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See detailNeuromorphic reinforcement learning
Dethier, Julie ULg; Ernst, Damien; Sepulchre, Rodolphe

Conference (2012, March 29)

Living organisms are able to successfully perform challeng- ing tasks such as perception, classification, association, and control. In hope for similar successes in artificial systems, neuromorphic ... [more ▼]

Living organisms are able to successfully perform challeng- ing tasks such as perception, classification, association, and control. In hope for similar successes in artificial systems, neuromorphic engineering uses neurophysiological models of perception and information processing in biological sys- tems to emulate their functions but also resemble their struc- ture [1]. In this abstract, we focus on the basal ganglia (BG), brain region in control of primitive functions of the nervous system, and specifically on their involvement in action selec- tion and reinforcement learning (RL). We hypothesize that neuromorphic-inspired systems will greatly benefit the RL community. [less ▲]

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See detailNeuromuscular transmission in migraine patients with prolonged aura
Ambrosini, Anna; MAERTENS DE NOORDHOUT, Alain ULg; SCHOENEN, Jean ULg

in Acta Neurologica Belgica (2001), 101(3), 166-70

P/Q Ca2+ channels are genetically abnormal in most cases of familial hemiplegic migraine (FHM) and may be involved in other types of migraine. They are also found at the neuromuscular junctions, where ... [more ▼]

P/Q Ca2+ channels are genetically abnormal in most cases of familial hemiplegic migraine (FHM) and may be involved in other types of migraine. They are also found at the neuromuscular junctions, where they control stimulation-induced acetylcholine release. Prolonged aura is a very frequent clinical feature in FHM patients. The objective of this study was thus to explore neuromuscular transmission in migraine with typical and prolonged aura patients. We performed single fiber electromyography (SFEMG) in such patients and compared them to a group of healthy volunteers. Results were expressed as mean jitter (MCD) and percentage of single endplate abnormalities. Mean MCD was on average comparable in controls and migraineurs. By contrast, single endplate abnormalities were only found in patients (p < 0.01), especially in those with prolonged aura (p < 0.001). These results suggest subtle impairment of neuromuscular transmission in a subgroup of migraineurs characterized by prolonged aura, which might be due to dysfunctioning P/Q Ca(2+)-channels. [less ▲]

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See detailNeuromuscular transmission in migraine: a single-fiber EMG study in clinical subgroups.
Ambrosini, Anna; Maertens De Noordhout, Alain ULg; Schoenen, Jean ULg

in Neurology (2001), 56(8), 1038-43

OBJECTIVE: To search for impairment of neuromuscular transmission by single-fiber electromyography (SFEMG) in patients with common forms of migraine. BACKGROUND: P/Q Ca(2+) channels are genetically ... [more ▼]

OBJECTIVE: To search for impairment of neuromuscular transmission by single-fiber electromyography (SFEMG) in patients with common forms of migraine. BACKGROUND: P/Q Ca(2+) channels are genetically abnormal in most cases of familial hemiplegic migraine (International Headache Society [IHS] code 1.2.3) and may be involved in other types of migraine. Besides in the brain, these channels are found in motor nerve endings, where they control stimulation-induced acetylcholine release. If they are functionally abnormal, the neuromuscular transmission might be impaired. METHODS: Sixty-two migraineurs (18 without aura, IHS code 1.1; 19 with typical aura, IHS code 1.2.1; 10 with prolonged aura, IHS code 1.2.2; 15 with and without aura) and 16 healthy control subjects underwent stimulation SFEMG. Results were expressed as the mean value of consecutive differences (MCD) and percentage of single-fiber abnormalities (abnormal jitter or impulse blocking). RESULTS: Average MCD was comparable in control subjects and migraineurs (17.1 +/- 2.6 versus 17.5 +/- 4.7 microsec). By contrast, single-fiber abnormalities were found in 17 patients but in none of the control subjects (p = 0.036). Most of these patients had unilateral sensorimotor symptoms and/or aphasia and/or loss of balance during the aura. SFEMG abnormalities were significantly correlated with the occurrence of these clinical features and with a diagnosis of migraine with prolonged aura. CONCLUSIONS: Stimulation SFEMG shows mild abnormalities of neuromuscular transmission in a subgroup of migraineurs with aura, characterized by clinical features frequently found in human P/Q Ca(2+) channelopathies. These abnormalities might thus be due to genetically modified P/Q Ca(2+) channels. [less ▲]

