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Biomedical subjects

Y Taché

Publications and source records attributed to Y Taché.

18 recordsLinked to original sources
PubMed1979

Role of putative neurotransmitters in prolactin, GH and LH response to acute immobilization stress in male rats.

Immobilization for 30 min induced a significant rise of prolactin (Prl), a significant reduction of growth hormone (GH), and no modification of plasma luteinizing hormone (LH) values in male rats. Depletion of brain catecholamine stores increased Prl and decreased LH levels while GH secretion was not affected. Blockade of beta-adrenergic receptors reduced GH and increased LH values. Plasma GH levels were also drastically reduced by depletion of brain serotonin (SER) levels and by atropine, and were increased by blockade of the H1 histamine (HIS) receptor. The anti-gamma-aminobutyric acid (GABA) agent picrotoxin significantly reduced Prl and GH plasma levels. Depletion of brain catecholamine stores or blockade of beta-adrenergic receptors antagonized the restraint-induced rise of plasma Prl values, while the decrease of GH elicited by stress was not modified by any pharmacological manipulation. These results indicate that although several putative neurotransmitters (PN) of the central nervous system (CNS) are implicated in the modulation of baseline levels of Prl, GH and LH, only the stress-induced activation of Prl secretion appears to be mediated by a PN, namely through a noradrenergic, beta-adrenergic route.

5,6-Dihydroxytryptamine↗
PubMed1979

Adenohypophyseal hormone response to chronic stress in dexamethasone-treated rats.

The influence of dexamethasone treatment on the basal values of corticosterone, GH, prolactin (PRL), LH and FSH, as well as on the adenohypophyseal hormone response to chronic stress was studied in female rats. Dexamethasone acetate (25 micrograms/100 b.w.), given by gavage twice daily for 10 days, decreased the resting plasma levels of corticosterone, GH, LH and PRL, whereas the FSH titers remained normal. The secretion of ACTH (evaluated indirectly through corticosterone concentrations) and of GH appeared to be most sensitive to the suppressive effect of dexamethasone. The same hormonal response pattern was induced by 8 h of daily immobilization for 10 days, except that ACTH release was enhanced and the plasma LH titers dropped more drastically. Dexamethasone administration in combination with restraint did not alter the characteristic hormonal profile of chronic stress, despite the fact that ACTH secretion was completely blocked. These data suggest that the inhibition of PRL, LH and GH secretion following severe, chronic stress is not causally related to the sustained elevation of plasma ACTH.

Animals↗
PubMed1979

Effects of neuropeptides on adenohypophyseal hormone response to acute stress in male rats.

The effects of bombesin and other unrelated oligopeptides on hormonal changes induced by stress were studied in conscious adult male rats. Restraint in the cold for 1 h increased plasma corticosterone and PRL levels and decreased GH values but had no effect on LH levels. Bombesin (5 microgram), given intracerebroventricularly (ivt) before stress, inhibited the PRL rise without affecting corticosterone, GH, or LH response. A complete blockade of PRL rise was observed with doses of bombesin ranging from 5 microgram to 100 ng ivt, regardless of the duration (15, 30, 45, or 60 min) or the nature (cold exposure or restraint at room temperature) of the stressor agents. Bombesin was 10(3) more potent as a PRL inhibitor when given ivt than when given iv, and its ivt effect was not reversed by naloxone (1 or 10 mg/kg). Among other unrelated peptides tested (beta-endorphin, neurotensin, substance P, and TRH; 5 microgram ivt), only neurotensin decreased plasma PRL levels in rats subjected to restraint in the cold for 1 h. These results show that in conscious male rats, centrally administered bombesin has a very potent and long acting inhibitory effect on PRL release induced by acute stress. Since a bombesin-like peptide has been found in rat brain, its physiological role in PRL regulation remains to be elucidated.

Animals↗
PubMed1978

Pattern of adenohypophyseal hormone changes induced by various stressors in female and male rats.

