References of "Rigo, Jean-Michel"
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See detailCultured Oligodendrocyte Progenitors Derived from Cerebral Cortex Express a Glycine Receptor Which Is Pharmacologically Distinct from the Neuronal Isoform
Belachew, Shibeshih ULg; Rogister, Bernard ULg; Rigo, Jean-Michel et al

in European Journal of Neuroscience (1998), 10(11), 3556-64

Using the whole-cell patch-clamp technique, we demonstrate glycine-induced currents in oligosphere-derived oligodendrocyte progenitors cultured from newborn rats. Similar inward currents are also ... [more ▼]

Using the whole-cell patch-clamp technique, we demonstrate glycine-induced currents in oligosphere-derived oligodendrocyte progenitors cultured from newborn rats. Similar inward currents are also triggered by beta-alanine and taurine, two established glycine receptor agonists. In our recording conditions, glycine-gated currents in oligodendrocyte progenitors reverse about 0 mV and are reversibly inhibited by the glycine competitive antagonist strychnine, the Cl- channel blocker picrotoxinin and the non-competitive antagonist cyanotriphenylborate. The oligodendrocyte progenitors glycine receptor (GlyR) differs from the corresponding neuronal receptor: [3H]strychnine binding data and the strychnine inhibition curve of glycine-induced currents in oligodendrocyte progenitor cultures suggest the existence of two strychnine binding sites on the oligodendroglial GlyR. Using total RNA isolated from oligodendrocyte progenitors cultures, reverse transcription-polymerase chain reaction analysis of glycine receptor subunit expression shows the presence of alpha2 and beta subunits and immunocytochemical stainings confirm that this GlyR contains an alpha subunit which is not alpha1. The molecular structure of the oligodendroglial GlyR could be either homopentameric alpha2 or heteromeric alpha2beta but in both cases, the sequence of the alpha2 or beta subunits have to be different from the known neuronal sequences in order to explain, respectively, the cyanotriphenylborate (alpha2) and picrotoxinin (beta) sensitivities. This work thus demonstrates that GlyR are expressed by oligodendrocytes obtained not only from spinal cord but also from supraspinal structures. The pharmacological properties and presumably the molecular structure of oligodendroglial GlyR are original. The physiological meaning of the presence of such receptors on developing and mature oligodendrocytes remains unknown. [less ▲]

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See detailDevelopmental Regulation of Neuroligand-Induced Responses in Cultured Oligodendroglia
Belachew, Shibeshih ULg; Malgrange, Brigitte ULg; Rigo, Jean-Michel et al

in Neuroreport (1998), 9(6), 973-80

Using whole-cell patch-clamp techniques, we show that oligosphere-derived oligodendrocyte progenitor cells (OP) display GABA-, glutamate-, 5-HT-, glycine- and acetylcholine-gated inward currents. When OP ... [more ▼]

Using whole-cell patch-clamp techniques, we show that oligosphere-derived oligodendrocyte progenitor cells (OP) display GABA-, glutamate-, 5-HT-, glycine- and acetylcholine-gated inward currents. When OP differentiate into oligodendrocytes (ODC), the amplitude of peak currents elicited by saturating concentrations of these transmitters decreases except for 5-HT. Intracellular Ca2+ concentration changes induced by microperfusion of glutamate, 5-HT, TRH, met-enkephalin and substance P were monitored using a fluo-3-based calcium imaging system. When OP cells differentiate into ODC, a global decrease of the proportion of responding cells is observed. During type-2 astrocytes commitment, this proportion decreases for 5-HT, TRH- and metenkephalin stimulations whereas it remains constant for substance P and glutamate. These data demonstrate a development regulation of neurotransmitter- and neuropeptide-induced responses within the oligodendroglial lineage. [less ▲]

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See detailDiazepam-Insensitive Gabaa Receptors on Postnatal Spiral Ganglion Neurones in Culture
Malgrange, Brigitte ULg; Rigo, Jean-Michel; Lefebvre, Philippe ULg et al

in Neuroreport (1997), 8(3), 591-6

Using dissociated spiral ganglion cell cultures obtained from 3-day-old rat cochlea, we investigated the response of auditory neurones to gamma-aminobutyric acid (GABA) using patch-clamp techniques. In ... [more ▼]

