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Biomedical subjects

R Collu

Publications and source records attributed to R Collu.

At least 19 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

Further studies on the relationship of adrenal and gonadal steroids in pubertal development in female rats.

Surgical adrenalectomy or the administration of aminoglutethimide, corticosterone (B), and androstenedione (delta 4) to the immature female rat had no effect on the timing of vaginal membrane opening. Dehydroepiandrosterone (DHA) and estrone (E1) significantly hastened vaginal patency. Aminoglutethimide increased pituitary LH content while FSH content was decreased. An anti-17 beta-E2 antibody increased pituitary LH content and plasma concentration suggesting enhanced synthesis and release of LH. Pituitary FSH content was unaltered while plasma FSH decreased. Aminoglutethimide increased adrenal and ovarian but not pituitary weight while the antibody had no effect. Since little DHA is present in rat plasma and adrenal and since only estrogens have any effect on the onset of puberty, it is likely that the adrenal is not directly involved in pubertal development in the female rat.

Adrenal Glands↗
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

The effect of TRH on the release of TSH, PRL and GH in man under basal conditions and following methysergide.

Pretreatment with methysergide, a blocker of serotoninergic receptors, significantly reduced the TSH response to TRH in six male volunteers. The TRH-induced PRL release was also slightly decreased, while plasma GH levels were not significantly modified by TRH either during the control period or after methysergide. These results indicate that alterations of central nervous system monoaminergic pathways may modify the hypophysiotropic effects of TRH.

Adult↗
PubMed1978

Effects of clofibrate on plasma tryptophan, growth hormone, and prolactin and on brain tryptophan and serotonin in prepubertal rats.

The effects of clofibrate administration (200 mg/kg, po) on somatic growth, plasma levels of lipids, tryptophan, growth hormone (GH), and prolactin (PRL), as well as on brain concentrations of tryptophan and 5-hydroxytryptamine (5-HT) were studied in prepubertal male rats. The drug did not significantly alter ponderal growth, but an appreciable reduction of tail length was observed in rats treated for 30 days. Triglyceride concentrations in plasma showed a 43% diminution after 30 days of treatment, whereas free fatty acid (FFA) levels were not modified. Clofibrate administration for 7, 15, or 30 days caused a fall in total tryptophan and a significant increase of the free fraction in plasma with no change in brain tryptophan levels. Brain 5-HT was generally unaffected but a marked elevation of this parameter was noted in rats treated for 15 days. Plasma GH and PRL concentrations remained unaltered. It may be concluded from these findings that the slight reduction of somatic growth, the diminution of triglycerides, and the increase of free tryptophan in plasma, induced by chronic clofibrate treatment, are not associated with variations in brain tryptophan and 5-HT levels or with modifications of plasma GH and PRL titers.

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↗
PubMed1978

Reevaluation of levodopa-propranolol as a test of growth hormone reserve in children.

The growth hormone (GH) reserve of 15 short children was evaluated with the levodopa-propranolol test (DPT) and the sequential arginine-insulin test (AIT). Four patients failed to respond to both tests and were classified as hyposomatotropic. In the other 11 children, the mean GH peak response to the DPT was significantly higher than that to the AIT, mainly because five subjects who had a normal response to the DPT failed to respond to the AIT. These children had a generally poor yearly growth increment prior to testing associated in three with an obvious emotional problem, and were found at follow-up to have resumed a normal growth pattern. These data confirm the effectiveness of the DPT as a test of GH reserve. Although hypoglycemia can occur occasionally during test, this procedure is safer and easier to perform than the widely used AIT. Finally, the DPT seems to detect a category of children who have a temporary growth failure and nonresponse to the usual GH tests but who are not hyposomatotropic and consequently do not require human GH.

Adolescent↗
PubMed1978

Antagonism by taurine of morphine induced growth hormone secretion.

The intraperitoneal (IP) or intraventricular (IVT) administration of small amounts of taurine did not modify pentobarbital-induced sleep or pituitary hormone release. However, the drastic increment in plasma GH values induced by morphine administration was completely blocked by the IVT injection of the amino acid. Whether taurine plays a physiological role in the control of GH secretion is highly speculative.

Animals↗
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↗