Plasma modifications of adenohypophyseal hormones were investigated in groups of female and male rats stressed for 15, 30 min, 1, 2, 4 or 6 h, either by cold (4 degrees C), forced muscular exercise (FME), or immobilization. GH levels in both female and male rats were consistently decreased by the 3 stressing agents. Immobilization in the female and the 3 stressors in the male elicited an early secretory response of prolactin (Prl), while only in immobilized female rats plasma LH levels showed an early, short-lived increment. A more prolonged exposure to stress had an inhibitory influence on plasma Prl and LH levels in both sexes. FSH concentrations were not modified in females, but were decreased in male rats submitted to either one of the 3 stressors. In both male and female rats plasma TSH levels rose during cold exposure, while they were decreased by FME and by immobilization. Our data indicate that the character of the hormonal secretory response during stress is nonspecific. Indeed, to the exception of the specific stimulation of TSH release by cold, stress-induced hormonal changes are not related to the nature but rather to the intensity and duration of the stressing agent.

Animals↗
PubMed1978

Pattern of adenohypophyseal hormone changes in male rats following chronic stress.

To delineate the pattern of adenohypophyseal hormone secretion following chronic stress, adult male rats were exposed daily to 6 h of cold, forced exercise or immobilization for 3, 6, 10, 15, 28 or 42 consecutive days. Groups of these animals were sacrificed at the end of the last stress sessions, and plasma growth hormone (GH), luteinizing hormone (LH), prolactin (Prl) and follicle-stimulating hormone (FSH) levels were measured by radioimmunoassay (RIA). Irresspective of the different stimuli used, long-term stress induced a morphologic and hormonal response characterized by decreased ponderal growth, adrenal enlargement, thymus involution and significant diminutions in GH, Prl and LH levels with no modifications in FSH titers. The magnitude and duration of these changes varied with the severity of the stressors.

Adrenal Glands↗
PubMed1977

Antagonism of pentobarbital-induced hormonal changes by TRH in rats.

In adult male rats, injection of TRH into a lateral ventricle of the brain 5 min prior to pentobarbital (PB) administration caused a significant dose-related inhibition of prolactin (PRL) release, in doses ranging from 500 to 5 ng. Among 8 TRH analogues devoid of thyrotropin-releasing activity, 6 were found to significantly suppress PB-induced PRL secretion at an intraventricular dose level of 10 microgram, and the 3 most effective in this respect were also able to counteract growth hormone (GH) release elicited by PB. The derivative [1,3'-DCM2]TRH was still potent enough to block PB-induced PRL secretion at an intraventricular dosage of 50 ng. The peptide ACTH 4--10 was ineffective, whereas another ACTH derivative H-Met(O2)-Glu-His-Phe-D-Lys-Phe-OH (Org 2766) reduced PRL release. TRH did not affect the increase of plasma PRL induced by acute stress. alpha-Methyl-p-tyrosine (alpha-MT) failed to influence the inhibiting effect of TRH on GH secretion but significantly reduced that on PRL release. p-Chlorophenylalanine (PCPA) completely blocked the antagonistic effect of TRH on all PB-induced hormonal changes, suggesting that serotoninergic mechanisms may be involved in the extra-pituitary effect of TRH.

Adrenocorticotropic Hormone↗
PubMed1977

Effects of chronic stress on pituitary hormone release induced by combined hemi-extirpation of the thyroid, adrenal and ovary in rats.

Morphologic and hormonal changes, induced by combined ablation of a thyroid lobe, one adrenal and one ovary, were studied over a 15-day period in rats, some of whom were subjected to 8 h of daily immobilization. The compensatory hypertrophy (CH) of the contralateral glands in non-stressed animals was associated with a significant increase in the plasma levels of LH (from the 1st to the 10th day), prolactin (PRL, from the 3rd to the 6th day), FSH (on the 3rd day) and corticosterone (from the 6th to the 15th day), whereas GH titers were not altered. Immobilization for 1, 3, 6, 10 or 15 days inhibited the b.w. gain, induced involution of the thymus, enhanced compensatory enlargement of the adrenal, and blocked the CH of the ovary and, to a lesser degree, of the thyroid. This chronic stressor produced a marked rise in plasma corticosterone, antagonized the surge of PRL, FSH and LH, and decreased the plasma levels of GH. On the basis of these morphological and hormonal variations, it appears that severe chronic stress in hemi-thyroidectomized-adrenalectomized-ovariectomized animals further increases the ACTH response but antagonizes the increased secretion of the other pituitary hormones.

