A5056953658- Neurogenesis and neuroplasticity mechanisms
- Neuroscience and Neuropharmacology Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Ion channel regulation and function
- MicroRNA in disease regulation
- Ion Transport and Channel Regulation
- Connexins and lens biology
- Ion Channels and Receptors
- Epigenetics and DNA Methylation
- Hedgehog Signaling Pathway Studies
- Axon Guidance and Neuronal Signaling
- Neurological Disease Mechanisms and Treatments
- Nerve injury and regeneration
- Regulation of Appetite and Obesity
- RNA and protein synthesis mechanisms
- Neuroscience and Neural Engineering
- Circadian rhythm and melatonin
- 3D Printing in Biomedical Research
- Biochemical Analysis and Sensing Techniques
- Biochemical effects in animals
- Autism Spectrum Disorder Research
- Medicinal Plant Pharmacodynamics Research
- Cardiac electrophysiology and arrhythmias
- Mesenchymal stem cell research
- Caveolin-1 and cellular processes
Czech Academy of Sciences, Institute of Experimental Medicine
2010-2024
Inserm
2022-2024
Collège de France
2022-2024
Université Paris Sciences et Lettres
2022-2024
Centre National de la Recherche Scientifique
2022-2024
Wellcome/MRC Cambridge Stem Cell Institute
2019-2024
University of Cambridge
2019-2024
Charles University
2010-2024
Centre Interdisciplinaire de Recherche en Biologie
2022-2024
Medical Research Council
2019-2021
Abstract Fragile X syndrome (FXS) is an inherited form of intellectual disability caused by the loss mRNA-binding fragile mental retardation protein (FMRP). FXS characterized neuronal hyperexcitability and behavioral defects, however mechanisms underlying these critical dysfunctions remain unclear. Here, using male Fmr1 knockout mouse model FXS, we identify abnormal extracellular potassium homeostasis, along with impaired channel Kir4.1 expression function in astrocytes. Further, reveal that...
The mediobasal hypothalamus (MBH; arcuate nucleus of the [ARH] and median eminence [ME]) is a key nutrient sensing site for production complex homeostatic feedback responses required maintenance energy balance. Here, we show that refeeding after an overnight fast rapidly triggers proliferation differentiation oligodendrocyte progenitors, leading to new oligodendrocytes in ME specifically. During this nutritional paradigm, perineuronal nets (PNNs), emerging regulators ARH metabolic functions,...
Throughout the brain, astrocytes form networks mediated by gap junction channels that promote activity of neuronal ensembles. Although their inputs on information processing are well established, how molecular shape network patterns remains unclear. Here, using astroglial connexin-deficient mice, in which disconnected and bursting abnormal, we show astrocyte strengthen via dynamic regulation extracellular potassium levels, independently glutamate homeostasis or metabolic support. Using a...
To understand the structural alterations that underlie early and late changes in hippocampal diffusivity after hypoxia/ischemia (H/I), apparent diffusion coefficient of water (ADC W ) were studied 8-week-old rats H/I using diffusion-weighted magnetic resonance imaging (DW-MRI). In CA1 region, ADC analyses performed during 6 months reperfusion compared with cell number/cell-type composition, glial morphology, extracellular space (ECS) parameters obtained by real-time iontophoretic method....
The ethacrynic acid derivative, 4-(2-butyl-6,7-dichlor-2-cyclopentylindan-1-on-5-yl) oxobutyric (DCPIB) is considered to be a specific and potent inhibitor of volume-regulated anion channels (VRACs). In the CNS, DCPIB was shown neuroprotective through mechanisms principally associated its action on VRACs. We hypothesized that could also regulate activity other astroglial involved in cell volume homeostasis.Experiments were performed rat cortical astrocytes primary culture hippocampal situ....
Recently, we have identified two astrocytic subpopulations in the cortex of GFAP-EGFP mice, which astrocytes are visualized by enhanced green-fluorescent protein (EGFP) under control human glial fibrillary acidic (GFAP) promotor. These subpopulations, termed high response- (HR-) and low (LR-) astrocytes, differed extent their swelling during oxygen-glucose deprivation (OGD). In present study focused on identifying ion channels or transporters that might underlie different capabilities these...
Polydendrocytes (also known as NG2 glial cells) constitute a fourth major cell type in the adult mammalian central nervous system (CNS) that is distinct from other types. Although much evidence suggests these cells are multipotent vitro, their differentiation potential vivo under physiological or pathophysiological conditions still controversial. To follow fate of polydendrocytes after CNS pathology, permanent middle cerebral artery occlusion (MCAo), commonly used model focal ischemia, was...
Astrocytes respond to ischemic brain injury by proliferation, the increased expression of intermediate filaments and hypertrophy, which results in glial scar formation. In addition, they alter ion channels, receptors transporters that maintain ionic/neurotransmitter homeostasis. Here, we aimed demonstrate Hcn1-4 genes encoding hyperpolarization-activated cyclic nucleotide-gated (HCN) channels reactive astrocytes following focal cerebral ischemia (FCI) or global (GCI) characterize their...
The proper function of the nervous system is dependent on balance ions and water between intracellular extracellular space (ECS). It has been suggested that interaction aquaporin-4 (AQP4) transient receptor potential vaniloid isoform 4 (TRPV4) channels play a role in cell volume regulation, indirectly, ECS volume. Using real-time iontophoretic method, we studied changes diffusion parameters: fraction α (α = fraction/total tissue volume) tortuosity λ (λ2 free/apparent coefficient) mice with...
Abstract The cerebral cortex develops from dorsal forebrain neuroepithelial progenitor cells. Following the initial expansion of cell pool, these cells generate neurons all cortical layers and then astrocytes oligodendrocytes. Yet, regulatory pathways that control maintenance pool are currently unknown. Here we define six basic pathway components regulate proliferation cortically specified human stem (cNESCs) in vitro without loss developmental potential. We show activation FGF inhibition...
Accumulating evidence indicates that increased intracellular Na(+) concentration ([Na(+) ]i ) in astroglial cells is associated with the development of brain edema under ischemic conditions, but underlying mechanisms are still elusive. Here, we report primary cultured rat cortical astrocytes, elevations [Na(+) reflecting those achieved during ischemia cause a marked decrease hypotonicity-evoked current mediated by volume-regulated anion channel (VRAC). Pharmacological manipulations revealed...
Summary The cerebral cortex develops from dorsal forebrain neuroepithelial progenitor cells. Initial expansion of the cell pool is followed by generation neurons all cortical layers and later, astrocytes oligodendrocytes. However, regulatory pathways that control maintenance are currently unknown. Here we define six basic pathway components regulate proliferation cortically specified human stem cells (cNESCs) in vitro without loss developmental potential. We show activation FGF inhibition...
Abstract Throughout the brain, astrocytes form networks mediated by gap-junction channels that promote activity of neuronal ensembles. Although their inputs on information processing are well established, how molecularly gap junction shape network patterns remains unclear. Here using astroglial connexin-deficient mice, in which disconnected and bursting abnormal, we found astrocyte strengthen via dynamic regulation extracellular potassium levels, independently glutamate homeostasis or...
Posters639age of both pre-and postsynaptic structures.The revealed ultrastructural changes were prevented by the application NMDA receptor antagonist, D-AP5.Conclusion: These data provide evidence dynamic, activity-dependent interactions between processes glial cells and their partners suggest that glia can participate in activity-induced structural synapse remodeling.