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Biomedical subjects

S E Greer

Publications and source records attributed to S E Greer.

47 records · Page 3Linked to original sources
PubMed1984

Heterogeneity of activity of the prolactin-releasing factor in the bovine hypothalamo-neurohypophysial complex.

Fresh samples of bovine hypothalamic median eminence or hypophysial stalk extracted with 0.1 M-HCl and fractionated on Sephadex G-100 had two prolactin-releasing factor (PRF) components, the major one in the void volume (PRF-A) and the minor one in an elution position (partition coefficient (Kav) = 0.333) immediately after PRF-A (PRF-B). Similar fractionation of bovine posterior pituitary extracts showed two PRF peaks: PRF-A and another in a more retarded position than PRF-B (Kav = 0.645; PRF-C). Storage of bovine stalk extract at -20 degrees C for 1 year caused a shift from higher molecular weight PRF into PRF-C. Thyrotrophin-releasing hormone stimulated prolactin secretion, but its dose-response slope and chromatographic mobility were quite different from those for bovine tissue extracts. Secretion of prolactin induced by extracts of bovine hypophysial stalk is calcium dependent and is inhibited by dopamine.

Animals↗
PubMed1983

Nycterohemeral difference in inhibition of stress-induced ACTH in adrenalectomized rats.

To determine the interactions among the determinants of ACTH secretion, we examined the influence of circadian rhythmicity on glucocorticoid suppression of ACTH. Adrenalectomized rats were injected with the same amount of corticosterone at 0900 and 1800 h, and plasma ACTH concentrations were determined under basal conditions and after a standard ether stress. At 0900 h, corticosterone suppressed both basal and stress-induced plasma ACTH concentrations. At 1800 h, the same treatment suppressed basal ACTH secretion but not the stress-induced rise. Although the same amount of corticosterone was injected at both times of day, the plasma corticosterone concentration 5 min after injection was higher at 1800 h than at 0900 h. This study indicates that there is a nycterohemeral difference in feedback suppression of stress-induced ACTH secretion by a given dose of corticosterone. The daily variation in feedback inhibition may be due to the additive effect of the evening surge stimulus and the stress stimulus that together override the feedback signal.

Adrenalectomy↗
PubMed1983

Hyposmolar stimulation of in vitro pituitary secretion of luteinizing hormone: a potential clue to the secretory process.

Diluting the perifusion medium with water caused a striking prompt increase in LH secretion from perifused, acutely dispersed adenohypophseal cells. The minimum effective proportion of water was 4%; the quantity of hormone secreted was proportional to the dilution of the medium up to greater than 50% water. Secretion was not induced if the dilution was made with 5% aqueous mannitol to maintain isotonicity. The LH secretory responses to hyposmolarity or to LHRH were qualitatively indistinguishable. We suggest that expansion of the outer cell membrane may be an important initial component of the mechanism of secretion from adenohypophyseal cells.

Animals↗
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↗
PubMed1978

Studies on the site of action of vasopressin in inducing adrenocorticotropin secretion.

Hypophysectomized rats bearing three transplanted pituitaries under the kidney capsule responded to synthetic lysine vasopressin or pitressin with a significant elevation of plasma corticosterone, whereas hypophysectomized rats with no grafts did not. This response was completely abolished by pretreatment of animals with dexamethasone but was unaltered by central hypothalamic destruction. Corticotropin-releasing factor content of the hypothalamic median eminence, hypophyseal stal-, or pars nervosa of the posterior pituitary of intact rats was unchanged 5 or 10 min after ip injection of vasopressin compared to the basal level. We conclude that vasopressin and dexamethasone act directly on the adenohypophysis in vivo to exert their stimulatory or inhibitory effect on ACTH secretion.

Adrenocorticotropic Hormone↗
PubMed1977

Distribution of corticotrophin releasing factor activity within the hypothalamic-pituitary complex of rats and cattle.

An assay system involving cultured rat adenohypophysial cells from either intact or adrenalectomized donors was used to study the distribution of corticotrophin releasing factor (CRF) activity in the hypothalamic-pituitary complex of rats and cattle. In the rat hypothalamus, CRF activity was most concentrated in the median eminence, but CRF was present in the stalk and the posterior pituitary gland in much higher concentrations than in the median eminence in both species. The dose--response slopes for the median eminence, stalk and pars nervosa of the posterior pituitary gland were parallel to each other, suggesting a qualitative similarity between the CRF activity in these tissues. Rat posterior pituitary glands may also contain another CRF component which has a much flatter dose--response curve, but is detectable in smaller quantities of posterior pituitary tissue than is the other type of CRF.

