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Start Over Author "Desrues L" Journal journal of molecular endocrinology
4 results on '"Desrues L"'

3. Role of calcium in thyrotrophin-releasing hormone-stimulated release of melanocyte-stimulating hormone from frog neurointermediate lobe

Author

Lamacz, M., Tonon, M. C., Louiset, E., Desrues, L., Cazin, L., Guy, J., Pelletier, G., and Vaudry, H.

Abstract

The effect of modifications of extracellular calcium concentrations on α-MSH release has been studied using perifused frog neurointermediate lobes. Increasing concentrations of calcium (from 2 to 10 mmol/l) gave rise to a dose-related stimulation of α-MSH secretion, whereas reduction of Ca2+from 2 to 15 mmol/l partially inhibited α-MSH release. The direct effect of extracellular Ca2+on α-MSH secretion was confirmed by the dose-dependent stimulation of α-MSH release induced by the calcium ionophore A23187. Perifusion with a calcium-free medium or blockade of Ca2+channels by 4 mmol Co2+/l both resulted in an inhibition of spontaneous and TRH-induced α-MSH release. Conversely, administration of verapamil or methoxy-verapamil (10 μmol/l each) did not alter basal secretion and had no effect on the response of the glands to TRH. Nifedipine (10 μmol/l), which was able to block KCl (20 mmol/l)-evoked α-MSH release, induced a slight inhibition of basal α-MSH secretion, indicating that extracellular Ca2+levels may regulate α-MSH release in part by Ca2+influx through voltage-dependent Ca2+channels. In contrast TRH-induced α-MSH release was not affected by nifedipine or dantrolene (10 μmol/l), and BAY-K-8644 (1 μmol/l) did not significantly modify the response of neurointermediate lobes to TRH. Taken together, these results suggest that TRH-induced α-MSH secretion is associated with calcium influx across the plasma membrane and that calcium entry caused by TRH may occur through nifedipine/verapamil-insensitive Ca2+channels.

Published
1988
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4. Mechanism of action of gamma-aminobutyric acid on frog melanotrophs.

Author

Desrues L, Vaudry H, Lamacz M, and Tonon MC

Subjects
Adenylyl Cyclases metabolism, Animals, Baclofen pharmacology, Calcium metabolism, Calcium Channels metabolism, Colforsin pharmacology, Cyclic AMP biosynthesis, GABA-A Receptor Agonists, GABA-B Receptor Agonists, In Vitro Techniques, Inositol Phosphates biosynthesis, Male, Models, Biological, Rana ridibunda, Receptors, GABA-A drug effects, Receptors, GABA-A metabolism, Receptors, GABA-B drug effects, Receptors, GABA-B metabolism, Signal Transduction, Taurine analogs & derivatives, Taurine pharmacology, Melanocyte-Stimulating Hormones metabolism, Pituitary Gland, Posterior drug effects, Pituitary Gland, Posterior physiology, gamma-Aminobutyric Acid pharmacology
Abstract

We have previously demonstrated that gamma-aminobutyric acid (GABA) is a potent regulator of secretory and electrical activity in melanotrophs of the frog pituitary. The aim of the present study was to investigate the intracellular events which mediate the response of melanotrophs to GABA. We first observed that GABA (1-100 microM) inhibited both basal and forskolin-stimulated cyclic AMP (cAMP) formation. The inhibitory effect of GABA on cAMP levels was mimicked by the GABAB receptor agonist baclofen (100 microM) and totally abolished by a 4-h pretreatment with pertussis toxin (0.1 microgram/ml). In contrast, the specific GABAA agonist 3-aminopropane sulphonic acid (3APS) did not affect cAMP production. Both GABA and 3APS (100 microM each) induced a biphasic effect on alpha-MSH release from perifused frog neurointermediate lobes, i.e. a transient stimulation followed by an inhibition of alpha-MSH secretion. Administration of forskolin (10 microM) prolonged the stimulatory phase and attenuated the inhibitory phase evoked by GABA and 3APS, indicating that cAMP modulates the response of melanotrophs to GABAA agonists. Ejection of 3APS (1 microM) in the vicinity of cultured melanotrophs caused a massive increase in intracellular calcium concentration ([Ca2+]i). The stimulatory effect of 3APS on [Ca2+]i was abolished when the cells were incubated in a chloride-free medium. The formation of inositol trisphosphate was not affected by 3APS, suggesting that the increase in [Ca2+]i cannot be ascribed to mobilization of intracellular calcium stores. omega-Conotoxin did not alter the secretory response of frog neurointermediate lobes to 3APS, while nifedipine blocked the stimulation of alpha-MSH secretion induced by 3APS. In conclusion, the present data indicate that, in frog pituitary melanotrophs, (i) the stimulatory phase evoked by GABAA agonists can be accounted for by an influx of calcium through L-type calcium channels, (ii) the inhibitory effect evoked by GABAB agonists can be ascribed to inhibition of adenylate cyclase activity and (iii) cAMP attenuates the inhibitory phase evoked by GABAA agonists. Taken together, these data suggest that activation of GABAB receptors may modulate GABAA receptor function.

Published
1995
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