David Orduz

ORCID: 0000-0002-4198-2691
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Neurogenesis and neuroplasticity mechanisms
  • Ion channel regulation and function
  • Neuroscience and Neural Engineering
  • Neural dynamics and brain function
  • Photoreceptor and optogenetics research
  • Vestibular and auditory disorders
  • Genetics and Neurodevelopmental Disorders
  • Genetic Neurodegenerative Diseases
  • Anesthesia and Neurotoxicity Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Congenital heart defects research
  • Neonatal and fetal brain pathology
  • Autism Spectrum Disorder Research
  • Hearing, Cochlea, Tinnitus, Genetics
  • Pluripotent Stem Cells Research
  • Cardiac electrophysiology and arrhythmias
  • Mitochondrial Function and Pathology
  • MicroRNA in disease regulation
  • Glycogen Storage Diseases and Myoclonus
  • Advanced Memory and Neural Computing

Inserm
2015-2019

Neurophysiologie et nouvelles microscopies
2016-2019

Gfi Informatique (France)
2019

Université Paris Cité
2007-2016

Sorbonne Université
2016

Sorbonne Paris Cité
2015-2016

Délégation Paris 5
2015

Université Libre de Bruxelles
2009-2015

Brain Physiology Lab
2007

Centre National de la Recherche Scientifique
2007

Gene mutations and gene copy number variants are associated with autism spectrum disorders (ASDs). Affected products often part of signaling networks implicated in synapse formation and/or function leading to alterations the excitation/inhibition (E/I) balance. Although network parvalbumin (PV)-expressing interneurons has gained particular attention ASD, little is known on PV’s putative role respect ASD. Genetic mouse models represent powerful translational tools for studying genetic...

10.1038/tp.2015.19 article EN cc-by-nc-sa Translational Psychiatry 2015-03-10

The contribution of neuronal dysfunction to neurodegeneration is studied in a mouse model spinocerebellar ataxia type 1 (SCA1) displaying impaired motor performance ahead loss or atrophy cerebellar Purkinje cells. Presymptomatic SCA1 mice show reduction the firing rate cells (both vivo and slices) associated with efficiency main glutamatergic synapse onto increased A-type potassium current. channel Kv4.3 appears be internalized response stimulation accumulates presymptomatic mice. are...

10.1523/jneurosci.0905-11.2011 article EN cc-by-nc-sa Journal of Neuroscience 2011-08-17

NG2 cells, oligodendrocyte progenitors, receive a major synaptic input from interneurons in the developing neocortex. It is presumed that these precursors integrate cortical networks where they act as sensors of neuronal activity. We show cells somatosensory cortex form transient and structured network with follows its own rules connectivity. Fast-spiking interneurons, highly connected to target proximal subcellular domains containing GABAA receptors γ2 subunits. Conversely, non-fast-spiking...

10.7554/elife.06953 article EN cc-by eLife 2015-04-22

Striatal fast spiking interneurons (FSIs) modulate output of the striatum by synchronizing medium-sized spiny neurons (MSNs). Recent studies have broadened our understanding FSIs, showing that they are implicated in severe motor disorders such as parkinsonism, dystonia and Tourette syndrome. FSIs only striatal to express calcium-binding protein parvalbumin (PV). This selective expression PV raises questions about functional role this Ca(2+) buffer controlling FSI dynamics and, consequently,...

10.1113/jphysiol.2012.250795 article EN The Journal of Physiology 2013-04-04

The first wave of oligodendrocyte precursor cells (firstOPCs) and most GABAergic interneurons share common embryonic origins. Cortical firstOPCs are thought to be replaced by other OPC populations shortly after birth, maintaining a consistent density making postnatal interactions between ontogenetically-related unlikely. Challenging these ideas, we show that cortical firstOPC subpopulation survives forms functional cell clusters with lineage-related interneurons. Favored origin, display...

