Maximum lateral dimensions of laser‐induced oxidation of thin tellurium films: A negative feedback effect

1989 ◽  
Vol 65 (10) ◽  
pp. 4033-4035 ◽  
Author(s):  
M. Wautelet
Keyword(s):  
Negative Feedback ◽  
Feedback Effect

EFFECT OF HYPOTHALAMIC DEAFFERENTATION ON THE CONTROL OF LUTEINIZING HORMONE SECRETION

1970 ◽  
Vol 46 (1) ◽  
pp. 1-7 ◽  
Author(s):  
S. TALEISNIK ◽  
M. E. VELASCO ◽  
J. J. ASTRADA
Keyword(s):  
Luteinizing Hormone ◽  
Negative Feedback ◽  
Positive Feedback ◽  
Hormone Secretion ◽  
Feedback Effect ◽  
Luteinizing Hormone Secretion ◽  
Ovarian Steroids ◽  
Medial Hypothalamus ◽  
Lh Release ◽  
Positive Feedback Effect

SUMMARY The influence that the interruption of the neural afferents to the hypothalamus exerts on ovulation and on the release of luteinizing hormone (LH) was studied in the rat. Animals with retrochiasmatic sections interrupting the neural connexions between the medial hypothalamus and the preoptic area (POA) showed constant oestrus and failed to ovulate. Animals in which the dorsal neural afferents to the POA were transected had oestrous cycles and ovulated normally. The positive feedback effect of progesterone on LH release in spayed animals primed either with 20 μg. oestradiol benzoate or 2·5 mg. testosterone propionate 3 days before was studied. Transection of the dorsal afferents to the POA favoured an increase in plasma LH, but in animals with retrochiasmatic sections the response was abolished. However, the negative feedback effect of ovarian steroids operated after both types of transection because an increase in plasma LH occurred after ovariectomy. It is concluded that the negative feedback effect of ovarian steroids acts on the medial hypothalamus which can maintain a tonic release of gonadotrophins in the absence of steroids. In contrast, the POA involved in the positive feedback effect of progesterone is concerned with the phasic release of LH.

FEEDBACK EFFECTS OF THYROXINE ON THE HYPOTHALAMUS AND PITUITARY OF GOLDFISH, CARASSIUS AURATUS

1971 ◽  
Vol 51 (1) ◽  
pp. 31-39 ◽  
Author(s):  
R. E. PETER
Keyword(s):  
Negative Feedback ◽  
Positive Feedback ◽  
Carassius Auratus ◽  
Feedback Effect ◽  
Inhibitory Factor ◽  
Pituitary Stalk ◽  
Thyroid Activity ◽  
Feedback Effects ◽  
Goldfish Carassius Auratus ◽  
Positive Feedback Effect

SUMMARY The effect on thyroid activity of a systemically ineffective dose of thyroxine (T4) implanted in the hypothalamus or pituitary of goldfish was tested. Thyroid activity was decreased by T4 implantation in either location, indicating that T4 has a negative feedback effect on the pituitary causing a decrease in thyrotrophin secretion, and a positive feedback effect on the hypothalamus stimulating the secretion of thyrotrophin inhibitory factor (TIF). Fish with a T4 or blank-control implant in the pituitary that had a damaged pituitary stalk, as a result of the operative procedures, were hyperthyroid, suggesting either that TIF is more effective in suppressing thyrotroph activity than T4 and that the effect of T4 was masked by the absence of TIF, or, less likely, that T4 negative feedback in the pituitary is not effective independent of TIF. The results were compared with the information about T4 feedback in mammals.

scholarly journals Dynorphin-Kappa Opioid Receptor Signaling Partly Mediates Estrogen Negative Feedback Effect on LH Pulses in Female Rats

2013 ◽  
Vol 59 (3) ◽  
pp. 266-272 ◽  
Author(s):  
Mst. Parvin MOSTARI ◽  
Nahoko IEDA ◽  
Chikaya DEURA ◽  
Shiori MINABE ◽  
Shunji YAMADA ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Negative Feedback ◽  
Kappa Opioid Receptor ◽  
Feedback Effect ◽  
Female Rats ◽  
Receptor Signaling ◽  
Kappa Opioid

Effects of ovarian hormones on brain opioid binding sites in castrated female rats

1992 ◽  
Vol 263 (3) ◽  
pp. E507-E511 ◽  
Author(s):  
D. Dondi ◽  
P. Limonta ◽  
R. Maggi ◽  
F. Piva
Keyword(s):  
Negative Feedback ◽  
Positive Feedback ◽  
Binding Sites ◽  
Serum Levels ◽  
Estradiol Benzoate ◽  
Inhibitory Effect ◽  
Feedback Effect ◽  
Female Rats ◽  
Opioid Binding ◽  
Positive Feedback Effect

These experiments were performed to analyze whether treatments of ovariectomized female rats with ovarian steroid regimens able to induce either an increase (positive feedback effect) or a decrease (negative feedback effect) of serum levels of luteinizing hormone (LH) have some impact on the characteristics of mu-opioid binding sites in circumscribed areas of the brain. The increase of serum levels of LH elicited by a treatment with estradiol benzoate (EB) plus progesterone (P; positive feedback effect) was accompanied by a significant decrease in the number of mu-binding sites in the hypothalamus and in the corpus striatum. The decrease in serum levels of LH induced by a treatment with EB alone (negative feedback effect) brought about a significant increase of the number of mu-binding sites in the thalamus and in the hippocampus. These results seem to suggest that the release of LH induced by EB plus P may involve a decrease of hypothalamic mu-binding sites. Apparently, the inhibitory effect on LH release exerted by EB alone does not involve any change of the density of these binding sites in the hypothalamus.

