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L Ferland

Publications and source records attributed to L Ferland.

50 records · Page 3Linked to original sources
PubMed1976

Site of the in vivo stimulatory effect of prostaglandins on LH release.

A possible direct effect of prostaglandins E1 and E2 (PGE1 and PGE2) on luteinizing hormone (LH) release at the pituitary level was studied in vitro using anterior pituitary cells in primary culture, a system approximately 10-fold more sensitive to stimulation of LH release than previously used hemipituitaries. No effect of PGE1 or PGE2 could be detected on the time course of basal or LH-RH-stimulated LH release or on the LH responsiveness to LH-RH. This absence of a direct effect of PGEs at the pituitary level on LH release was confirmed by in vivo experiments using female rats under Surital anesthesia in the afternoon of proestrus. After intravenous injection, under these conditions, 15(S)-15-methyl PGE2 was 3-5 times more potent than PGE2 to increase plasma LH levels while PGE1 had about 50% the potency of PGE2. Injection of sheep anti-LH-RH serum one hour before PGE1 or PGE2 injection not only lowered basal plasma LH levels but prevented the rise induced by PGEs. These data indicate clearly that the increased plasma LH levels observed after in vivo PGE injection are secondary to a stimulation of LH-RH release while PGEs do not appear to have a significant effect on LH release at the pituitary level.

Animals↗
PubMed1976

Inhibition by six somatostatin analogs of plasma growth hormone levels stimulated by thiamylal and morphine in the rat.

Administration of sodium thiamylal (50 mg/kg,i.p.) and morphine (3 mg/animal,s.c.) leads to high plasma levels of growth hormone (GH) with a maximum measured approximately 30 min after injection. When the same dose of morphine is administered 60 and 120 min later and small additional doses of thiamylal are injected to maintain the animals deeply anesthetized, constant high levels of plasma GH are maintained up to the last interval studied (3 h). This in vivo model has been used to evaluate the potency and duration of action of somatostatin and of six of its analogs by serial blood sampling of animals bearing a cannula inserted into the right superior vena cava. A significant inhibitory effect of somatostatin (45% inhibition) is observed 15 min after a s.c. injection of 1 mug of the peptide while a near maximal effect (90-95% inhibition) is found at a dose of 25 mug. Both the degree of inhibition and duration of action of somatostatin are dose-dependent. Inhibitory activities equivalent to 1-250 mug of somatostatin can be measured with the model described. [Tyr1] somatostatin, [D-Ala1]somatostatin, [N-acetyl-Cys3] somatostatin and [N-benzoyl-Cys3] somatostatin have activities indistinguishable from somatostatin itself while [D-Lys4] somatostatin and [des-amino1, des-carboxy14] somatostatin have approximately 10% the activity of the natural hypothalamic peptide. This in vivo model offers advantageous characteristics of precision and reproducibility for the evaluation of potency of inhibitors of GH release.

Animals↗
PubMed1976

Inhibitory activity of analogues of luteinizing hormone-releasing hormone (LH-RH) in vitro and in vivo.

Improved inhibitors of LH-RH are those which, beside removal of the histidine residue at position 2 of LH-RH, include replacement of glycine at position 6 by a D-amino acid. A still better modification is replacement of the histidine residue at position 2 by D-phenylalanine. As examples, when tested in pituitary cells in culture, [Des-His2]LH-RH, [Des-His2, D-Leu6]LH-RH, [Des-His2, D-Phe6]-LH-RH, [D-Phe2]LH-RH, [D-Phe2, D-Leu6]LH-RH and [D-Phe2, D-Phe6]LH-RH inhibit 50% of LH release induced by LH-RH at molar ratios (MR50S) of 3000, 500, 60, 1000, 150 and 25, respectively. [D-Phe2, D-Phe6, D-Phe7]LH-RH, [D-Phe2, Phe3, D-Phe6]LH-RH and [D-Phe2, Phe5, D-Phe6]LH-RH have MR50 values of respectively 400, 100, and 75. When evaluated in vivo, some of the mentioned structural modifications permit inhibition of LH-RH action at molar ratios lower than observed in vitro. At a 500 molar ratio, [D-Phe2, Phe5, D-Phe6]-LH-RH inhibits the plasma LH rise induced by LH-RH by 75% up to 5 h after its injection. When administered at 12.00 hours at the dose of 2 mg, this analogue inhibits the spontaneous pro-oestrus LH surge and ovulation by 85 and 75%, respectively.

Animals↗
PubMed1976

Effect of pharmacological blockade of ACTH and TSH secretion on the acute stimulation of prolactin release by exposure to cold and ether stress.