Adrenal Glands↗
PubMed1977

Thyrotropin-releasing hormone in rat brain: nyctohemeral variations.

The concentration of thyrotropin-releasing hormone (TRH) was measured by specific radioimmunoassay in three different brain regions of rats sacrificed every 4 h over a 24 h period. TRH concentration reached a zenith at 1200 h both in the hypothalamus and the amygdala but did not vary in the forebrain. These results indicate that a nyctohemaral variation of TRH levels exists in hypothalamic and extrahypothalamic brain areas.

Amygdala↗
PubMed1977

Influence of Steroidal enzyme inducers on the toxicity of pyrogallol, pargyline and nialamide.

In rats, the toxic manifestations of overdosage with with parcyline (a monoamine oxidase inhibitor) or pyrogallol (a catechol-o-methyltransferase inhibitor) were diminished by treatment with the more potent steroidal (pregnenolone-16alpha-carbonitrile, spironolactone, etc.) or nonsteroidal (phenobarbital) catatoxic substances. Except for significant protection offered by glucocorticoids (triamcinolene, prednisolone acetate) against pargyline, all other pretreatments (progesterone, estradiol, desoxycorticosterone acetate, etc.) either had no influence on or increase the deleterious effects of the two amine inhibitors. Nialamide intoxication was exacerbated by most of these conditioners.

Animals↗
PubMed1976

Effect of rat stalk median eminence extracts on rat GH secretion in vivo.

Estradiol (0.2 mug), injected subcutaneously for 10 days to adult male rats, increased plasma growth hormone (GH) levels as compared with oil-treated controls. In estradiol-pretreated (10 days), urethane-anesthetized rats, the first as well as the second of two successive intracarotid injections, at 1-hour intervals, of one rat stalk median eminence equivalent evoked a significant rise in plasma radioimmunoassayable GH. Under the same conditions, cerebral cortex extracts (1 equivalent) induced a slight elevation whereas vasopressin (30 mU) or serotonin (200 ng) were ineffective. These results indicate that estrogen-primed, urethane-anesthetized rats can be used to demonstrate GH-releasing activity in rat SME extracts.

Animals↗
PubMed1975

Inhibition of the effects of alfathesin and other steroid anesthetics by catatoxic steroids in rats.

In rats, the sleeping time induced by overdosage with eight steroid anesthetics--alfathesin, 3-(3-oxo-17beta-hydroxy-19-nor-4-androsten-17alpha-yl)-propionic acid-lactone (SC-8109), 21-hydroxy=5alpha-pregnane-3,20-dione (P-234), 4-pregnene-3,11,20-trione (Bio.66), 17-hydroxy-3-oxo-4-androstene-17alpha-propionic acid-gamma-lactone(SC-5233),3alpha-hydroxy-5beta-pregnane-11,20-dione, 5beta-pregnane-3,11,20-trione (U-1373), and hydroxydione--was abolished or considerably reduced by a variety of catatoxic compounds, particularly 3beta-hydroxy-20-oxo-5-pregnene-16alpha-carbonitrile (PCN), 9alpha-fluoro-11beta,17-dihydroxy-3-oxo-4-androstene-17alpha-propionic acid potassium salt (CS-1), prednisolone, ethylestrenol and spironolactone. Phenobarbital and diphenylhydantoin, two non-steroidal stimulators of hepatic microsomal drug metabolism, were also highly effective. In contrast, triamcinolone, estradiol,progesterone, desoxycorticosterone and hydroxydione, which exert little or no catatoxic activity, failed to significantly diminish anesthesia or sedation.

Alfaxalone Alfadolone Mixture↗