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Stéphane OLIET

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PhD, McGill University (1994)
Posdoc, UCSF (1994-1997) HFSP fellow
CR1 CNRS, Inserm U378(2001)
HDR, Université Bordeaux 2 (2003)
DR1 CNRS, Neurocentre Magendie Inserm (2009)

Expertise: Astrocyte, gliotransmitters, plasticity, synapse, NMDA receptors

95 publication(s) since Juillet 1991:

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The indicated IF have been collected by the Web of Sciences in

01/09/1998 | J Neurosci   IF 6.1
Evidence for a hypothalamic oxytocin-sensitive pattern-generating network governing oxytocin neurons in vitro.
Jourdain P, Israel JM, Dupouy B, Oliet SH, Allard M, Vitiello S, Theodosis DT, Poulain DA

During lactation and parturition, magnocellular oxytocin (OT) neurons display a characteristic bursting electrical activity responsible for pulsatile OT release. We investigated this activity using hypothalamic organotypic slice cultures enriched in magnocellular OT neurons. As shown here, the neurons are functional and actively secrete amidated OT into the cultures. Intracellular recordings were made from 23 spontaneously bursting and 28 slow irregular neurons, all identified as oxytocinergic with biocytin and immunocytochemistry. The bursting electrical activity was similar to that described in vivo and was characterized by bursts of action potentials (20.1 +/- 4.3 Hz) lasting approximately 6 sec, over an irregular background activity. OT (0.1-1 microM), added to the medium, increased burst frequency, reducing interburst intervals by 70%. The peptide also triggered bursting in 27% of nonbursting neurons. These effects were mimicked by the oxytocin receptor (OTR) agonist [Thr4, Gly7]-OT and inhibited by the OTR antagonist desGly-NH2d(CH2)5[D-Tyr2,Thr4]OVT. Burst rhythmicity was independent of membrane potential. Hyperpolarization of the cells unmasked volleys of afferent EPSPs underlying the bursts, which were blocked by CNQX, an AMPA/kainate receptor antagonist. Our results reveal that OT neurons are part of a hypothalamic rhythmic network in which a glutamatergic input governs burst generation. OT neurons, in turn, exert a positive feedback on their afferent drive through the release of OT.

We have found that two distinct forms of long-term depression (LTD), one dependent on the activation of NMDA receptors (NMDARs) and the other dependent on the activation of metabotropic glutamate receptors (mGluRs), coexist in pyramidal cells of the CA1 region of the hippocampus of juvenile rats (11-35 days). Both forms were pathway specific, required membrane depolarization, and were blocked by chelating postsynaptic Ca2+ with BAPTA. The mGluR-LTD, but not the NMDAR-LTD, was blocked by the T-type Ca2+ channel blocker Ni2+ and intracellular administration of a protein kinase C inhibitory peptide. In contrast, the protein phosphatase inhibitor Microcystin LR blocked NMDAR-LTD, but not mGluR-LTD. NMDAR-LTD is associated with a decrease in the size of quantal excitatory postsynaptic currents, whereas for mGluR-LTD there was no change in quantal size, but a large decrease in the frequency of events. While mGluR-LTD did not interact with NMDAR-dependent long term potentiation (LTP), NMDAR-LTD was capable of reversing LTP. Prior saturation of mGluR-LTD had no effect on NMDAR-LTD. NMDAR-LTD and mGluR-LTD thus appear to be mechanistically distinct forms of synaptic plasticity in that they share neither induction nor expression mechanisms.

06/1997 | Neuron   IF 14.4
Two distinct forms of long-term depression coexist in CA1 hippocampal pyramidal cells.
Oliet SH, Malenka RC, Nicoll RA

Two distinct forms of long-term depression (LTD), one dependent on the activation of NMDA receptors (NMDARs) and the other dependent on the activation of metabotropic glutamate receptors (mGluRs), are shown to coexist in CA1 hippocampal pyramidal cells of juvenile (11-35 day-old) rats. Both forms were pathway specific and required membrane depolarization and a rise in postsynaptic Ca2+. mGluR-LTD, but not NMDAR-LTD, required the activation of T-type Ca2+ channels, group 1 mGluRs, and protein kinase C, while NMDAR-LTD, but not mGluR-LTD, required protein phosphatase activity. NMDAR-LTD was associated with a decrease in the size of quantal excitatory postsynaptic currents, whereas for mGluR-LTD there was no change in quantal size, but a large decrease in the frequency of events. NMDAR-LTD, but not mGluR-LTD, reversed NMDAR-dependent long-term potentiation, and NMDAR-LTD was unaffected by prior saturation of mGluR-LTD. These findings indicate that NMDAR-LTD and mGluR-LTD are mechanistically distinct forms of synaptic plasticity.

1997 | Annu Rev Physiol   IF 17.9
Osmoreceptors in the central nervous system.
Bourque CW, Oliet SH

Osmoreceptors regulate sodium and water balance in a manner that maintains the osmotic pressure of the extracellular fluid (ECF) near an ideal set point. In rats, the concerted release of oxytocin and vasopressin, which is determined by the firing rate of magnocellular neurosecretory cells (MNCs), plays a key role in osmoregulation through the effects of natriuresis and diuresis. Changes in excitatory synaptic drive, derived from osmosensitive neurons in the organum vasculosum lamina terminalis (OVLT), combine with endogenously generated osmoreceptor potentials to modulate the firing rate of MNCs. The cellular basis for osmoreceptor potentials has been characterized using patch-clamp recordings and morphometric analysis in MNCs isolated from the supraoptic nucleus of the adult rat. In these cells, stretch-inactivated cationic channels transduce osmotically evoked changes in cell volume into functionally relevant changes in membrane potential. The experimental details of these mechanisms are reviewed in their physiological context.

