References of "MOONEN, Gustave"
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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 detailExperimental modulation of neurotransmitter phenotype in adult dorsal root ganglion neurons.
Schoenen, Jean ULg; Delrée, P.; Jammaer, R. et al

Conference (1990, June 30)

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See detailIn vitro and in vivo modulation of neurotransmitter phenotype in adult dorsal root ganglion neurons.
Schoenen, Jean ULg; Delrée, P.; Jammaer, R. et al

Conference (1990, June 16)

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See detailAn in vivo model of varicella-zoster virus latent infection of dorsal root ganglia
Sadzot-Delvaux, Catherine ULg; Merville, Marie-Paule ULg; Delrée, P. et al

in Journal of Neuroscience Research (1990), 26(1), 83-89

We describe here the first in vivo model of varicella-zoster virus (VZV) latent infection in the adult rat peripheral nervous system. Infected Mewo cells were injected subcutaneously along the spine of ... [more ▼]

We describe here the first in vivo model of varicella-zoster virus (VZV) latent infection in the adult rat peripheral nervous system. Infected Mewo cells were injected subcutaneously along the spine of healthy adult rats. No clinical sign of infection was observed even 9 months after inoculation. Humoral immune response to VZV was detected in all infected animals throughout the study (9 months). The presence of viral material in dissociated and cultured dorsal root ganglia (DRG) from inoculated animals was studied by immunoperoxidase and in situ hybridization. When DRGs from infected animals were plated in culture from 1 month and up to 9 months after inoculation, viral nucleic acids and proteins were detected in neurons. Furthermore, trypsinization and subcultivation of infected neurons in culture is needed to reactivate infectious virus at least in some of the neurons. This model provides a useful tool for studying 1) the molecular mechanisms leading to an in vivo latency, 2) the role of the immune system, in particular cellular immunity, on the establishment, maintenance, and reactivation of latency, 3) the neurotropism of mutant viruses, and 4) the effects of antiviral agents. [less ▲]

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See detailAcute and persistent varicella-zoster virus infection of human and murine neuroblastoma cell lines
Bourdon-Wouters, C.; Merville, Marie-Paule ULg; Sadzot-Delvaux, Catherine ULg et al

in Journal of Neuroscience Research (1990), 26(1), 90-97

Human and murine neuroblastoma cell lines were infected in vitro with varicella-zoster virus (VZV). Infected human neuroblastoma cells (IMR-32) supported the synthesis of abundant viral antigens as ... [more ▼]

Human and murine neuroblastoma cell lines were infected in vitro with varicella-zoster virus (VZV). Infected human neuroblastoma cells (IMR-32) supported the synthesis of abundant viral antigens as detected by indirect immunoperoxidase labeling using human serum rich in anti-VZV antibodies and did not survive the infection. In situ hybridization (ISH) with VZV-cloned probes revealed a strong hybridization signal in these infected cells. During cultivation, the virus was released in the culture medium, and viral polypeptides were revealed by Western blotting of infected cells, using either a monoclonal anti-gpI antibody or a rabbit antiserum. All these findings indicate that IMR-32 cells support a productive and lytic infection by VZV, whether infected by cell-free virus or by cocultivation with infected cells. Murine neuroblastoma cells (neuro-2A) survived VZV infection and did not produce any infectious virus. No VZV-specific proteins were detected in infected cells either by immunolabeling or by Western blotting. However, viral nucleic acids could be detected by ISH, indicating that mouse neuroblastoma cells displayed a nonproductive, nonlytic infection. Infected neuro-2A cells have been examined by ISH using probes corresponding to immediate early (IE) genes 4, 62, and 63 and late (L) gene 31 encoding gpII. A strong hybridization signal was detected when infected cells were probed with a fragment containing the IE genes 62 and 63. Lower levels of hybridization were detected with the other probes, corresponding to IE or L genes. These systems allow comparative molecular analysis of persistent and acute infection of nerve cells by VZV. [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 detailNeurono-Glial Interactions and Neural Plasticity
Moonen, Gustave ULg; Rogister, Bernard ULg; Leprince, Pierre ULg et al

in Coleman, Paul; Higgins, G.; Phelps, C. (Eds.) Progress In Brain research: Neuronal Plasticity in aging and dementia (1990)

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See detailIn vitro and in vivo modulation of neurotransmitter phenotype in adult rat DRG neurons
Schoenen, Jean ULg; Delrée, P.; Martin, Didier ULg et al

in Rapport annuel de la Fondation Médicale Reine Elisabeth (1990)

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See detailIn vitro and in vivo modulation of neurotransmitter phenotype in adult DRG neuron.
Schoenen, Jean ULg; Delrée, P.; Martin, Didier ULg et al

