Biomedical subjects

A Benyassi

Publications and source records attributed to A Benyassi.

8 recordsLinked to original sources

PubMed2001

Glucocorticoid receptors and serotonin N-acetyltransferase activity in the fish pineal organ.

This study aimed to determine whether glucocorticoid receptors are expressed in the photosensitive trout pineal organ, and whether glucocorticoids modulate melatonin secretion. On Western blots from pineal extracts, an antibody directed against trout glucocorticoid receptor labeled a single band at the expected size (approximately 100 kDa). Dexamethasone inhibited pineal arylalkylamine N-acetyltransferase activity (AANAT2; serotonin --> N-acetylserotonin) in a dose-dependent manner after 6 h of culture in the dark (IC50 2.10(-8) M). RU486 (10(-7) M) alone had a partial agonistic activity, whereas it antagonized the effects of 10(-8) M dexamethasone. Hydroxyindole-O-methyltransferase activity (N-acetylserotonin --> melatonin) remained unaffected. This is the first demonstration that glucocorticoid receptors are present in the pineal organ and that glucocorticoids modulate melatonin production.

Acetylserotonin O-Methyltransferase↗

PubMed2000

Melatonin synthesis: arylalkylamine N-acetyltransferases in trout retina and pineal organ are different.

Serotonin N-acetyltransferase (AANAT) is the first enzyme in the conversion of serotonin to melatonin. Changes in AANAT activity determine the daily rhythm in melatonin secretion. Two AANAT genes have been identified in the pike, pAANAT-1 and pAANAT-2, expressed in the retina and in the pineal, respectively. The genes preferentially expressed in these tissues encode proteins with distinctly different kinetic characteristics. Like the pike, trout retina primarily expresses the AANAT-1 gene and trout pineal primarily expresses the AANAT-2 gene. Here we show that the kinetic characteristics of AANAT in these tissues differ as in pike. These differences include optimal temperature for activity (pineal: 12 degrees C; retina: 25 degrees C) and relative affinity for indoleethylamines compared to phenylethylamines. In addition, retinal AANAT exhibited substrate inhibition, which was not seen with pineal AANAT. The kinetic differences between AANAT-1 and AANAT-2 appear to be defining characteristics of these gene subfamilies, and are not species specific.

Acetyl Coenzyme A↗

PubMed1994

Rapid changes in somatostatin and TRH mRNA in whole rat hypothalamus in response to acute cold exposure.

Acute cold stimulus induces activation of the thyreotropic axis characterized by a rapid increase in plasma thyrotropin (TSH). Since pituitary TSH release is mainly regulated by two hypothalamic hormones: thyrotropin-releasing hormone (TRH) and somatostatin, the aim of this study was to analyse whether changes in the steady state mRNA levels and peptide content of these neurohormones occur under acute cold stimulation in rats. Northern blot analysis of hypothalamic somatostatin mRNA levels after 15, 30, 60 or 180 min of cold exposure revealed a 2.0-fold increase after 15 min at 4 degrees C. This augmentation was followed by a return to control values at 30 min. However, the hypothalamic content of somatostatin was not significantly modified at any cold exposure time. TRH mRNA showed a similar pattern to somatostatin, with a 2.5-fold increase after 15 min at 4 degrees C. In contrast, hypothalamic TRH content was significantly decreased after 15 min cold exposure, returning to control values at 30 min. The increase in mRNA levels was specific for the two hypothalamic hormones, since there was no concomitant variation in GAPDH mRNA used as negative control. These results suggest that the organism is quickly aroused by cold stimulus, triggering rapid activation in transcription of the two neurohormones involved in the regulation of the thyreotrope axis. Since the peptide contents did not show the same pattern, a quantitative change in transcription or in mRNA stability does not appear to be a prerequisite for increased peptide expression, suggesting that somatostatin and TRH gene expressions could be regulated at translational or post-translational steps.

Animals↗

PubMed1993

Chronic stress affects in vivo hypothalamic somatostatin release but not in vitro GH responsiveness to somatostatin in rats.

One week after stereotaxical implantation of a push-pull cannula into the median eminence (ME), rats were stressed by immobilization for 2 h daily for 7 days. Thereafter, ME was perfused for 1 h in basal, stress and recovery conditions, respectively, and somatostatin (SRIH) was measured in perfusate fractions. Pituitaries were in vitro perifused to assess GH responsiveness to SRIH. In the stressed group, basal SRIH release was significantly higher than in the control group and stress caused a significant sharp peak in neurohormone release. GH responsiveness to SRIH was not affected in pituitaries obtained from stressed donors. High SRIH levels secreted under chronic stress thus did not impair the GH pituitary response to SRIH.

Animals↗

PubMed1993

Antidepressant/anxiolytic ipsapirone inhibits cold-induced hypothalamic TRH release.

