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Biomedical subjects

M A Greer

Publications and source records attributed to M A Greer.

At least 91 records · Page 5Linked to original sources
PubMed1981

Hypoglycemia stimulates ACTH secretion through a direct effect on the basal hypothalamus.

The primary site of action of insulin hypoglycemia to induce ACTH secretion was investigated in rats with medial basal hypothalamic ablation (MBHA), medial basal hypothalamic deafferentation (MBHD), and chlorpromazine-morphine-pentobarbital (C-M-P) treatment. Plasma corticosterone (B) concentration was used as an index of ACTH secretion. Hypoglycemia failed to provoke ACTH secretion in MBHA and C-M-P treated animals, while it stimulated ACTH secretion in MBHD animals to the same extent as in controls. The rise in plasma B induced by synthetic lysine-vasopressin injection was not significantly different between MBHA and control animals, indicating pituitary ACTH reserve was not affected by the operation. Our data indicate that hypoglycemia stimulates ACTH secretion through a primary effect in the medial basal hypothalamus and not in the extrahypothalamic CNS or adenohyphophysis.

Adrenocorticotropic Hormone↗
PubMed1981

Evidence that thyrotropin and prolactin are not secreted by the posterior pituitary of the rat.

After eutopic hypophysectomy of the host, transplants under the renal capsule of three whole pituitaries or of the adenohypophysis alone were capable of maintaining plasma PRL concentration equal to or greater than that of intact controls. The basal plasma TSH levels in rats with these types of heterotopic pituitaries was below that of intact controls but was significantly increased by TRH or chronic antithyroid treatment. Rats with posterior pituitary (intermediate and neural lobe) heterotopic transplants were incapable, under any conditions tested, of raising the plasma PRL or TSH concentration above that seen in hypophysectomized controls without pituitary transplants. In a further experiment, selective extirpation of the anterior or posterior lobe of the eutopic pituitary was performed. Plasma concentrations of TSH and PRL in rats with anterior lobectomy were not significantly different from those of hypophysectomized controls but were significantly higher than those of hypophysectomized controls in rats with posterior lobectomy. These data indicate that only the adenohypophysis secretes physiologically significant quantitites of these two hormones. (Endocrinology 108: 382, 1981)

Animals↗
PubMed1981

Thyrotropin secretory response to thyrotropin-releasing hormone in the hypothyroid perinatal rat: further evidence of thyrotroph independence of the hypothalamus during early ontogenesis.

Propylthiouracil fed to pregnant rats for the last week of gestation to induce maternal and fetal hypothyroidism induced a 3-fold rise in plasma TSH concentration in the newborn pups compared to a 4-fold rise in their mothers. Subcutaneous administration of 1 ng/g BW TRH caused a greater rise in plasma TSH in the hypothyroid pups than in their mothers. These results, in combination with published data, indicate that the apparent independence of pituitary-thyroid function from TRH control during early ontogenesis in the rat is primarily due to delayed maturation of the hypothalamic TRH system.

Animals↗
PubMed1981

Delineation of the hypothalamic area controlling thyrotropin secretion in the rat.

Discrete midline hypothalamic lesions were made in male rats in the region of the paraventricular nuclei (PVN), ventromedial nuclei, and medial preoptic area (mPO) using modified Halasz C-shaped knives. In euthyroid rats, small lesions, including the PVN and little surrounding tissue, or large lesions, including portions of the dorsomedial nucleus, anterior hypothalamus, and preoptic area in addition to the PVN, caused a similar 60% drop in the plasma TSH concentration within 2 days which persisted for at least 3 weeks. PVN lesions also produced a significant decrease in plasma TSH in hypothyroid rats and diminished both the increase in plasma TSH in response to thyroidectomy and the decrease induced by ether inhalation. Ventromedial nuclei lesions preserving the PVN inconsistently decreased plasma TSH. mPO lesions anterior to the PVN induced a transient elevation of plasma TSH and GH only in hypothyroid rats. TRH-stimulated TSH secretion was not affected by any of the lesions. The results suggest: 1) the PVN and their immediate vicinity are of primary importance for maintaining a normal TSH response to the stimuli investigated, and 2) the mPO area tonically inhibits TSH secretion, presumably through its role in somatostatin secretion.