Using dissociated spiral ganglion cell cultures obtained from 3-day-old rat cochlea, we investigated the response of auditory neurones to gamma-aminobutyric acid (GABA) using patch-clamp techniques. In our recording conditions, GABA elicited inward currents in > 95% of the neurones which reversed around 0 mV. Similar inward currents were measured using isoguvacin, a specific agonist of GABAA receptors. GABA-gated currents were reversibly inhibited by the channel blocker picrotoxin and the GABA competitive antagonist bicuculline. These functional GABAA receptors are characterized by an insensitivity to benzodiazepines and a relatively high sensitivity to beta-carbolines and barbiturates. These results show that the GABAA receptor pharmacological properties of spiral ganglion neurones are close to those of cerebellar granule cells. [less ▲]

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See detailAstroglia-released factor with negative allosteric modulatory properties at the GABA A receptor.
Rigo, Jean-Michel; Belachew, Shibeshih ULg; Coucke, Paul et al

in Biochemical Pharmacology (1996), 52(3), 465-473

We have previously shown, using whole-cell patch-clamp techniques, that astrocytes release a negative allosteric modulator of the gamma-aminobutyric acid type A receptor (GABAA receptor) with beta ... [more ▼]

We have previously shown, using whole-cell patch-clamp techniques, that astrocytes release a negative allosteric modulator of the gamma-aminobutyric acid type A receptor (GABAA receptor) with beta-carboline-like properties, thus, likely to act at the benzodiazepine site. Here, using patch-clamp and binding techniques, we confirm that the low-molecular-weight fraction of astroglia-conditioned medium (ACM lmf) contains a factor(s) that negatively modulates GABAA-receptor function. This factor, like beta-carbolines, enhances the specific binding of [35S]t-butyl bicyclophosphorothionate (TBPS) to adult rat cortical membranes in the presence of GABA. However, it fails to interact with various ligands of the benzodiazepine (BZD) site of the GABAA receptor ([3H]flunitrazepam, [3H]Ro 15-1788 and [3H]Ro 15-4513). The question of the actual binding site of the astroglia-derived factor on the GABAA receptor, thus, remains open and can be addressed only after the purification of the active molecule(s) of ACM Imf has been completed, and a labeled form of the endogenous ligand becomes available. Taken together, however, the data suggest that type 1 astrocytes are able to modulate the effects of the main inhibitory neurotransmission in the central nervous system. [less ▲]

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See detailAstroglia-Released Factor Shows Similar Effects as Benzodiazepine Inverse Agonists
Rigo, Jean-Michel; Belachew, Shibeshih ULg; Lefebvre, P. P. et al

in Journal of Neuroscience Research (1994), 39(4), 364-76

Media conditioned by cultured neonatal cerebral cortex microexplants (CCM) or astrocytes (ACM) contain low molecular weight (< 1,000 Da) substance(s) which inhibits the gamma aminobutyric acid (GABA ... [more ▼]

Media conditioned by cultured neonatal cerebral cortex microexplants (CCM) or astrocytes (ACM) contain low molecular weight (< 1,000 Da) substance(s) which inhibits the gamma aminobutyric acid (GABA)-induced inward current recorded in cerebellar granule cells and hippocampal neurons in culture using the whole-cell patch-clamp technique. This effect is specific for CCM and ACM, as medium conditioned by PC12 cells (PC12CM) does not affect the GABA response of these cells. It is also specific for GABA-induced currents because glutamate-induced currents do not change either in amplitude or in shape in the presence of CCM or ACM. The inhibitory effect on the GABA response in cerebellar granule cells of both ACM and CCM could be suppressed by flumazenil, a specific benzodiazepine (BZD) antagonist and could be mimicked by two BZD inverse agonists. These data thus demonstrate the presence of a BZD inverse agonist-like activity in CCM and ACM. This effect of ACM on different neuronal cell types was heterogenous since no detectable effect could be observed on the GABA-induced current in GABA-responsive dorsal root ganglion (DRG) neurons, presumably reflecting a functional heterogeneity of the GABAA receptors present in these different neuronal subsets. By the release of such an endogenous BZD inverse agonist-like activity, glia cells could possibly modulate GABAA receptor-mediated responses. [less ▲]

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See detailSyngeneic Grafting of Adult Rat Drg-Derived Schwann Cells to the Injured Spinal Cord
Martin, Didier ULg; Schoenen, Jean ULg; Delree, P. et al

in Brain Research Bulletin (1993), 30(3-4), 507-14

A subdural inflatable micro-balloon was used to induce closed traumatic contusion to adult rat spinal cord. This spinal cord injury model was associated with reproducible and graded neurological deficits ... [more ▼]

