Neurocentre Magendie

Pascal FOSSAT





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7 publication(s) depuis Juin 2005:


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2014 | J Physiol   IF 4.8
Extracellular signal-regulated kinase phosphorylation in forebrain neurones
contributes to osmoregulatory mechanisms

Dine J, Ducourneau V, Fenelon V, Fossat P, Amadio A, Eder M, Israel JM, Oliet SH, Voisin D

Abstract:





03/2012 | Cereb Cortex   IF 8.3
Glial D-serine gates NMDA receptors at excitatory synapses in prefrontal cortex.
Fossat P, Turpin FR, Sacchi S, Dulong J, Shi T, Rivet JM, Sweedler JV, Pollegioni L, Millan MJ, Oliet SH, Mothet JP

Abstract:
N-methyl-D-aspartate receptors (NMDARs) subserve numerous neurophysiological and neuropathological processes in the cerebral cortex. Their activation requires the binding of glutamate and also of a coagonist. Whereas glycine and D-serine (D-ser) are candidates for such a role at central synapses, the nature of the coagonist in cerebral cortex remains unknown. We first show that the glycine-binding site of NMDARs is not saturated in acute slices preparations of medial prefrontal cortex (mPFC). Using enzymes that selectively degrade either D-ser or glycine, we demonstrate that under the present conditions, D-ser is the principle endogenous coagonist of synaptic NMDARs at mature excitatory synapses in layers V/VI of mPFC where it is essential for long-term potentiation (LTP) induction. Furthermore, blocking the activity of glia with the metabolic inhibitor, fluoroacetate, impairs NMDAR-mediated synaptic transmission and prevents LTP induction by reducing the extracellular levels of D-serine. Such deficits can be restored by exogenous D-ser, indicating that the D-amino acid mainly originates from glia in the mPFC, as further confirmed by double-immunostaining studies for D-ser and anti-glial fibrillary acidic protein. Our findings suggest that D-ser modulates neuronal networks in the cerebral cortex by gating the activity of NMDARs and that altering its levels is relevant to the induction and potentially treatment of psychiatric and neurological disorders.




20/01/2010 | J Neurosci   IF 5.9
Glia-Dependent Switch of Kainate Receptor Presynaptic Action
Bonfardin V, Fossat P, Theodosis D, Oliet S

Abstract:
Presynaptic kainate receptors (KARs) exert a modulatory action on transmitter release. This effect can be switched from facilitation to inhibition by an increased concentration of KAR agonists. We here report that activation of presynaptic GluK1-containing KARs facilitates GABA release on oxytocin and vasopressin neurons in the supraoptic nucleus of the hypothalamus. Increase in ambient levels of glutamate associated with the physiological reduction of astrocytic coverage of oxytocin neurons in lactating rats switches this KAR-mediated facilitation to inhibition of GABAergic transmission. This effect was reproduced in both oxytocin and vasopressin neurons of virgin rats when glutamate transporters were blocked pharmacologically, thereby establishing that enhanced levels of extracellular glutamate induce the switch in KAR-mediated action. The facilitation of GABA release was inhibited with philanthotoxin, a Ca(2+)-permeable KAR antagonist, suggesting that this effect was associated with an ionotropic mode of action. Conversely, KAR-mediated inhibition was compromised in the presence of U73122, a phospholipase C inhibitor, in agreement with the involvement of a metabotropic pathway. We thus reveal that physiological astrocytic plasticity modifies the mode of action of presynaptic KARs, thereby inversing their coupling with GABA release.




20/01/2010 | J Neurosci   IF 5.9
Knockdown of L calcium channel subtypes: differential effects in neuropathic pain.
Fossat P*, Dobremez E*, Bouali-Benazzouz R, Favereaux A, Bertrand SS, Kilk K, Leger C, Cazalets JR, Langel U, Landry M, Nagy F

Abstract:





01/2007 | Eur J Neurosci   IF 3
L-type calcium channels and NMDA receptors: a determinant duo for short-term nociceptive plasticity.
Fossat P, Sibon I, Le Masson G, Landry M, Nagy F

Abstract:
In the dorsal horn of the spinal cord, pain-transmitting neurons exhibit action potential windup, a form of short-term plasticity, which consists of a progressive increase in neuronal response during repetitive stimulation of nociceptive input fibers. Windup depends on N-methyl-D-aspartate (NMDA) receptor activation, but previous in vitro studies indicated that windup also relies on intrinsic plateau properties of spinal neurons. In the present study, we considered the possible involvement of these properties in windup in vivo. For this purpose, we first studied a nociceptive flexion reflex in the rat. We showed that windup of the reflex is actually suppressed by blockers of L-type calcium current and Ca(2+)-activated non-specific cationic current (Ican), the two main depolarizing conductances of plateau potentials. We further showed that, during windup, NMDA receptors provide a critical excitatory component in a dynamic balance of excitatory and inhibitory inputs which ultimately activates L-type calcium channels. The nociceptive reflex involves at least two neuronal groups, which may express intrinsic amplification properties, motor neurons and dorsal horn neurons. By means of extracellular recordings in the dorsal horn, we showed that windup of dorsal horn neuron discharge was sensitive to the modulators of L-type calcium current. Altogether, our results suggest that, in vivo, windup also depends on the amplification properties of spinal neurons, the triggering of which requires previous activation of NMDA receptors.




06/2005 | Eur J Neurosci   IF 3
Distribution and regulation of L-type calcium channels in deep dorsal horn neurons after sciatic nerve injury in rats
Dobremez E, Bouali-Benazzouz R, Fossat P, Monteils L, Dulluc J, Nagy F, Landry M

Abstract:





06/2005 | Eur J Neurosci   IF 3
Distribution and regulation of L-type calcium channels in deep dorsal horn neurons after sciatic nerve injury in rats.
Dobremez E, Bouali-Benazzouz R, Fossat P, Monteils L, Dulluc J, Nagy F, Landry M

Abstract: