Christophe Melon

ORCID: 0000-0002-8517-6886
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Neurological disorders and treatments
  • Parkinson's Disease Mechanisms and Treatments
  • Neurotransmitter Receptor Influence on Behavior
  • Receptor Mechanisms and Signaling
  • Neuroscience and Neural Engineering
  • Genetic Neurodegenerative Diseases
  • Diet and metabolism studies
  • Neurogenesis and neuroplasticity mechanisms
  • Treatment of Major Depression
  • Transcranial Magnetic Stimulation Studies
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Photoreceptor and optogenetics research
  • Advanced MRI Techniques and Applications
  • Nerve injury and regeneration
  • Electromagnetic Fields and Biological Effects
  • Mitochondrial Function and Pathology
  • Schizophrenia research and treatment
  • Pluripotent Stem Cells Research
  • Medicinal Plants and Neuroprotection
  • Alzheimer's disease research and treatments
  • Cholinesterase and Neurodegenerative Diseases
  • Olfactory and Sensory Function Studies
  • Nicotinic Acetylcholine Receptors Study
  • Vitamin C and Antioxidants Research

Institut de Biologie du Développement Marseille
2011-2024

Centre National de la Recherche Scientifique
2008-2022

Aix-Marseille Université
2009-2021

Institut de Microbiologie de la Méditerranée
2011

Infection et inflammation
2005

Mécanismes Centraux et Périphériques de la Neurodégénérescence
2004

Bayer (Germany)
1998-2004

AVL (France)
1995-2001

Servier (France)
1999-2000

Centre Hospitalier Universitaire de Saint-Pierre
1978

The present study evaluated, via a combined electrophysiological and dialysis approach, the potential influence of serotonin (5-HT)(2C) as compared to 5-HT(2A) 5-HT(2B) receptors on dopaminergic, adrenergic, serotonergic transmission in frontal cortex (FCX). Whereas selective antagonist MDL100,907 failed modify extracellular levels dopamine (DA), noradrenaline (NA) or 5-HT simultaneously quantified single dialysate samples freely-moving rats, 5-HT(2B)/5-HT(2C) SB206,553 dose-dependently...

10.1002/(sici)1098-2396(20000601)36:3<205::aid-syn5>3.0.co;2-d article EN Synapse 2000-06-01

Abstract There is growing experimental evidence for the implication of glutamate‐mediated mechanisms both in pathophysiology Parkinson's disease and development dyskinesias with long‐term administration l ‐3,4‐dihydroxyphenylalanine ( ‐DOPA). However, impact this treatment on glutamate transmission basal ganglia has been poorly investigated. In study, we examined effects 6‐hydroxydopamine‐induced lesion nigral dopamine neurons or without subsequent chronic ‐DOPA several parameters system...

10.1111/j.1460-9568.2004.03591.x article EN European Journal of Neuroscience 2004-09-01

Evidence exists that a reinforcement in monoaminergic transmission the frontal cortex (FCX) is associated with antidepressant (AD) properties. Herein, we examined whether blockade of alpha2-adrenergic receptors modified influence monoamine reuptake inhibitors on FCX levels serotonin (5-HT), noradrenaline (NAD), and dopamine (DA). The selective receptor agonist S 18616 (0.16 mg/kg, s.c.) suppressed extracellular NAD, DA, 5-HT (by 100, 51, 63%, respectively) single dialysates freely moving...

10.1046/j.1471-4159.1997.69062616.x article EN Journal of Neurochemistry 1997-12-01

Abstract Alterations of striatal synaptic transmission have been associated with several motor disorders involving the basal ganglia, such as Parkinson’s disease. For this reason, we investigated role group‐III metabotropic glutamate (mGlu) receptors in regulating striatum by electrophysiological recordings and using our novel orthosteric agonist (3 S )‐3‐[(3‐amino‐3‐carboxypropyl(hydroxy)phosphinyl)‐hydroxymethyl]‐5‐nitrothiophene (LSP1‐3081) l ‐2‐amino‐4‐phosphonobutanoate (L‐AP4). Here,...

10.1111/j.1471-4159.2009.06036.x article EN Journal of Neurochemistry 2009-03-14

The solute carrier family SLC25 drives the import of a large diversity metabolites into mitochondria, key cellular structure involved in many metabolic functions. Mutations mitochondrial glutamate SLC25A22 (also named GC1) have been identified early epileptic encephalopathy and migrating partial seizures infancy but pathophysiological mechanism GC1 deficiency is still unknown, hampered by absence an vivo model. This mainly expressed astrocytes principal gate for entry mitochondria. A...