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See detailNeuron-Specific Enolase as a Marker of in Vitro Neuronal Damage. Part I: Assessment of Neuron-Specific Enolase as a Quantitative and Specific Marker of Neuronal Damage
Hans, Pol ULg; Bonhomme, Vincent ULg; Collette, Julien ULg et al

in Journal of Neurosurgical Anesthesiology (1993), 5(2), 111-6

Enolase in cerebrospinal fluid is a sensitive marker for many types of neurological injuries including head injury and ischemia. We assessed neuron-specific enolase (NSE) as a quantitative and specific ... [more ▼]

Enolase in cerebrospinal fluid is a sensitive marker for many types of neurological injuries including head injury and ischemia. We assessed neuron-specific enolase (NSE) as a quantitative and specific biochemical marker of neuronal damage in an experimental model of kainate neurotoxicity. Rat hippocampal cultures were treated with various concentrations of kainate. NSE release into the culture medium was compared with neuronal death estimated either by direct cell counting or by lactate dehydrogenase (LDH) release, largely used to quantify neuronal injury. A dose-response relationship was observed between kainate concentration and the amount of NSE released (r = -0.69; p < 0.05) as well as a significant correlation between NSE release and neuronal death (r = 0.64; p < 0.05). Likewise, a significant correlation was found between LDH and NSE release (r = 0.85; p < 0.05). The specificity of NSE as an indicator of neuronal death was demonstrated using immunocyto-chemistry labeling and measurement of NSE release by pure astrocyte cultures. We concluded that NSE is a reliable, quantitative, and specific marker of neuronal injury. [less ▲]

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See detailNeuron-Specific Enolase as a Marker of in Vitro Neuronal Damage. Part II: Investigation of the Astrocyte Protective Effect against Kainate-Induced Neurotoxicity
Bonhomme, Vincent ULg; Hans, Pol ULg; Collette, Julien ULg et al

in Journal of Neurosurgical Anesthesiology (1993), 5(2), 117-20

The protective effect of astrocytes on hippocampal neurons against kainate-induced toxicity was investigated using neuron-specific enolase as an indicator of neuronal death. Astrocyte-rich and astrocyte ... [more ▼]

The protective effect of astrocytes on hippocampal neurons against kainate-induced toxicity was investigated using neuron-specific enolase as an indicator of neuronal death. Astrocyte-rich and astrocyte-poor mixed rat hippocampal cultures were submitted to various concentrations of kainate. At each kainate concentration, the amount of NSE released by neurons was significantly greater in astrocyte-poor than in astrocyte-rich cultures (p < 0.05). This protective effect was not observed when neuronal survival was tested on astrocyte-poor cultures in astrocyte-conditioned culture medium with or without 10(-4) M kainate. In conclusion, astrocytes significantly attenuate kainate toxicity on hippocampal neurons, and this effect is not mediated by a diffusible factor. [less ▲]

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See detailNeuron-Specific Enolase as a Predictor of Death or Poor Neurological Outcome After Out-of-Hospital Cardiac Arrest and Targeted Temperature Management at 33 degrees C and 36 degrees C.
Stammet, Pascal ULg; Collignon, Olivier; Hassager, Christian et al

in Journal of the American College of Cardiology (2015), 65(19), 2104-14

BACKGROUND: Neuron-specific enolase (NSE) is a widely-used biomarker for prognostication of neurological outcome after cardiac arrest, but the relevance of recommended cutoff values has been questioned ... [more ▼]