Glucocorticoid-mediated responses of plasma ACTH and anterior pituitary pro-opiomelanocortin, growth hormone and prolactin mRNAs during adjuvant-induced arthritis in the rat

1992 ◽  
Vol 9 (3) ◽  
pp. 273-281 ◽  
Author(s):  
A. Stephanou ◽  
N. J. Sarlis ◽  
R. A. Knight ◽  
S. L. Lightman ◽  
H. S. Chowdrey
Keyword(s):  
Mrna Expression ◽  
Hpa Axis ◽  
Negative Feedback ◽  
Anterior Pituitary ◽  
Feedback Inhibition ◽  
Feedback Effect ◽  
High Dose ◽  
Plasma Acth ◽  
Pomc Mrna ◽  
Prolactin Mrna

ABSTRACT Adjuvant arthritis (AA) in the rat leads to chronic stimulation of the hypothalamic-pituitary-adrenal (HPA) axis and the loss of its diurnal rhythmicity. We have investigated the effects of adrenalectomy (ADX) and different levels of corticosterone replacement upon plasma ACTH levels and anterior pituitary pro-opiomelanocortin (POMC), GH and prolactin mRNAs during the development of AA. In control ADX animals, we observed the negative feedback effects of exogenous corticosterone on plasma ACTH and anterior pituitary POMC mRNA. In the ADX animal with AA, however, the increased POMC mRNA which was observed was not reduced by exogenous corticosterone on day 7 of AA, although the negative feedback effect of corticosterone on plasma ACTH was intact. On day 14, however, even high dose corticosterone replacement failed to have a significant feedback effect on the raised levels of plasma ACTH. In control ADX animals, corticosterone replacement resulted in increased anterior pituitary GH mRNA and reduced prolactin mRNA. In contrast, in ADX animals with AA, GH mRNA was reduced and there was a further decrease in prolactin mRNA. In these animals, corticosterone replacement did not affect GH or prolactin mRNA expression. These data demonstrate a disruption of the normal mechanisms underlying feedback inhibition of the HPA axis by glucocorticoids during AA. Similarly, the glucocorticoid-dependent regulation of GH and prolactin mRNA expression is altered in AA.

Dexamethasone inhibits ovine corticotrophin-releasing factor (oCRF), arginine vasopressin (AVP), and oCRF + AVP stimulated release of ACTH during the last third of pregnancy in the sheep fetus

1987 ◽  
Vol 65 (6) ◽  
pp. 1186-1192 ◽  
Author(s):  
Laurie J. Norman ◽  
John R. G. Challis
Keyword(s):  
Negative Feedback ◽  
Arginine Vasopressin ◽  
Late Pregnancy ◽  
Feedback Effect ◽  
Plasma Acth ◽  
Fetal Sheep ◽  
Corticotrophin Releasing Factor ◽  
Basal Release ◽  
Sheep Fetus ◽  
Acth Release

We examined the hypothesis that in fetal sheep during late pregnancy exogenous glucocorticoids might affect differentially the pituitary response, measured as changes in plasma ACTH concentrations, to the systemic administration of ovine corticotrophin-releasing factor (oCRF), arginine vasopressin (AVP), or oCRF + AVP. At d 113–116 of pregnancy, equimolar injections of oCRF and AVP given separately provoked similar significant increases in plasma ACTH; the change in ACTH over basal values was significantly greater than the sum of the two separate responses when AVP + oCRF were given together. Exogenous dexamethasone did not affect basal ACTH concentrations, but suppressed significantly the responses to oCRF, AVP, and oCRF + AVP. At d 126–130, there was a significant ACTH response to CRF alone and to AVP + oCRF, but not to AVP alone. The response during the first 30 min postinjection to oCRF was significantly less than that to AVP + oCRF. Plasma Cortisol rose after each peptide injection. Exogenous dexamethasone suppressed both basal and stimulated responses to each peptide. At the amounts injected, there was no significant ACTH or Cortisol response to oCRF, AVP, or oCRF + AVP at d 136–140, but dexamethasone suppressed basal ACTH and Cortisol concentrations at this time. We conclude that stimulated, but not basal, release of ACTH is subject to the negative feedback effect of exogenous glucocorticoid by d 113–116 of gestation in fetal sheep. Both basal and stimulated release of ACTH and Cortisol are suppressed after d 125. At the amount of exogenous dexamethasone given, oCRF, AVP, and oCRF + AVP-stimulated responses are affected similarly. Our results suggest different controls of basal and stimulated ACTH release from the pituitary at d 113–116 of gestation. Our findings would be consistent with the pituitary as a level of action for the negative feedback effect of corticosteroids on stimulated ACTH release throughout the last third of pregnancy in fetal sheep.

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