01/03/1996 | Science   IF 41
Bidirectional control of quantal size by synaptic activity in the hippocampus.
Oliet SH, Malenka RC, Nicoll RA

Analysis of strontium-induced asynchronous release of quanta from stimulated synapses revealed that long-term potentiation and long-term depression in the CA1 region of the mammalian hippocampus are associated with an increase and a decrease, respectively, in quantal size. At a single set of synapses, the increase in quantal size seen with long-term potentiation was completely reversed by depotentiating stimuli. Long-term potentiation and depression are also associated with an increase and decrease, respectively, in the frequency of quantal events, consistent with an all-or-none regulation (up or down) of clusters of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, a change in the release of transmitter, or both.

Stretch-sensitive ion channels are ubiquitous, yet evidence of their role in mechanotransduction remains scarce. The presence of stretch-inactivated cation channels in supraoptic neurons is consistent with the osmoreceptor potentials regulating vasopressin release. However, whether osmosensitivity depends on mechanical gating and ion flux through stretch-inactivated channels is unknown. Here we report that changes in channel open probability associated either with modification of pipette pressure or with external osmolality selectivity result from variations in closed time. While channel mechanosensitivity and osmotically evoked changes in cell volume are not affected by gadolinium, similar concentrations of the lanthanide inhibit cation permeation through the single channels and macroscopic osmoreceptor potentials. Mechanotransduction through stretch-inactivated channels is therefore necessary for osmoreception in supraoptic neurons.

1996 | J Physiol Paris   IF 2.7
Expression mechanisms of long-term potentiation in the hippocampus.
Isaac JT, Oliet SH, Hjelmstad GO, Nicoll RA, Malenka RC

We have taken a number of different experimental approaches to address whether long-term potentiation (LTP) in hippocampal CA1 pyramidal cells is due primarily to presynaptic or postsynaptic modifications. Examination of miniature EPSCs or EPSCs evoked using minimal stimulation indicate that quantal size increasing during LTP. The conversion of silent to functional synapses may contribute to the LTP-induced changes in mEPSC frequency and failure rate that previously have been attributed to an increase in the probability if transmitter release.

09/1995 | J Neuroendocrinol   IF 3
Effects of activin-A on neurons acutely isolated from the rat supraoptic nucleus.
Oliet SH, Plotsky PM, Bourque CW

Nerve fibers containing activin-like immunoreactivity have been shown to be present within the area of the supraoptic nucleus. In this study, whole-cell patch-clamp recordings from supraoptic magnocellular neurosecretory cells were used to characterize the electrophysiological effects of this peptide. Nanomolar concentrations of recombinant activin-A caused the appearance of a voltage-independent current reversing near -40 mV. At resting potential, membrane depolarization caused by this current was sufficient to accelerate action potential discharge, suggesting that activin receptors expressed on magnocellular neurosecretory cells may play a role in the control of neurohypophysial hormone release.

09/1994 | Front Neuroendocrin   IF 7.9
Osmoreceptors, osmoreception, and osmoregulation.
Bourque CW, Oliet SH, Richard D

Mammals have evolved sophisticated behavioral and physiological responses to oppose changes in the osmolality of their extracellular fluid. The behavioral approach consists of regulating the intake of salt and water through changes in sodium appetite and thirst. The physiological approach comprises adjustments of renal excretion of water and sodium which are achieved through changes in the release of antidiuretic and natriuretic hormones. Individually, these osmoregulatory responses are controlled by 'osmoreceptors': groups of specialized nerve cells capable of transducing changes in external osmotic pressure into meaningful electrical signals. Some of these sensors are located in the region of the hepatic portal vein, a strategic site allowing early detection of the osmotic impact of ingested foods and fluids. Changes in systemic osmolality, however, are detected centrally, within regions that include the medial preoptic area, the median preoptic nucleus, the organum vasculosum lamina terminalis (OVLT), the subfornical organ, and the supraoptic nucleus (SON). While studies have indicated that these central and peripheral osmoreceptors participate in the control of osmoregulatory responses, little is known of the mechanisms by which this is achieved. One notable exception, however, consists of the osmotic control of electrical activity in SON neurons which, in the rat, contributes to the regulation of natriuresis and diuresis through effects on the secretion of oxytocin and vasopressin. Previous studies have shown that these cells are respectively excited and inhibited by hypertonic and hypotonic conditions. Experiments in vitro indicate that these responses result from both the endogenous osmosensitivity of these cells and changes in synaptic drive. Patch-clamp analysis has revealed that SON neurons are respectively depolarized and hyperpolarized by increases and decreases in external osmolality and that these intrinsic responses result from changes in the activity of mechanosensitive cationic channels. Moreover, intracellular recordings in hypothalamic explants have shown that changes in electrical activity are associated with proportional changes in the frequency of glutamatergic excitatory postsynaptic potentials derived from osmosensitive OVLT neurons. Both of these mechanisms, therefore, may participate in the osmotic regulation of neurohypophysial hormone release in situ.

Recognizing that osmotic pressure is a principal factor controlling antidiuresis, Verney introduced the term 'osmoreceptor' to designate the mysterious cerebral structures that regulate vasopressin release from the posterior pituitary. While hormone secretion from the neurohypophysis is influenced by synaptic inputs from other osmoresponsive neurons, magnocellular neurosecretory cells currently provide our most comprehensive model of signal detection in an osmoreceptor.