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

99 publication(s) depuis Juillet 1991:

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1996 | J Physiol Paris
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
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
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.

Whole cell patch-clamp recordings were obtained from isolated rat supraoptic nucleus magnocellular neurosecretory cells (MNCs). Under current clamping, hyperosmolality produced by the addition of 10-30 mM mannitol depolarized each of 25 cells tested. In contrast, reducing fluid osmolality from 295 to 265 mosmol/kgH2O had the reverse effect, hyperpolarizing 18 of 21 MNCs. Voltage-clamp recordings in 43 cells revealed that the effects of hypo- and hyperosmolality, respectively, were caused by decreases and increases in a nonselective cation conductance reversing near -41 mV. Current-voltage analysis in Na(+)-free solution revealed that the reversal potentials of currents elicited by increases and decreases in osmolality both shifted to a value near -90 mV, suggesting that a single ionic conductance is modulated by these stimuli. The relation between cationic conductance and osmolality was specific, sensitive (+2.14%.mosmol-1.kgH2O-1), and well-fit by linear regression (r = 0.96; n = 22 cells) between 275 and 325 mosmol/kgH2O. These results indicate that MNCs express a depolarizing current that is active under steady-state conditions and that the up- or downregulation of this current contributes to the excitation or inhibition of these cells upon acute exposure to hypo- or hyperosmolar conditions.

22/07/1993 | Ann N Y Acad Sci
Extrinsic and intrinsic modulatory mechanisms involved in regulating the electrical activity of supraoptic neurons.
Bourque CW, Oliet SH, Kirkpatrick K, Richard D, Fisher TE


Vasopressin is a peptide hormone synthesized by neurons of the supraoptic and paraventricular nuclei, which project axon terminals to the neurohypophysis. Consistent with its antidiuretic properties, vasopressin release rises as a function of plasma osmolality, a response that results from accelerated action potential discharge. Previous studies have shown that increases in fluid osmolality depolarize supraoptic neurons in the absence of synaptic transmission, suggesting that these cells behave as intrinsic osmoreceptors. The mechanism by which changes in osmolality are transduced into an electrical signal is unknown, however. Here we report that changes in cell volume accompany physiological variations in fluid osmolality and that these modulate the activity of mechanosensitive cation channels in a way that is consistent with the macroscopic regulation of membrane voltage and action potential discharge. These findings define a function for stretch-inactivated channels in mammalian central neurons.

1. Magnocellular neurosecretory cells (MNCs) were isolated from the supraoptic nucleus of adult Long-Evans rats using an enzymatic procedure. Immunocytochemical staining with antibodies against vasopressin and oxytocin revealed that MNCs can be identified by size. The membrane properties of these cells were examined at 32-34 degrees C using intracellular recording methods. 2. Isolated MNCs displayed a mean (+/- S.E.M.; n = 109) resting membrane potential of -64.1 +/- 1.0 mV, an input resistance of 571 +/- 34 M omega, and a time constant of 8.7 +/- 0.4 ms. Measurements of specific resistivity and input capacitance revealed that the soma of these cells accounts for a mere 20% of their total somato-dendritic membrane in situ. 3. Voltage-current relations measured near -60 mV were linear negative to spike threshold. From more hyperpolarized membrane potentials, voltage responses to depolarizing current steps displayed transient outward rectification and delayed impulse discharge. 4. Action potentials (76.6 +/- 0.9 mV) triggered from an apparent threshold of -59.3 +/- 0.1 mV broadened progressively at the onset of spontaneous or current-evoked spike trains. Steady-state spike duration increased as a logarithmic function of firing frequency with a maximum near 25 Hz. These effects were abolished in Ca(2+)-free solutions. 5. In all cells, evoked spike trains were followed by a prolonged Ca(2+)-sensitive after-hyperpolarization. In contrast, only a small proportion (16%) of MNCs displayed spontaneous bursting activity or depolarizing after-potentials following brief current-evoked bursts. 6. Isolated MNCs responded to amino acids (glutamate and GABA) and to the neuropeptide cholecystokinin, indicating that receptors for these neurotransmitters are expressed postsynaptically by MNCs and are retained following dissociation. 7. Increasing the osmolality of the superfusing solution by 5-30 mosmol kg-1 caused a membrane depolarization associated with a decrease of input resistance and accelerated spontaneous spike discharge in each of thirty-six MNCs tested. Current-clamp analysis suggested that these responses resulted from the activation of a cationic conductance. Excitatory effects of hyperosmolality were not observed in non-magnocellular neurones (n = 6).

1. The sensitivity of cromakalim-activated current (Icrom) to manipulations of extracellular cationic composition was examined in whole-cell voltage clamp recordings from freshly-dispersed, adult guinea-pig ventricular myocytes. In bathing media with different concentrations of K+ (1, 2.5, 5.4 and 12 mM) the Icrom reversal potential (Erev) varied in strict correspondance with the K+ equilibrium potential and inward Icrom amplitude was proportional to the external K+ concentration. 2. Replacement of 12mM K+ with 12mM Rb+ induced a slight positive shift of Erev indicating that PRb+/PK+ = 1.06. K+ replacement with 12mM Cs+ reduced or abolished inward Icrom and produced a negative shift of Erev by at least 50 mV; an upper limit of PCs+/PK+ was fixed at 0.18. 3. Addition of Rb+ (1-30 mM) to 2.5 mM K(+)-containing medium produced a concentration-dependent increase in inward Icrom and positive shift of Erev suggesting that K+ and Rb+ have similar permeabilities and conductivities and do not interfere with each other in the channel. 4. CS+ (0.01-30 mM), added to medium containing 12 mM Rb+, induced a potent, voltage-dependent inhibition of inwardly rectifying current (IK1; IC50 = 0.2-3 mM). Voltage-dependent inhibition of inward Icrom was observed only at considerably higher CS+ concentrations (IC50 = 4-30 mM). Extracellular Rb+ and CS+ did not substantially alter the amplitude of outward Icrom. 5. The results support the contention that the ATP-sensitive K+ channel is the primary target of cromakalim action in ventricular myocytes.