Animals↗
PubMed1981

Non-specific adsorption of corticotrophin-releasing factor (CRF) to powdered glass.

CRF activity from various sources (rat hypothalamic median eminence and posterior pituitary, bovine hypophyseal stalk, and human peripheral blood) was adsorbed to finely ground glass (Quso, Corning, CRF activity was eluted from the glass with 30% acetone. Up to 85% of the total CRF activity originally present in the crude CRF preparation was adsorbed to Quso or Corning glass; up to 25% of the original total CRF activity was recovered from the glass with 30% acetone. We conclude that CRF is among the hormones adsorbed by glass.

Adrenocorticotropic Hormone↗
PubMed1980

Hippocampal inhibition of pituitary-adrenocortical function in female rats.

To assess the influence of the hippocampus on ACTH secretion, plasma ACTH concentrations were compared in hippocampectomized and control rats under conditions of differing plasma corticosterone concentrations. In the PM, hippocampectomized rats had higher basal and 2-min ether-stress-induced ACTH concentrations than did cortex-removed controls. Basal PM plasma corticosterone concentrations were also significantly elevated in the hippocampectomized group. In the AM, there were no between-group differences. Adrenalectomy abolished the PM differences between cortical-control and hippocampectomized rats. PM hypersecretion of ACTH in the absence of the hippocampus suggests that this structure contributes an inhibitory component to the neural mechanisms regulating ACTH release. The fact that this increase in hormone concentrations is limited to the PM indicates that there is a circadian variation in hippocampal action.

Adrenocorticotropic Hormone↗
PubMed1979

Effects of destruction of the suprachiasmatic nuclei on the circadian rhythms in plasma corticosterone, body temperature, feeding and plasma thyrotropin.

To study the role of the suprachiasmatic nuclei (SCN) in generating circadian rhythms in female rats, lesions were placed in the SCN or in the medial preoptic (PO) region. Serial blood sampling at 4-hour intervals at 3 and 13 weeks after surgery indicated that complete SCN destruction abolished rhythmic fluctuation in plasma corticosterone levels in individual rats. Partial destruction produced less interference, while medial PO lesions that spared the SCN were without effect. Similar effects were noted on daily changes in body temperature at 10 weeks after surgery; however, some rats showed evidence of dissociation of these two rhythmic functions in that some lesions appeared to affect one and not the other. In ancillary studies, it was found that all lesioned groups showed nocturnal feeding patterns similar to those of the controls and that the diurnal pattern in plasma thyrotropin (TSH) levels was altered by complete destruction of the SCN. These data suggest that the SCN are essential for the circadian rhythms in pituitary-adrenal function and body temperature and that separate pacemarkers may be present in these nuclei for these two periodic functions. The SCN may also control rhythmic TSH secretion, but these nuclei and the medial PO region do not appear essential for nocturnal feeding.

Animals↗
PubMed1979

Acute effects of hypothalamic ablation on plasma thyrotropin and prolactin concentrations in the suckling rat: evidence that early postnatal pituitary-thyroid regulation is independent of hypothalamic control.

Hypothalamic ablation was performed at various periods postnatally in animals previously administered propylthiouracil to raise plasma TSH concentrations. There was no significant change in plasma Tsh up to 8 h after hypothalamic ablation in pups 1--4 days old, whereas hypophysectomy of such pups produced a 60% fall in plasma TSH within 4 h. By the 5th postnatal day, hypothalamic ablation produced a 30% fall in plasma TSH within 4 h (P less than 0.05). By the 12th postnatal day and thereafter, the fall in plasma TSH after hypothalamic ablation was not significantly different from that seen in adults, except in 30-day-old rats in which there was a lesser effect of hypothalamic ablation on plasma TSH (P less than 0.01 in comparison to 23-day-old and adult groups). The greatest effect of hypothalamic ablation on plasma TSH was in 45-day-old animals (P less than 0.01 in comparison to adults). No significant change was produced in plasma PRL within 4 h postoperatively at any age. Our data indicate that regulation of TSH secretion in the rat is independent of hypothalamic control until after the 5th postnatal day and is fully developed by day 12. This corresponds temporally with the postnatal rise of plasma TSH, T4, and T3 and hypothalamic TRH to adult concentrations and indicates maturation of the hypothalamic regulation of TSH secretion.