BACKGROUND: Neuron-specific enolase (NSE) is a widely-used biomarker for prognostication of neurological outcome after cardiac arrest, but the relevance of recommended cutoff values has been questioned due to the lack of a standardized methodology and uncertainties over the influence of temperature management. OBJECTIVES: This study investigated the role of NSE as a prognostic marker of outcome after out-of-hospital cardiac arrest (OHCA) in a contemporary setting. METHODS: A total of 686 patients hospitalized after OHCA were randomized to targeted temperature management at either 33 degrees C or 36 degrees C. NSE levels were assessed in blood samples obtained 24, 48, and 72 h after return of spontaneous circulation. The primary outcome was neurological outcome at 6 months using the cerebral performance category score. RESULTS: NSE was a robust predictor of neurological outcome in a baseline variable-adjusted model, and target temperature did not significantly affect NSE values. Median NSE values were 18 ng/ml versus 35 ng/ml, 15 ng/ml versus 61 ng/ml, and 12 ng/ml versus 54 ng/ml for good versus poor outcome at 24, 48, and 72 h, respectively (p < 0.001). At 48 and 72 h, NSE predicted neurological outcome with areas under the receiver-operating curve of 0.85 and 0.86, respectively. High NSE cutoff values with false positive rates </=5% and tight 95% confidence intervals were able to reliably predict outcome. CONCLUSIONS: High, serial NSE values are strong predictors of poor outcome after OHCA. Targeted temperature management at 33 degrees C or 36 degrees C does not significantly affect NSE levels. (Target Temperature Management After Cardiac Arrest [TTM]; NCT01020916). [less ▲]

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See detailNeuronal and glial expression of the inducible HSP70 in forebrain ischemia
Xu, D.; Plumier, Jean-Christophe ULg; Robertson, Harold A. et al

Poster (1995)

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See detailNeuronal and psychological underpinnings of pathological gambling
Singer, Bryan F.; Anselme, Patrick ULg; Robinson, Mike J.F. et al

in Frontiers in Behavioral Neuroscience (2014), 8, 230

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See detailNeuronal and psychological underpinnings of pathological gambling (E-Book)
Singer, Bryan F; Anselme, Patrick ULg; Robinson, Mike JF et al

Book published by Frontiers in Behavioral Neuroscience (2014)

Like in the case of drugs, gambling hijacks reward circuits in a brain which is not prepared to receive such intense stimulation. Dopamine is normally released in response to reward and uncertainty in ... [more ▼]

Like in the case of drugs, gambling hijacks reward circuits in a brain which is not prepared to receive such intense stimulation. Dopamine is normally released in response to reward and uncertainty in order to allow animals to stay alive in their environment – where rewards are relatively unpredictable. In this case, behavior is regulated by environmental feedbacks, leading animals to persevere or to give up. In contrast, drugs provide a direct, intense pharmacological stimulation of the dopamine system that operates independently of environmental feedbacks, and hence causes “motivational runaways”. With respect to gambling, the confined environment experienced by gamblers favors the emergence of excitatory conditioned cues, so that positive feedbacks take over negative feedbacks. Although drugs and gambling may act differently, their abnormal activation of reward circuitry generates an underestimation of negative consequences and promotes the development of addictive/compulsive behavior. In Parkinson’s and Huntington’s disease, dopamine-related therapies may disrupt these feedbacks on dopamine signalling, potentially leading to various addictions, including pathological gambling. The goal of this Research Topic is to further our understanding of the neurobiological mechanisms underlying the development of pathological gambling. This eBook contains a cross-disciplinary collection of research and review articles, ranging in scope from animal behavioral models to human imaging studies. [less ▲]

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See detailNeuronal circuitries of emotional regulation in depressed patients before and after a mindfulness training
Cojan, Yann; Desseilles, Martin ULg

Scientific conference (2011, April 08)

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See detailNeuronal Control of Astrocytes Proliferation
Rogister, Bernard ULg; Leprince, Pierre ULg; Martin, Didier ULg et al

in Fedoroff, S.; Juurlink, B. H. J.; Doucette, R. (Eds.) Biology and pathology of astrocyte-neuron interactions (1993)

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See detailNeuronal Differentiation in the Adult Brain: Cdk6 as the Molecular Regulator
Caron, Nicolas ULg; Genin, Emmanuelle ULg; Vandenbosch, Renaud ULg et al

in Hayat, Eric (Ed.) TUMORS OF THE CENTRAL NERVOUS SYSTEM (2013)

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See detailNeuronal injury in NCX3 knockout mice following permanent focal cerebral ischemia and in NCX3 knockout cortical neuronal cultures following oxygen-glucose deprivation and glutamate exposure
Cross, J. L.; Meloni, B. P.; Bakker, A. J. et al

in Journal of Experimental Stroke & Translational Medicine (2009), 2(1), 3-9

In this study we subjected NCX3 knockout and wildtype mice to permanent focal cerebral ischemia by intraluminal middle cerebral artery occlusion. Analysis of brain sections by 2,3,5-Triphenyl-2H ... [more ▼]