Acute exposure of male rats to cold (5C)leads to a rapid increase of plasma levels of thyrotropin (TSH), prolactin (PRL), corticosterone, and L-thyroxine. Exposure to ether is similarly followed by a rapid increase of plasma levels of PRL and corticosterone, while TSH release is inhibited. Acute treatment with dexamethasone (500 mug) inhibits almost completely the PRL response to both exposure to cold and ether stress, while the plasma TSH response to cold is only delayed and the decrease of plasma TSH observed after ether stress is unchanged. Basal plasma levels of both TSH and PRL are lowered after treatment with the steroid. Thyroxine treatment lowers the plasma TSH concentration to undetectable levels without affecting the plasma PRL response to cold or ether exposure. The present data suggest that the rise of plasma PRL observed after cold exposure is not related to TRH and may suggest that common mechanisms control ACTH and PRL secretion during acute stress exposure.

Adrenocorticotropic Hormone↗
PubMed1975

Changes of pituitary sensitivity to LH-RH during the rat estrous cycle.

The plasma LH (luteinizing hormone) response to 200 ng of LH-RH (LH-releasing hormone) injected subcutaneously at different stages of the estrous cycle in normal rats under Surital anesthisia was maximal during the afternoon of proestrus and lowest on diestrus I. The area under the plasma LH curve measured at 13:00 on proestrus was approximately 7-fold higher than that obtained at 15:30 h on diestrus I. Intermediate responses were found on diestrus II, estrus and morning of proestrus. An approsimately 2.5-fold higher LH response was observed on proestrus than on diestrus I after injection of [D-Ala2, des Gly-NH2-10] LH-RH ethylamide at 15:00 h. That these marked changes of LH response are not secondary to interference by endogenous LH-RH, changes of the metabolism or transport of exogenous LH-RH or modification of plasma LH clearance is ascertanied by the finding of similar changes of pituitary sensitivity to LH-RH under in vitro conditions using pituitaries collected at the same stag-s of the estrous cycle. As measured both in vivo and in vitro, not only the amplitude but also the speed of LH response are maximal during the afternoon of proestrus and minimal on diestrus I.

Animals↗
PubMed1975

Inhibitory activity of four analogs of luteinizing hormone-releasing hormone in vivo.

Four analogs of luteinizing hormone-releasing hormone (LH-RH), [des-His2,D-Ala6]-LH-RH, [des-His2,D-Ala6, des-Gly-NH2(10)1-LH-RH ethylamide, [des-His2,D-Leu6]-LH-RH, and [D-Phe2,D-Leu6]-LH-RH, at 300-fold molar ratios (analog/LH-RH) led to an almost complete inhibition of LH response to LH-RH in anesthetized 4-day cycling rats on the afternoon of proestrus. At a 75-fold molar ratio, [des-His2,D-Ala6]-LH-RH still inhibited the LH-RH-induced LH release by 50%. The ethylamide substitution at the COOH terminus of [des-His2,D-Ala6]-LH-RH did not significantly improve the inhibitory activity of the molecule.

Animals↗
PubMed1975

Effect of exposure to cold on hypothalamic TRH activity and plasma levels of TSH and prolactin in the rat.

No significant change in hypothalamic TRH content was found in rats during acute (5-240 min) exposure to cold (5 degrees C), in spite of rapid and sustained elevations in plasma TSH and thyroxine. Plasma PRL rose markedly in the first 15 min, but returned to normal thereafter. Chronic exposure to cold (32 days) was characterized by elevated plasma and pituitary levels of both TSH and PRL in the presence of an unaltered hypothalamic TRH content. If increased TRH release from the hypothalamus occurs during exposure to cold, as suggested by the pituitary-thyroid stimulation, either it is compensated for by an equal rise in synthesis, or the extra amount released is negligible in comparison with the hypothalamic content of TRH. The acute PRL response to exposure to cold may be related to an acute TRH release but could also result from the accompanying stress response acting by a mechanism independent of TRH.

Animals↗
PubMedDate not supplied

Influence of estrogens on tuberoinfundibular and striatal dopaminergic systems in the rat.

As assessed by changes of prolactin secretion in rat anterior pituitary cells in culture, estrogens can exert a potent antidopaminergic activity at the pituitary level. Androgens and progestins can reverse the effect of estrogens. An interaction of sex steroids at the hypothalamic level on dopamine release and at the pituitary level on dopamine action could also be demonstrated in vivo. Moreover, estrogens exert a similar antidopaminergic activity at the striatal level on dopaminergic agent-induced acetylcholine accumulation. The observation of a modulation by estrogens of the symptoms of Parkinson's disease and tardive dyskinesias suggests the implication of sex steroids in neurology, psychiatry and behavior.

Animals↗
PubMedDate not supplied

Influence of estrogens on tuberoinfundibular and striatal dopaminergic systems in the rat.

As assessed by changes of prolactin secretion in rat anterior pituitary cells in culture, estrogens can exert a potent antidopaminergic activity at the pituitary level. Androgens and progestins can reverse the effect of estrogens. An interaction of sex steroids at the hypothalamic level on dopamine release and at the pituitary level on dopamine action could also be demonstrated in vivo. Moreover, estrogens exert a similar antidopaminergic activity at the striatal level on dopaminergic-agent-induced acetylcholine accumulation. The observation of a modulation by estrogens of the symptoms of Parkinson's disease and tardive dyskinesias suggests the implication of sex steroids in neurology, psychiatry and behavior.

Androgens↗