10.3389/fncel.2017.00149 article EN cc-by Frontiers in Cellular Neuroscience 2017-05-31

Abstract Hyperactivity of striatal glutamatergic synaptic transmission in response to dopamine depletion plays a major role the pathogenesis parkinsonian motor symptoms. In present study we investigated impact, on this hyperactivity, chronic dyskinesiogenic L‐DOPA treatment, combined or not with high‐frequency stimulation (HFS) subthalamic nucleus (STN). vitro patch‐clamp recordings were performed from spiny neurons hemiparkinsonian rats (intranigral 6‐OHDA injection). Here show that...

10.1111/j.1460-9568.2006.05047.x article EN European Journal of Neuroscience 2006-09-01

This study examined the cellular changes produced in striatum by chronic l -DOPA treatment and prolonged subthalamic nucleus high-frequency stimulation (STN–HFS) applied separately, successively, or association, 6-hydroxydopamine-lesioned rat model of Parkinson's disease (PD). Only animals showing severe -DOPA-induced dyskinesias (LIDs) were included, STN–HFS was for 5 d at an intensity efficient alleviating akinesia without inducing dyskinesias. alone induced FosB/ΔFosB immunoreactivity,...

10.1523/jneurosci.2949-06.2007 article EN cc-by-nc-sa Journal of Neuroscience 2007-02-28

The thalamic centromedian–parafascicular (CM/Pf) complex, mainly represented by Pf in rodents, is proposed as an interesting target for the neurosurgical treatment of movement disorders, including Parkinson9s disease. In this study, we examined functional impact subchronic high-frequency stimulation (HFS) 6-hydroxydopamine-lesioned hemiparkinsonian rat model. Pf-HFS had significant anti-akinetic action, evidenced alleviation limb use asymmetry (cylinder test). Whereas action was moderate,...

10.1523/jneurosci.1404-10.2010 article EN Journal of Neuroscience 2010-07-21

Striatal cholinergic interneurons (CINs) respond to salient or reward prediction-related stimuli after conditioning with brief pauses in their activity, implicating them learning and action selection. This pause is lost animal models of Parkinson's disease. How this signal regulates the striatal network remains an open question. Here, we examine impact CIN firing inhibition on glutamatergic transmission between cortex medium spiny neurons expressing dopamine D1 receptor (D1 MSNs). Brief...

10.1016/j.celrep.2022.111034 article EN cc-by-nc-nd Cell Reports 2022-07-01

Abstract Nigral depletion of the main brain antioxidant GSH is earliest biochemical event involved in Parkinson’s disease pathogenesis. Its causes are completely unknown but increasing number evidence suggests that glutamate transporters [excitatory amino acid (EAATs)] route by which precursors may enter cell. In this study, we report dopamine (DA) neurons, express excitatory carrier 1, preferentially affected EAAT dysfunction when compared with non‐DA neurons. rat embryonic mesencephalic...

10.1111/j.1471-4159.2007.05146.x article EN Journal of Neurochemistry 2007-11-27

Recent evidence points to a neuroprotective action of bee venom on nigral dopamine neurons in animal models Parkinson's disease (PD). Here we examined whether also displays symptomatic by acting the pathological functioning basal ganglia rat PD models. Bee effects were assessed combining motor behavior analyses and vivo electrophysiological recordings substantia nigra pars reticulata (SNr, output structure) pharmacological (neuroleptic treatment) lesional (unilateral intranigral...

10.1371/journal.pone.0142838 article EN cc-by PLoS ONE 2015-11-16

The long-term effects and action mechanisms of subthalamic nucleus (STN) high-frequency stimulation (HFS) for Parkinson's disease still remain poorly characterized, mainly due to the lack experimental models relevant clinical application. To address this issue, we performed a multilevel study in freely moving hemiparkinsonian rats undergoing 5-week chronic STN HFS, using portable constant-current microstimulator. In vivo metabolic neuroimaging by (1) H-magnetic resonance spectroscopy (11.7...

10.1111/jnc.13438 article EN Journal of Neurochemistry 2015-11-18

Abstract TP53INP1 is a stress-induced protein, which acts as dual positive regulator of transcription and autophagy whose deficiency has been linked with cancer metabolic syndrome. Here, we addressed the unexplored role its Drosophila homolog dDOR in maintenance neuronal homeostasis under chronic stress, focusing on dopamine (DA) neurons normal ageing- Parkinson’s disease (PD)-related context. Trp53inp1 − / mice displayed additional loss DA substantia nigra compared to wild-type (WT) mice,...

10.1038/s41419-021-03742-4 article EN cc-by Cell Death and Disease 2021-05-08
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