In this study we subjected NCX3 knockout and wildtype mice to permanent focal cerebral ischemia by intraluminal middle cerebral artery occlusion. Analysis of brain sections by 2,3,5-Triphenyl-2H-tetrazolium chloride staining, 12 hours after middle cerebral artery occlusion revealed no difference in infarct volume between NCX3 knockout and wildtype mice. In addition, we evaluated the effect of NCX3 protein knockdowri on neuronal viability in primary cortical neuronal cultures following in vitro ischemia (oxygen-glucose deprivation) and L-glutamate (glutamate) exposure. In vitro experiments revealed that neuronal viability was higher in NCX3 knockout neuronal cultures than in the wildtype cultures following ischemic and glutamate insults. The reduced sensitivity of neurons from NCX3 knockout mice to in vitro ischemia and excitotoxicity indicates that NCX3 calcium entry mode activity contributes to calcium overload and neuronal death. However our in vivo finding of e lack of differential sensitivity on infarct volume in NCX3 knockout and wildtype mice suggests that any benefit of reduced NCX3 activity is overridden following permanent focal cerebral ischemia. Taken together, these f]ndings suggest that reduced NXC3 activity limits calcium neurotoxicity during severe transient, but not during severe sustained ischemic insults. These results have important implications for the development of the NCX3 protein as a therapeutic target to reduce ischemic brain injury [less ▲]

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See detailNeuronal localization of the 25-kDa specific thiamine triphosphatase in rodent brain
Czerniecki, Jan ULg; Chanas, Grazyna; Verlaet, Myriam ULg et al

in Neuroscience (2004), 125(4), 833-840

Thiamine triphosphate (ThTP) is found in small amounts in most organisms from bacteria to mammals, but little is known about its physiological role. In vertebrate tissues, ThTP may act as a phosphate ... [more ▼]

Thiamine triphosphate (ThTP) is found in small amounts in most organisms from bacteria to mammals, but little is known about its physiological role. In vertebrate tissues, ThTP may act as a phosphate donor for the phosphorylation of certain proteins; this may be part of a new signal transduction pathway. We have recently characterized a highly specific 25-kDa thiamine triphosphatase (ThTPase) that is expressed in most mammalian tissues. The role of this enzyme may be the control of intracellular concentrations of ThTP. As the latter has been considered to be a neuroactive form of thiamine, we have studied the distribution of ThTPase mRNA and protein in rodent brain using in situ hybridization and immunohistochemistry. With both methods, we found the strongest staining in hippocampal pyramidal neurons, as well as cerebellar granule cells and Purkinje cells. Some interneurons were also labeled and many ThTPase mRNA-positive and immunoreactive cells were distributed throughout cerebral cortical gray matter and the thalamus. White matter was not significantly labeled. ThTPase immunoreactivity seems to be located mainly in the cytoplasm of neuronal perikarya. Immunocytochemical data using dissociated cultured cells from hippocampal and cerebellum showed that the staining was more intense in neurons than in astrocytes. The protein was rather uniformly located in the perikarya and dendrites, suggesting that ThTP and ThTPase may play a general role in neuronal metabolism rather than a specific role in excitability. There was no apparent correlation between ThTPase expression and selective vulnerability of certain brain regions to thiamine deficiency. (C) 2004 IBRO. Published by Elsevier Ltd. All rights reserved. [less ▲]

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See detailNeuronal migration disorders and epilepsies
Misson, Jean-Paul ULg; Dubru, Jean-Marie ULg; Leroy, Patricia et al

in Nehlig, Astrid; Motte, Jacques (Eds.) Childhood epilepsies and brain development (1999)

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See detailNeuronal migration in the murine cerebrum proceeds in parallel to raidial fibers : Analysis based upon double labeling of migrating neurons and radial fibers
Misson, Jean-Paul ULg; Austin, C.; Takahashi, T. et al

in Comptes Rendu des Journées Annuelles de la Société Belge de Pédiatrie (1990)

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See detailNeuronal replacement in the ischemic brain
Plumier, Jean-Christophe ULg

Scientific conference (2003)

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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 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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