10.1038/s41467-019-11904-4 article EN cc-by Nature Communications 2019-09-18

Morphological studies have provided ample evidence for synaptic connections between cerebellar Purkinje cells (PCs), but the functional properties of these synapses remain elusive. We report on direct recordings synaptically connected PCs in mice slices. In filled with a fluorescent dye to aid axon visualization and postsynaptic target identification, presynaptic action potentials elicited unitary inhibitory currents neighboring 10% potential tested. 11 pairs, had delay onset 1.62 +/- 0.16...

10.1073/pnas.0707489104 article EN Proceedings of the National Academy of Sciences 2007-10-26

The B05 transgenic SCA1 mice, expressing human ataxin-1 with an expanded polyglutamine tract in cerebellar Purkinje cells (PCs), recapitulate many pathological and behavioral characteristics of the neurodegenerative disease spinocerebellar ataxia type 1 (SCA1), including progressive PC loss. We transplanted neural precursor (NPCs) derived from subventricular zone GFP-expressing adult mice into white matter when they showed absent (5 weeks), initial (13 significant (24 weeks) Only cell loss,...

10.1523/jneurosci.0647-09.2009 article EN cc-by-nc-sa Journal of Neuroscience 2009-10-21

Programmed cell death and early activity contribute to the emergence of functional cortical circuits. While most neuronal populations are scaled-down by death, some subpopulations entirely eliminated, raising question importance such demise for wiring. Here, we addressed this issue focusing on Cajal-Retzius neurons (CRs), key players in development that eliminated postnatal mice part via Bax-dependent apoptosis. Using Bax-conditional mutants CR hyperpolarization, show survival electrically...

10.7554/elife.50503 article EN cc-by eLife 2019-12-31

Cajal-Retzius cells (CRs), the first-born neurons in developing cerebral cortex, coordinate crucial steps construction of functional circuits. CRs are thought to be transient, as they disappear during early postnatal life both mice and humans, where their abnormal persistence is associated with pathological conditions. Embryonic comprise at least three molecularly functionally distinct subtypes: septum, ventral pallium/pallial-subpallial boundary (PSB), hem. However, whether subtype-specific...

10.1016/j.celrep.2016.11.074 article EN cc-by-nc-nd Cell Reports 2016-12-01

Calcium binding proteins, such as parvalbumin, are abundantly expressed in very distinctive patterns the central nervous system but their physiological function remains poorly understood. Notably, at level of striatum, parvalbumin is only fast spiking (FS) interneurons, which form a inhibitory network modulating output striatum by synchronizing medium-sized spiny neurons (MSN). So far existing conductance-based computational models for FS did not allow study coupling between concentration...

10.3389/fnmol.2012.00078 article EN cc-by Frontiers in Molecular Neuroscience 2012-01-01

Optogenetic and pharmacogenetic techniques have been effective to analyze the role of neuronal activity in controlling oligodendroglia lineage cells behaving juvenile adult mice. This kind studies is also high interest during early postnatal development since important changes dynamics occur first two weeks. Yet, manipulation difficult implement at an age because high-level, specific protein expression less reliable neonatal Here we describe a protocol allowing for optogenetic stimulation...

10.3389/fncel.2018.00477 article EN cc-by Frontiers in Cellular Neuroscience 2018-12-06

Purkinje cells (PC) control spike timing of neighboring PC by their recurrent axon collaterals. These synapses underlie fast cerebellar oscillations and are characterized a strong facilitation within time window <20 ms during paired-pulse protocols. express high levels the Ca(2+) buffer protein calbindin D-28k (CB). As expected from absence buffer, presynaptic action potential-evoked [Ca(2+)]i transients were previously shown to be bigger in boutons young (second postnatal week) CB-/- mice,...

10.3389/fncel.2014.00364 article EN Frontiers in Cellular Neuroscience 2014-11-05

GENERAL COMMENTARY article Front. Cell. Neurosci., 21 July 2015Sec. Non-Neuronal Cells Volume 9 - 2015 | https://doi.org/10.3389/fncel.2015.00274

10.3389/fncel.2015.00274 article EN cc-by Frontiers in Cellular Neuroscience 2015-07-21
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