Acute administration of the serotonin (5-HT)1A receptor agonist ipsapirone has been previously shown to elicit a dose-dependent decrease of cold-elicited thyrotropin (TSH) secretion. Therefore, the aim of the present study was to evaluate, by means of a push-pull cannula implanted in the median eminence (ME), whether ipsapirone acts primarily through an inhibition of cold-elicited thyrotropin-releasing hormone (TRH) release. Ipsapirone administration (10 mg kg-1 i.p., 30 min before cold) prevented cold-elicited TRH release, thereby confirming the above hypothesis. In addition, this study further validates push-pull perfusion in the ME as a key tool for measuring TRH secretion in vivo.

Animals↗

PubMed1993

Role of somatostatin in the acute immobilization stress-induced GH decrease in rat.

In the present work we have investigated to what extent somatostatin (SRIF) release from median eminence (ME) is affected by stress immobilization (IMO) in unanesthetized rats stereotaxically implanted with a push-pull cannula (PPC). One week after implantation, the ME was perfused with artificial cerebrospinal fluid for 1 hour in basal, stress and recovery conditions respectively. Samples were collected every 15 min and SRIF was measured by RIA. In another group of animals, a jugular cannula was inserted the day before and plasma samples were taken off simultaneously with the ME perfusate for GH and SRIF analysis respectively. SRIF release from the ME is rapidly (15 min) and significantly increased (58 +/- 11 vs 28 +/- 5 pg/15 min; n = 7; P < 0.01) in rats bearing only PPC. Intriguingly, animals bearing a jugular catheter plus a PPC showed no increase in SRIF release during the first 15 min of IMO in spite of a striking decrease of plasma GH (27.2 +/- 3.8 vs 3.6 +/- 1.3 ng/ml; n = 6; P < 0.001) observed at this time. However, in spite that the animals responded with a significant increase in SRIF, the response was later and more reduced than in animals without jugular cannula. Since our two rat groups--as result of jugular cannula surgery 24 hours before--showed differences such as a food intake, body weight gain, plasma GH levels and basal SRIF release, we think that these differences could explain the modifications in the regulatory mechanisms involved in GH control under acute stress.

Animals↗

PubMed1993

Chronic but not acute exposure to stress is associated with hypothalamic vasoactive intestinal polypeptide (VIP) release into median eminence.

The influence of stress on hypothalamic VIP release into the pituitary portal blood has not been assessed at present despite the fact that this peptide has been implicated in the control of several pituitary hormones and especially in the release of prolactin (PRL) caused by stress. In the present work the effect of stress on the in vivo release of VIP into the pituitary portal blood of male rats was evaluated by means of push-pull perfusion (PPP) of median eminence (EM). VIP content in the PPP liquid was successfully measured and their levels agree well with pituitary portal blood levels measured by other authors. Whereas plasma PRL levels strongly increased during acute immobilization (IMO), no changes in VIP secretion into the ME were observed. VIP release into the ME was also unaffected by exposure to ether. In contrast, in chronically immobilized rats a significant increase in VIP release into the ME was obtained in response to acute IMO. The present data argue against a major role of hypothalamic VIP in PRL release caused by acute stress and show that chronic stress qualitatively alters the signal of hypothalamic VIP to the pituitary.

Animals↗

PubMed1992

Gamma-aminobutyric acid-glutamate interaction in the control of somatostatin release from hypothalamic neurons in primary culture: in vivo corroboration.

Recent studies have provided new data on the neuroendocrine role of glutamate (the major excitatory neurotransmitter) on somatostatin release. The neuroendocrine role of gamma-aminobutyric acid (GABA) (the major inhibitory neurotransmitter) on this same secretion, is also well established. Our objective was thus to investigate whether GABA and glutamate, which have opposite neurotransmission signals, could interact in the control of hypothalamic somatostatin release. Pharmacological manipulations of the two types of receptors were performed in vitro on primary cultures of hypothalamic neurons secreting somatostatin. We found that tonic release of somatostatin was reduced by 76% in the presence of tetrodotoxin (TTX) and was regulated by endogenous secretion of glutamate and GABA. CGS 19755, a highly selective N-methyl-D-aspartate (NMDA) receptor antagonist, significantly reduced tonic somatostatin secretion whereas it was strongly increased by picrotoxin and bicuculline, two GABAA antagonists. When CGS 19755 was applied with picrotoxin, somatostatin release was the same as levels obtained in the control group with TTX. GABA reduced tonic somatostatin release (in the presence or absence of TTX), and glutamate-stimulated secretion in a dose-dependent manner. Picrotoxin stimulation of tonic somatostatin release was additive with that obtained after glutamate stimulation and was also dose-dependent. This interaction was also studied in vivo in unanesthetized rats bearing a push-pull cannula stereotaxically implanted into the median eminence. Ip injected CGS 19755 (an antagonist that can freely permeate the blood-brain barrier) completely blocked the peak secretion of somatostatin observed after ip picrotoxin administration, whereas there was no significant effect when it was injected alone. These findings corroborated our in vitro data and allow us to postulate that GABA and glutamate interact in the control of somatostatin.

Animals↗