphine (24·3 ± 3·9 vs 39·3± 6·5 pmol/l in controls), as was vasopressin (7·2 ± 1·5 vs 19·7 ± 4·5 pmol/l in controls). Intravenous infusion of oxytocin (2–5 mU/min for 144·3 ± 8·2 min; total infused 448·5 ± 61·9 mU) after i.c.v. morphine re-started parturition; all pups were born to these rats (mean time to pup 6, 110·3 ± 12·7 min) before the i.v. vehicle-infused rats given i.c.v. morphine re-started (mean time to pup 6, 406·3±125·2 min).
It is concluded that morphine given during parturition acts centrally through opioid receptors to inhibit oxytocin secretion, and impairs the expression of maternal behaviour. Reversal of the effects of morphine on parturition by i.v. oxytocin demonstrates the important role of oxytocin in fetus ejection and expulsion.
Journal of Endocrinology (1989) 121, 521–536
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Abstract
Medullary thyroid carcinoma (MTC) is an APUDoma (APUD refers to amine precursor uptake and decarboxylation) arising from the parafollicular cells. Diarrhoea has been reported in some 30% of patients, variously attributed to excess production of calcitonin (CT), serotonin (5-HT), vasoactive intestinal peptide (VIP) or other factors.
The regulatory factors in MTC were examined employing immunocytochemistry and RIA to tumours and their extracts. The patients were followed up for more than 15 years. CT and calcitonin gene-related peptide were universally expressed in all the tumours. The neuroendocrine markers chromogranin A (and its fragments pancreastatin and WE-14), neurone-specific enolase, protein gene product 9·5 and carcino-embryonic antigen were found in the majority of MTCs and might be useful as immunocytochemical markers. 5-HT, substance P, neurokinin A, glucagon and VIP could not be detected, excluding them as candidates in the diarrhoea of MTC.
Journal of Endocrinology (1997) 152, 275–281