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Biomedical subjects

W J Sheward

Publications and source records attributed to W J Sheward.

31 records · Page 2Linked to original sources
PubMed1989

The effects of knife cuts in the sub-paraventricular zone of the female rat hypothalamus on oestrogen-induced diurnal surges of plasma prolactin and LH, and circadian wheel-running activity.

To investigate the role of suprachiasmatic efferent connections in the expression of diurnal hormone rhythms, the efferent pathway from the suprachiasmatic nucleus (the putative circadian generator in the rat) to the subparaventricular zone (the main terminal area of suprachiasmatic efferents) was disrupted using bilateral horizontal knife cuts in ovariectomized oestrogen-treated rats. The position of the knife cut was assessed by observing its effect on vasoactive intestinal polypeptide immunoreactivity (a marker for suprachiasmatic efferents into the sub-paraventricular zone). The size of both the diurnal plasma LH and prolactin surges was markedly and consistently reduced over the 3-week period following the lesion in animals with a total deafferentation of the subparaventricular zone, compared with sham-operated animals or lesioned animals with an intact subparaventricular zone. When lesioned animals were grouped according to the presence or absence of damage to the preoptic area, no significant differences were found in the sizes of the plasma hormone surges. When similar knife cuts were given to animals whose activity cycles were observed, no significant effects were noted in the ability of the animals to synchronize to a light/dark regime or to free-run in constant light conditions. These results suggest that the suprachiasmatic nucleus influences the diurnal surges of plasma LH and prolactin in oestrogen-treated ovariectomized rats, initially by an interaction with the subparaventricular zone and not by a direct influence on gonadotrophin-releasing hormone neurones or other more rostral structures.

Animals↗
PubMed1986

Prolactin messenger ribonucleic acid levels in the normal and hypogonadal mouse pituitary gland.

The effects of estrogen on the synthesis of pituitary PRL mRNA and PRL and the release of PRL into plasma were investigated in male and female normal and hypogonadal (hpg) mice. Because the hpg mouse is totally deficient in hypothalamic GnRH, it provides an excellent model for investigating the effects of estrogen and GnRH on PRL synthesis and release in the presence of a totally inactive gonadotropin-gonadal system. Estrogen stimulated the synthesis and release of pituitary PRL in both sexes of normal and hpg mice, and this marked increase in PRL synthesis correlated with an equally dramatic increase in pituitary PRL mRNA levels. Administration of GnRH alone produced a slight but significant increase in pituitary PRL content, which is consistent with an action of GnRH on prolactotropes, either directly or by way of a paracrine action involving gonadotropes.

Animals↗
PubMed1985

LH-RH in the rat and mouse hypothalamus and rat hypophysial portal blood: confirmation of identity by high performance liquid chromatography.

The nature of the immunoreactive (IR) form of luteinizing hormone-releasing hormone (LH-RH) in rat hypophysial portal vessel blood and in extracts of hypothalamus from rats and normal and hypogonadal (hpg) mice was investigated using high performance liquid chromatography and two highly specific anti-LH-RH sera. In rat hypophysial portal blood and in hypothalamic extracts from rats and normal mice a single immunoreactive peak was present which corresponded in retention time to synthetic LH-RH. No LH-RH-IR was detected in hypothalamic extracts from the hpg strain of mouse.

Animals↗
PubMed1985

Effects of intravenously administered 6-hydroxydopamine on the content of monoamines in the median eminence and neurointermediate lobe of the rat.

The effects of intravenous administration of 6-hydroxydopamine (6-OHDA) on the content of catecholamines in the median eminence and neurointermediate lobe was studied in male rats. The results confirmed previous findings of a depletion of catecholamines in both regions as a result of this lesion, although the magnitude of the effect was less than that revealed by fluorescence histochemistry. Administration of desipramine before 6-OHDA injection produced a more specific lesion, depleting dopamine but leaving noradrenaline unaffected.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1985

Effect of immunoneutralization of thyrotrophin-releasing hormone on the release of thyrotrophin and prolactin during suckling or in response to electrical stimulation of the hypothalamus in the anaesthetized rat.

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.

Animal Population Groups↗
PubMed1984

Somatostatin-28(1-12)-like immunoreactive substance is secreted into hypophysial portal vessel blood in the rat.

Somatostatin-28(1-12)-like immunoreactivity was measured in extracts of rat hypophysial portal blood and peripheral blood. The concentration of somatostatin-28(1-12) was higher in portal than in peripheral extracts, and its release into portal vessel blood was increased 4- to 5-fold by electrical stimulation of the median eminence. These results show that somatostatin-28(1-12) may be a physiological neurohormone and/or neurotransmitter.

Animals↗
PubMed1984

The hypogonadal mouse pituitary contains bioactive LH.

Saline extracts of pituitary glands from normal and hpg male mice were assayed for LH by the testosterone production assay. The extract of hpg pituitary tissue stimulated testosterone production by mouse Leydig cells in a dose-dependent manner which paralleled that of normal mouse pituitary. The normal mouse pituitary was about 20 times as potent as hpg pituitary which is similar to the relative potency obtained by radioimmunoassay. These results show that differentiation of the gonadotrophs and the synthesis of some biologically active LH can occur in the absence of LHRH.

Animals↗
PubMed1983

Somatostatin-28 is an hormonally active peptide secreted into hypophysial portal vessel blood.

Somatostatin 14 and 28 (SS-14 and SS-28) have been measured in hypophysial portal blood of male Wistar rats. The concentration and total amount of SS released into portal blood were increased 6- to 7-fold by electrical stimulation of the median eminence. On HPLC, only two peaks of immunoreactivity were detected in extracts of portal plasma and these peaks corresponded with SS-14 and SS-28, respectively. The amount of SS-28 in portal plasma was, on a molar basis, similar or greater than that of SS-14 and this together with other evidence suggests that SS-28 is an hormonally active peptide.

Animals↗
PubMed1983

Prolactin measurements in normal and hypogonadal (hpg) mice: developmental and experimental studies.

Plasma and pituitary PRL levels are significantly greater in adult female than in male rats. This difference is thought to be brought about by ovarian steroids. We found a similar sex difference in pituitary PRL content in normal mice from 30 days of age. Ovariectomy reduced pituitary PRL content and this reduction was prevented by sc implants of estradiol-17 beta (E2). Implants of E2 also increased the pituitary PRL content in normal male mice to a level approaching that in normal females. The hypogonadal (hpg) mice did not show a sex difference in pituitary PRL content. Implantation of E2 into mutants of both sexes raised the pituitary content of PRL to the level in normal females. Treatment of intact but not ovariectomized hpg females with two injections/day of 6 micrograms FSH (NIH-FSH-S15) produced uterine growth and an increase in pituitary PRL content. Estrogen implants significantly increased plasma PRL concentrations in ovariectomized normal female and normal male mice but not in adult hpg male or female animals. These results show that elevation of the plasma E2 concentration increased significantly the synthesis of PRL in both normal and hpg mice of both sexes, and in the normal, but not the hpg mice, also increased the plasma concentration of PRL.

Aging↗
PubMed1983

Thyrotropin-releasing hormone in rat pituitary stalk blood and hypothalamus: studies with high performance liquid chromatography.

Immunoreactive TRH (TRH-IR) in rat pituitary stalk blood and hypothalamus was investigated with high performance liquid chromatography in conjunction with a sensitive RIA. The TRH-IR of ethanol extracts of stalk blood resolved into three peaks, whether the blood was collected with the pituitary gland in situ or after the gland had been removed. The first peak corresponded to authentic TRH. By contrast, all the immunoreactive TRH in pituitary and hypothalamic extracts and in peripheral blood to which hypothalamic or synthetic TRH had been added eluted as a single peak with the same retention time as authentic TRH. The additional IR peaks in stalk blood did not correspond to known metabolites of TRH, and, since absent from the hypothalamus, they are unlikely to represent stored TRH precursors. Although authentic TRH constituted only 37% of total TRH-IR in pituitary stalk blood, the amount released during the first hour into stalk blood (1.7 ng) in relation to hypothalamic content (approximately 5 ng) was still high (approximately 34%) compared with that of LHRH (approximately 0.6%) and somatostatin (approximately 0.3%).

Animals↗
PubMed1982

Immediate increases in plasma prolactin and neurophysin but not other hormones after electroconvulsive therapy.

Plasma prolactin, growth hormone, cortisol, luteinising-hormone-releasing hormone (LHRH), thyrotropin-releasing hormone (TRH), and nicotine and oestrogen stimulated neurophysin (NSN and ESN) were measured before and for 6 min after electroconvulsive therapy (ECT) in eight women with severe electroconvulsive therapy (ECT) in eight women with severe depression. Plasma concentrations of NSN and ESN had increased significantly (as much as 10-fold for NSN) within 1 min of the seizure, and concentrations of prolactin had increased within 2-4 min after the seizure. Whereas plasma prolactin and ESN either continued to increase or remained raised throughout the 6 min after seizure, the concentrations of NSN fell to reach a value at 6 min that was approximately 50% of the maximum. There were no increases in any of the other hormones or peptides within the 6 min period under study. Thus ECT has selective effects on hormone release which cannot be attributed simply to a generalised release of pituitary or hypothalamic hormones in response to brain stimulation and/or stress.

Adult↗
PubMed1982

Priming effect of luteinizing hormone releasing hormone in the hypogonadal mouse.

We have investigated the LH response to LH releasing hormone (LH-RH) in female hypogonadal (hpg) mice in which the hypothalamus contains no LH-RH and the pituitary gland contains significantly less LH than in normal mice. Both the releasing action and the priming effect of LH-RH were not significantly different in hpg compared with normal mice. Raised plasma concentrations of oestradiol-17 beta reduced pituitary responsiveness to LH-RH in normal but not in hpg mice. These results show that in the mouse neither long-term exposure to normal levels of LH-RH nor a normal pituitary content of LH are necessary for either the releasing or the priming action of LH-RH.

Animals↗