A subdural inflatable micro-balloon was used to induce closed traumatic contusion to adult rat spinal cord. This spinal cord injury model was associated with reproducible and graded neurological deficits and histopathological alterations. At various delays after injury, transplantations of syngeneic adult cultured dorsal root ganglion-derived Schwann cells were performed into the spinal cord lesion. The transplants were well integrated and reduced the microcystic posttraumatic cavitation as well as the gliosis. Schwann cells transplants were invaded by numerous regenerating neurites most of which, based upon their neurotransmitter contents, seem to originate from the dorsal root ganglion. [less ▲]

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See detailPlasticity of Developing and Adult Dorsal Root Ganglion Neurons as Revealed in Vitro
Delree, P.; Ribbens, Clio ULg; Martin, Didier ULg et al

in Brain Research Bulletin (1993), 30(3-4), 231-7

We review recent data on the plasticity of dorsal root ganglion (DRG) neurons as revealed during cultivation in vitro. Some experiments on cultured developing DRG neurons and on adult DRG neurons in vivo ... [more ▼]

We review recent data on the plasticity of dorsal root ganglion (DRG) neurons as revealed during cultivation in vitro. Some experiments on cultured developing DRG neurons and on adult DRG neurons in vivo are also mentioned. Cultured developing and adult DRG neurons can be switched from an apolar to a multipolar phenotype by fetal calf serum or fibronectin. The effect is concentration dependent and occurs through an early modification of cell-substratum interaction. Adult DRG neurons synthesize and release within hours after injury TGF beta-1, which is a mitogen and a differentiation factor for Schwann cells. Finally, adult DRG neurons express in vitro neurotransmitters that are not expressed in vivo. This neurotransmitter plasticity can be modulated in vitro by some growth factors and in vivo by distal or proximal axotomy. [less ▲]

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See detailThree-dimensional organ culture systems
Rogister, Bernard ULg; Rigo, Jean-Michel; Lefebvre, Philippe ULg et al

in Boulton, Alan; Baker, Glen; Walz, Wolfgang (Eds.) Practical Cell Culture Techniques (1992)

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See detailModulation of Proteolytic Activity During Neuritogenesis in the Pc12 Nerve Cell: Differential Control of Plasminogen Activator and Plasminogen Activator Inhibitor Activities by Nerve Growth Factor and Dibutyryl-Cyclic Amp
Leprince, Pierre ULg; Rogister, Bernard ULg; Delree, P. et al

in Journal of Neurochemistry (1991), 57(2), 665-74

Extracellular proteolysis is considered to be required during neuritic outgrowth to control the adhesiveness between the growing neurite membrane and extracellular matrix proteins. In this work, PC12 ... [more ▼]

Extracellular proteolysis is considered to be required during neuritic outgrowth to control the adhesiveness between the growing neurite membrane and extracellular matrix proteins. In this work, PC12 nerve cells were used to study the modulation of proteolytic activity during neuronal differentiation. PC12 cells were found to contain and release a 70-75-kDa tissue-type plasminogen activator (tPA) and a much less abundant 48-kDa urokinase-type plasminogen activator. A plasminogen activator inhibitor (PAI) activity with molecular sizes of 54 and 58 kDa was also detected in PC12 cell conditioned medium and formed high-molecular-mass complexes with released tPA. Release of PAI activity was dependent on treatment with nerve growth factor (NGF), whereas tPA synthesis and release were under control of a cyclic AMP-dependent mechanism and increased on treatment with dibutyryl-cyclic AMP [(But)2cAMP] or cholera toxin. Simultaneous treatment with NGF and (But)2cAMP resulted in increases of both tPA and PAI release and enhancement of tPA-PAI complex formation. The resulting plasminogen activator activity in conditioned medium was high in (But)2cAMP-treated cultures with short neuritic outgrowth but remained low in NGF- or NGF plus (But)2cAMP-treated cultures, where neurite extension was, respectively, large and very large. These results suggest that excess proteolytic activity may be detrimental to neuritic outgrowth and that not only PAI release but also tPA-PAI complex formation is associated with production of large and stable neuritic outgrowth. This can be understood as an involvement of PAI in the protection against neurite-destabilizing proteolytic activity. [less ▲]