Adrenalectomy↗
PubMed1975

The effect of iodine deficiency on thyroid function in the infant rat.

We have studied rats born to severely iodine-deficient mothers and subsequently maintained on a low-iodine diet (LID) from birth to 41 days. They were compared with controls born to mothers fed a high-iodine diet (HID). LID babies from birth on had large goiters, high thyroid labeled MIT/DIT ratios and radioiodine uptakes, high plasma TSH and low plasma T4 in comparison to HID controls. Thyroid labeled T3/T4 ratios were low in all babies at birth but were higher in the LID than HID babies from day 5 on and were greater than 1 after day 10, approximating the T3/T4 of the mothers. Coupling efficiency, as indicated by thyroid labeled (T3 + T4)/(MIT + DIT), was relatively low for the first 4 postnatal days for both the HID and LID babies and was associated with a lower plasma T4 than at later intervals. Injection of 0.05 mug 127I- simultaneously with 131I- caused an acute increase in labeled T4 and decrease in MIT formation in LID babies of all ages, but did not affect T3 synthesis. Doses of 127I- 20 times as large had no effect on labeled iodoamino acid synthesis in HID babies. Thyroid organic radioiodine content in newborn LID rats was 65% lower at 24 hr than at 4 hr after 131I injection, indicating that thyroid secretion was occurring. A few of the LID pups were "runts" approximately 60% the size of HID babies the same age. However, the overwhelming majority of LID babies maintained the same weight as HID controls from birth until weaning. After weaning, the LID babies grew at a slower rate than the HID controls. Relative thyroid weight, radioiodine metabolism and plasma TSH were no different in runts of various ages or in their mothers than in the "normal" LID controls. Adaptation was apparently adequate in the LID babies to maintain a nearly euthyroid state. We suggest that the low labeled T3/T4 ratio in the first few days of life in the LID babies may be due to a coupling deficiency in newborn rats resulting in a proportionately greater formation of iodotyrosines than of iodothyronines compared to older animals. This results in a greater intrathyroidal retention of iodine during intracellular thyroglobulin proteolysis and a more highly iodinated thyroglobulin in the LID babies than after normal coupling is achieved.

Animals↗
PubMed1975

Changes in plasma thyroxine, triiodothyronine, and TSH during adaptation to iodine deficiency in the rat.

We have measured plasma thyroxine (T4), triiodothyronine (T3), and TSH with specific radioimmunoassays in rats during adaptation to severe iodine deficiency after they had previously received regimens supplying various quantities of iodine. Rats were maintained on a high-iodine diet (HID) containing 3 mg iodine/kg or a low-iodine diet (LID) containing 30 mug iodine/kg supplemented with 0.1, 0.2, or 0.4 mug iodine/ml of drinking water before swtiching to KID alone. Frequent serial blood samples were obtained up to 3 months, using 6 or more animals for each time interval. In animals originally fed HID, T4 remained at 4-6 mug/100 ml unitl the tenth day of LID, then rapidly decreased to a value of less than 0.4 mug/100 ml at 1 month. TSH was initially 50 muU/ml and increased linearly to 165 muU/ml on day 16. Thence there was a much more rapid rate of rise to 640 muU/ml at 38 days. The rats changed to LID alone after having been fed LID with iodine supplementation underwent similar qualitative hormonal changes. However, the decrease in plasma T4 and the increase in plasma TSH occurred sooner in the rats which had drunk water containing only 0.1 or 0.2 mug iodine/ml than in the previous experiment. Rats which had received 0.4 mug iodine/ml showed a pattern essentially identical to that of the animals which had been fed HID. plasma T3 did not change significantly in any of the experiments, remaining at 60-90 ng/100 ml, although there was a tendency for the values to be somewhat lower after several weeks of LID. There was a highly significant negative correlation of plasma T4 with plasma TSH. There was no significant correlation of plasma T3 with either plasma T4 or plasma TSH. It is concluded that the combined physiologic effect of plasma T4 and T3 concentration is more important in determining TSH secretion through negative feedback effects on the hypothalamus and/or pituitary than is the concentration of plasma T3.

Animals↗