Conference (1990)

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See detailCultured neurons release an inhibitor of astroglia proliferation (astrostatine).
Rogister, Bernard ULg; Leprince, Pierre ULg; Bonhomme, Vincent ULg et al

in Journal of Neuroscience Research (1990), 25(1), 58-70

Using in vitro techniques, we looked for a possible downregulation of rat astroglia proliferation by neuronal cells. We demonstrate that medium conditioned by 7-day-old rat cerebellar granule neurons or ... [more ▼]

Using in vitro techniques, we looked for a possible downregulation of rat astroglia proliferation by neuronal cells. We demonstrate that medium conditioned by 7-day-old rat cerebellar granule neurons or by 16-day-old rat embryo hippocampal neurons strongly inhibits the proliferation of cultured astroglial cells. Two neuronal cell lines, the PC12 rat pheocromocytoma and the neuro 2A (N2A) murine neuroblastoma also release such an activity. This release in N2A-conditioned medium (CM) occurs when the cells are at high density and show a low proliferation rate. This activity is present in media conditioned by neuronal cells, but not in media conditioned by normal astrocytes, by two glioma cell lines, or by one fibroblastic cell line. This proliferation inhibitor addresses normal astrocytes: the proliferation of two glioma cell lines, of a fibroblastic cell line, and of the two neuronal cell lines (PC12, N2A) is not inhibited by N2A CM. Moreover, this activity is directed against type 1 astrocytes, but not against type 2. Using three different assays, we demonstrate that DNA synthesis by astroglial cells is inhibited. N2A CM has no cytotoxic effect on astrocytes and does not modify their overall protein synthesis. Using affinity and gel filtration chromatography, we show that this activity is associated with a protein whose molecular weight ranges between 15 and 20 kDa. The possible relationship between this N2A cell-derived astroglia proliferation inhibitor and other types of potential glial proliferation inhibitors has been investigated. A brain glycoprotein immunologically related to epidermal growth factor receptor (EGFR) was reported to inhibit astroglial cell proliferation in vitro. Using polyclonal and monoclonal antibodies against EGFR, we were unable to immunoprecipitate the astrocyte proliferation inhibitor in N2A CM or to demonstrate by immunoblotting the presence of an EGFR-like immunoreactivity in the N2A CM or in the active chromatographic fractions of N2A CM. Transforming growth factor beta (TGF beta) is a well-known modulator of the proliferation of various cell types and was shown to be present in N2A CM. Using a polyclonal anti-TGF beta antibody that recognizes TGF beta on Western blots of N2A CM, we were unable to immunoprecipitate the astrocyte proliferation inhibitor of N2A CM. It seems thus far that the neuronal astroglia proliferation inhibitor is a new protein for which we propose the name astrostatine. [less ▲]

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See detailEnhanced Release of Plasminogen Activator Inhibitor(S) but Not of Plasminogen Activators by Cultured Rat Glial Cells Treated with Interleukin-1
Rogister, Bernard ULg; Leprince, Pierre ULg; Delree, P. et al

in Glia (1990), 3(4), 252-7

Astroglial cells are known to proliferate during development of the nervous system, as well as during post-traumatic gliosis. We have previously shown that the proliferation of cultured astrocytes can be ... [more ▼]

Astroglial cells are known to proliferate during development of the nervous system, as well as during post-traumatic gliosis. We have previously shown that the proliferation of cultured astrocytes can be stimulated by the urokinase-type (uPA) of plasminogen activator (PA) and that astrocytes are able to release such uPA upon stimulation with basic fibroblast growth factor, which is known to act as a mitogen for these cells. Here we report studies on the effects of human interleukin-1 (IL-1) on the release of PA activity by cultured newborn rat astroglial cells. Whereas there is controversy in the literature as to whether IL-1 stimulates multiplication of astroglial cells, we failed to observe such an effect in our system. We did observe, however, a dose-dependent decrease in PA activity in the supernatant of the IL-1 treated cultures. Further analysis revealed that this apparent decrease in PA release was in fact due to an increased release of plasminogen activator inhibitor (PAI). A similar IL-1 induced increase in PAI release was also found to occur in cultures of transformed astrocytes (human glioma LN18) and in cultured Schwann cells, but not in cultures of neurons or neuronal tumour cells. Since protease inhibitors are known to possess neuritogenic properties, our results suggest that IL-1, by its capacity to induce PAI, may promote neuritogenesis. [less ▲]

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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 and in situ experimental modulation of neurotransmitters, phenotypic expression by adult dorsal root ganglion neurons
Schoenen, J.; Delrée, P.; Martin, Didier ULg et al

Conference (1989, November)

Detailed reference viewed: 7 (2 ULg)