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Depolarizing GABA/glycine synaptic events switch from excitation to inhibition during frequency increases.Multi-stability and pattern-selection in oscillatory networks with fast inhibition and electrical synapsesExtracellular neural microstimulation may activate much larger regions than expected by simulations: a combined experimental and modeling study.GABA(A) receptor and glycine receptor activation by paracrine/autocrine release of endogenous agonists: more than a simple communication pathway.Morphologically heterogeneous met-enkephalin terminals form synapses with tyrosine hydroxylase-containing dendrites in the rat nucleus locus coeruleus.Ontogenic changes of the GABAergic system in the embryonic mouse spinal cord.Glycine release from radial cells modulates the spontaneous activity and its propagation during early spinal cord development.Serotonin controls the maturation of the GABA phenotype in the ventral spinal cord via 5-HT1b receptors.Ontogenic changes of the spinal GABAergic cell population are controlled by the serotonin (5-HT) system: implication of 5-HT1 receptor family.NKCC1 cotransporter inactivation underlies embryonic development of chloride-mediated inhibition in mouse spinal motoneuron.Acetylcholine controls GABA-, glutamate-, and glycine-dependent giant depolarizing potentials that govern spontaneous motoneuron activity at the onset of synaptogenesis in the mouse embryonic spinal cord.Analysis of synaptic inputs and targets of physiologically characterized neurons in rat frontal cortex: combined in vivo intracellular recording and immunolabeling.VEGF modulates synaptic activity in the developing spinal cord.Nonsynaptic glycine release is involved in the early KCC2 expression.Expression of the glycinergic system during the course of embryonic development in the mouse spinal cord and its co-localization with GABA immunoreactivity.Embryonic alteration of motoneuronal morphology induces hyperexcitability in the mouse model of amyotrophic lateral sclerosisImplication of 5-HT in the Dysregulation of Chloride Homeostasis in Prenatal Spinal Motoneurons from the G93A Mouse Model of Amyotrophic Lateral SclerosisPersistent Sodium Current Drives Excitability of Immature Renshaw Cells in Early Embryonic Spinal NetworksRelaxation of synaptic inhibitory events as a compensatory mechanism in fetal SOD spinal motor networks
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P50
description
researcher ORCID ID = 0000-0003-3972-8229
@en
name
Pascal Branchereau
@ast
Pascal Branchereau
@en
Pascal Branchereau
@es
Pascal Branchereau
@nl
type
label
Pascal Branchereau
@ast
Pascal Branchereau
@en
Pascal Branchereau
@es
Pascal Branchereau
@nl
prefLabel
Pascal Branchereau
@ast
Pascal Branchereau
@en
Pascal Branchereau
@es
Pascal Branchereau
@nl
P31
P496
0000-0003-3972-8229