Animals↗
PubMed1979

Comparison of the effects of deafferentation and ablation of medial basal hypothalamus on thyrotropin and prolactin secretion.

To further delineate the interrelationships of neural control of TSH and prolactin secretion, medial basal hypothalamic deafferentation (MBHD) or medial basal hypothalamic ablation (MBHA) were performed in euthyroid or hypothyroid male rats. MBHD produced a prompt and significant fall in plasma TSH but no change in plasma prolactin. MBHA produced a more marked fall in plasma TSH and a 6-fold rise in plasma prolactin within 3 days postoperatively. Plasma TSH remained at a low level postoperatively, but plasma prolactin gradually declined from its peak 3-5 days postoperatively to approximately the initial basal levels 2 weeks postoperatively. MBHA did not appreciably impair the ability of TRH to stimulate TSH secretion or of perphenazine to stimulate prolactin secretion. Where the same experiments were performed in both euthyroid and hypothyroid rats, there was no qualitative difference between the two, although basal plasma TSH was higher and prolactin lower in the hypothyroid than in the euthyroid animals. Our data support the concept that the medial basal hypothalamus is important in stimulating TSH and inhibiting prolactin secretion. Dormant inhibitory influences on prolactin secretion, but not stimulatory influences on TSH secretion, may be aroused after hypothalamic ablation.

Animals↗
PubMed1978

Postnatal development of pituitary-thyroid function in male and female rats: comparison of plasma and thyroid T3 and T4 concentration.

Plasma T4, T3, and TSH, and total and 131l-labeled T4 and T3 in thyroid digests were determined in male and female rats from birth to 30--45 days postnatally. Mothers and offspring were fed a high-iodine Purina diet throughout. In both sexes, plasma T4 was less than 1 microgram/100ml at birth but rose linearly to a peak of 6--7 micrograms/100 ml at day 15. Plasma T3 remained low at 30--40 ng/100 ml until day 10, then rose steeply to 80--100 ng/100 ml at day 20--30. Plasma TSH had a bimodal distribution with an early peak in the intial 1--2 weeks of life and a second rise after day 30. Adult pattern sex differences in plasma TSH appeared by day 30. Labeled T3 was undetectable in thyroid digests until after day 7. Both labeled and stable T3 and T4 concentration and T3/T4 ratios rose progressively during the first 2 weeks of life. After day 7, stable and labeled intrathyroidal T3/T4 ratios were significantly correlated, but the latter was always higher than the former for any given age.

Animals↗
PubMed1978

Evidence that control of fetal thyrotropin secretion is independent of both the fetal and maternal hypothalamus.

Propylthiouracil (PTU) administered to pregnant rats from day 18-21 of gestation caused a significant increase in maternal and fetal thyroid weight and plasma TSH. Fetal encephalectomy on day 18 did not significantly affect basal or PTU-stimulated pituitary-thyroid function. Destruction of the basal hypothalamus in the mother on day 13 or 16 markedly reduced maternal plasma TSH and thyroxine and prevented a PTU-induced increase in thyroid size, but did not affect fetal pituitary-thyroid function. Plasma PRL, was undetectable in both intact and encephalectomized fetuses at 21 days but was increased greater than 6-fold to approximately 2 microgram/ml in the mothers by maternal hypothalamic destruction. We conclude that fetal pituitary-thyroid function in the rat is not dependent on either fetal or maternal hypothalamic TRH.

Animals↗