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See detailKainate and Nmda Toxicity for Cultured Developing and Adult Rat Spiral Ganglion Neurons: Further Evidence for a Glutamatergic Excitatory Neurotransmission at the Inner Hair Cell Synapse
Lefèbvre, Philippe ULg; Weber, T.; Leprince, Pierre ULg et al

in Brain Research (1991), 555(1), 75-83

In the inner ear, the excitatory amino acid glutamate is a proposed neurotransmitter acting at the synapse between hair cells and afferent auditory neurons. Using cultures of 5-day-old rat auditory ... [more ▼]

In the inner ear, the excitatory amino acid glutamate is a proposed neurotransmitter acting at the synapse between hair cells and afferent auditory neurons. Using cultures of 5-day-old rat auditory neurons, we show that the afferent auditory neuronal population can be divided, on the basis of its sensitivity to the neuronotoxic effect of glutamate and its analogs, in at least 3 subpopulations, one responding to N-methyl-D-aspartate (NMDA), one responding to kainate and a third minor one unresponsive to NMDA, kainic acid and glutamate. No toxic effect of quisqualate is observed. The use of specific antagonists (kynurenate and 2-amino-5-phosphonovalerate (DAP-5) demonstrates the specificity of the receptors to the excitatory amino acids on the afferent auditory neurons. Afferent auditory neurons from adult rats can also be cultured and in these preparations only the large neurons are sensitive to glutamate, kainate and NMDA while the small neurons are not responsive, suggesting that a glutamatergic neurotransmission occurs only at this synapse between the inner hair cells and the large radial afferent auditory neurons. We also show that, in vitro, the organ of Corti releases, in response to an increased potassium concentration and in the presence of calcium, a toxic activity for the afferent auditory neurons that is antagonized by kynurenate and DAP-5. Pathophysiological implications are discussed. [less ▲]

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See detailProtéases et inhibiteurs de protéases : implications multiples dans le développement et le vieillissement cérébral
Leprince, Pierre ULg; Rogister, Bernard ULg; Delrée, Paul et al

in Revue d'Oto-Neuro-Ophtalmologie (1991), 12(13), 30-38

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See detailPotassium-Induced Release of an Endogenous Toxic Activity for Outer Hair Cells and Auditory Neurons in the Cochlea: A New Pathophysiological Mechanism in Meniere's Disease?
Lefebvre, Philippe ULg; Weber, T.; Rigo, Jean-Michel et al

in Hearing Research (1990), 47(1-2), 83-93

In Meniere's disease, the increase of extracellular potassium concentration in the perilymph is thought to play a key role in determining the progressive loss of cochlear hair cells. In this paper, we ... [more ▼]

In Meniere's disease, the increase of extracellular potassium concentration in the perilymph is thought to play a key role in determining the progressive loss of cochlear hair cells. In this paper, we describe a serum-free culture preparation of hair cells from 5 day-old rat and report the release by the cochlea, in response to an increase of extracellular potassium concentration, of a cytotoxic activity active on hair cells and auditory neurons. The toxic activity is associated with low molecular weight (less than 10,000 Dalton) molecule(s) as revealed by ultrafiltration. Morphological studies performed on the organ of Corti incubated during 24 h in the presence of the cochlea-derived toxic activity (CTA), show that this factor is toxic for hair cells and not for supporting or surrounding cells. The release of CTA occurs both in the spiral ganglion and in the organ of Corti. We suggest that this cochlea-derived toxic activity may play an important role in the pathophysiology of the hearing loss that occurs during the progression of Meniere's disease. [less ▲]

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See detailNeuronotrophic Effect of Developing Otic Vesicle on Cochleo-Vestibular Neurons: Evidence for Nerve Growth Factor Involvement
Lefebvre, Philippe ULg; Leprince, Pierre ULg; Weber, T. et al

in Brain Research (1990), 507(2), 254-60

In the developing inner ear, the existence of a neuronal death and of a peripheral target-derived trophic effect on cochleovestibular neurons has been documented. Using cultures of rat cochleovestibular ... [more ▼]

In the developing inner ear, the existence of a neuronal death and of a peripheral target-derived trophic effect on cochleovestibular neurons has been documented. Using cultures of rat cochleovestibular neurons, we show that the E12 otic vesicle releases a factor promoting the survival and the neuritogenesis of these neurons, and that this effect is mimicked by NGF. The effect of the optic vesicle conditioned medium (OVCM) on cochleovestibular neurons is suppressed by anti-NGF antibodies. OVCM is neuronotrophic for NGF-sensitive sympathetic neurons, an effect that is also suppressed by anti-NGF antibodies, further demonstrating the presence of biologically active nerve growth factor. [less ▲]

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See detailMultiple roles for plasminogen activator system in nervous system development
Leprince, Pierre ULg; Rogister, Bernard ULg; Delrée, Paul et al

in Serine proteases and their serpin inhibitors in the Nervous System (1990)

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See detailTrophic and toxic influences on neurones
Leprince, Pierre ULg; Rigo, Jean-Michel; Rogister, Bernard ULg et al

in Current Aspects of the Neurosciences Vol.1 (1990)

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See detailCultured Astroglia Release a Neuronotoxic Activity That Is Not Related to the Excitotoxins
Leprince, Pierre ULg; Lefebvre, Philippe ULg; rigo, Jean-Michel et al

in Brain Research (1989), 502(1), 21-7

Neuronal death after brain injury is thought to be in part the result of the activity of the excitotoxins, a family of excitatory amino acids which are released by neurones. We have also described an ... [more ▼]

Neuronal death after brain injury is thought to be in part the result of the activity of the excitotoxins, a family of excitatory amino acids which are released by neurones. We have also described an astroglial cell-derived neuronotoxic activity of low molecular weight whose release can be induced by depolarizing events such as an increase in extracellular potassium concentration. We study here the relationship between this astroglia-derived neuronotoxic activity present in astroglia-conditioned medium (ACM) and the excitotoxins. Using a colorimetric assay of neuronal survival, we show that the ACM neuronotoxic activity, is able to induce the death of all types of neurones tested, including those which are insensitive to excitotoxins. Furthermore, the ACM neuronotoxic activity does not require for its action the extracellular ionic composition which is needed for the activity of excitotoxins. Finally, the ACM neuronotoxic activity is not blocked by competitive or non-competitive antagonists of the various classes of excitotoxin receptors. Those data demonstrate that the astroglia-derived neuronotoxic activity is not related to the excitotoxins. Still, because astrocytes can also be depolarized by members of the excitotoxin family, the possibility exists that the release of astroglia-derived neuronotoxic activity would follow the rise in extracellular excitatory amino acid concentration during nervous system injury. [less ▲]

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See detailIn Vitro Kinetics of a Newborn Rat Astroglia-Derived Neuronotoxic Activity
Leprince, Pierre ULg; rigo, Jean-Michel; Lefebvre, Philippe ULg et al

in Neuroscience Letters (1989), 102(2-3), 268-72

A low-molecular weight astrocyte-derived neuronotoxic activity (ANTA) was detected, using a colorimetric bioassay of cell survival, by its effect on cultured granule cells. This neuronotoxic activity was ... [more ▼]

A low-molecular weight astrocyte-derived neuronotoxic activity (ANTA) was detected, using a colorimetric bioassay of cell survival, by its effect on cultured granule cells. This neuronotoxic activity was found to be released rapidly from newborn rat astrocytes in culture upon incubation in 50 mM K+-containing growth medium. The release by astrocytes could be induced repetitively by successive incubations in high-K+ medium alternating with incubations in normal medium. Astrocytes were also found to inactivate rapidly isobutanol-extracted ANTA in normal K+-containing growth medium. Kinetic studies showed that ANTA induces a slow (greater than 12 h) degeneration of cultured granule cells. ANTA is shown here to be an intermediate of normal astrocyte metabolism and to display appropriate kinetic characteristics compatible with its proposed role in inducing part of the delayed neuronal loss that occurs after a brain injury (secondary neuronal death). [less ▲]

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See detailInteractions neurotrophiques dans l'oreille interne en développement ?
Lefebvre, Philippe ULg; Weber, Thierry; Rigo, Jean-Michel et al

in Acta Otolaryngologica Belgica (1989), 43(5), 403-409

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See detailDevelopmental Neurobiology and the physiopathology of brain injury
Moonen, Gustave ULg; Delrée, Paul; Leprince, Pierre ULg et al

in Stein, Don; Sabel, Bernhard (Eds.) Pharmacological approaches to the treatment of brain and spinal cord injury (1988)

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