The Experts below are selected from a list of 315 Experts worldwide ranked by ideXlab platform
A B Uzdensky - One of the best experts on this subject based on the ideXlab platform.
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crayfish mechanoreceptor neuron prevents photoinduced apoptosis of satellite Glial Cells
Brain Research Bulletin, 2006Co-Authors: Mikhail S Kolosov, A B UzdenskyAbstract:Abstract Interactions between neurons and glia play a key role in the development, functioning and survival of the nervous system. However, the influence of neurons on Glial Cells has received less attention than the role of glia in supporting neural functions. We here investigated the role of isolated crayfish stretch receptor neuron in the death of satellite Glial Cells under photodynamic impact. After staining with aluminum phthalocyanine photosens, the neuronal cell body was locally irradiated with a focused beam of He–Ne (633 nm, 200 W/cm 2 ) or semiconductor laser (650 nm, 50 W/cm 2 ). This rapidly abolished neuronal activity. The whole preparation was then subjected to total laser irradiation with lower intensity (633 nm, 0.3 W/cm 2 ), which induced death of Glial Cells. Double staining of the preparation with propidium iodide and Hoechst 33342 in the following 6–7 h allowed the visualization of necrotic, apoptotic and alive Cells. Previous neuron inactivation with the focused laser beam was found to increase photodynamically-induced apoptosis but not necrosis of satellite Glial Cells enwrapping the axon. Therefore, the intact neuronal cell body protected satellite Glial Cells against photoinduced apoptosis. Altogether the data indicate that mechanoreceptor neurons release some signaling molecules involved in the prevention of Glial apoptosis. This may provide integrity of the stretch receptor organ and its resistance to injurious factors.
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Photodynamic injury of isolated neuron and satellite Glial Cells: morphological study
IEEE Journal of Selected Topics in Quantum Electronics, 2003Co-Authors: D.e. Bragin, A.s. Kohany, A B UzdenskyAbstract:Potential application of photodynamic therapy (PDT) for treatment of brain tumors including gliomas is currently studied. However, PDT effect on normal Glial Cells is unknown. We have studied PDT effect using a simple model system - isolated crayfish mechanoreceptor consisting of receptor neuron and surrounding Glial Cells. Sulphonated alumophthalocyanine photosens (AlPcSn) localizes predominately in the Glial envelope around the neuron. PDT treatment with 10/sup -7/ M photosens inhibits and then irreversibly abolishes neuron activity for approximately 20 min. Then, in 1.7 h after PDT, the plasma membrane loses integrity and extracellular propidium iodide may enter into the cytosol and stain the nuclear chromatin. Neuron nucleus progressively shrinks but apoptotic nucleus fragmentation is not occurred. Such neuron death has been defined as delayed necrosis. Nuclei of the satellite Glial Cells also shrink. In 8 h after PDT treatment, some of them become fragmented that is characteristic for apoptosis, whereas others lose the plasma membrane integrity and die through necrosis. However, under PDT treatment Glial Cells not only die but also proliferate and their number is increased. This gliosis is probably aimed to neuron saving.
Magdalena Götz - One of the best experts on this subject based on the ideXlab platform.
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role of radial Glial Cells in cerebral cortex folding
Current Opinion in Neurobiology, 2014Co-Authors: Victor Borrell, Magdalena GötzAbstract:Radial Glial Cells play key roles during cerebral cortex development, as primary stem and progenitor Cells giving rise — directly or indirectly — to neurons and glia, but also acting as scaffold for the cerebral cortex architecture and migrating neurons. Recent work led to the discovery of novel types of radial Glial Cells with key roles in gyrification, the folding of the mammalian cerebral cortex in phylogeny and ontogeny. Here we summarize the cellular and molecular basis of this fascinating process allowing the expansion of the mammalian cerebral cortex with all its functional consequences.
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Potential of Glial Cells
Stem Cells Handbook, 2013Co-Authors: Magdalena Götz, Swetlana SirkoAbstract:In the adult mammalian brain, Glial Cells are among the most abundant cell type and perform many key functions in the central nervous system (CNS). MicroGlial Cells are derived from the mesoderm and are the major phagocytotic population in the adult brain. Conversely macroGlial Cells are derived from the ectoderm and comprise—astroglia, oligodendroglia, and NG2 glia. Most surprisingly, however, Glial Cells also act as stem and progenitor Cells, a role discovered about a decade ago in the developing CNS, where only a single type of glia exists, the radial glia, which are most likely precursors to the later astroglia. Intriguingly, some of these persist into the adult brain and act as adult neural stem Cells (NSCs). However, even some differentiated astroGlial Cells acquire NSC hallmarks after injury in the adult brain. Here we will review the knowledge about radial Glial Cells in the developing brain, their role in neurogenic niches of the adult brain, and the reaction of parenchymal astrocytes to injury with focus on their dedifferentiation and the features they share with radial Glial Cells and adult NSCs. This chapter therefore highlights novel sources of NSCs and their emergence from previously unexpected sites, such as the wound reaction after brain injury.
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Biology and Function of Glial Cells
Neurosciences - From Molecule to Behavior: a university textbook, 2013Co-Authors: Magdalena GötzAbstract:The nervous system is generally composed of two cell types, neurons and glia. During the evolution of nervous systems, both become more numerous, but the Glial Cells even more so than neurons. Glial Cells perform a complex panel of functions ranging from key roles in development to a diversity of functions in the adult nervous system.
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Glial Cells generate neurons the role of the transcription factor pax6
Nature Neuroscience, 2002Co-Authors: Nico Heins, Paolo Malatesta, Francesco Cecconi, Masato Nakafuku, Kerry L Tucker, M A Hack, Prisca Chapouton, Yvesalain Barde, Magdalena GötzAbstract:Radial Glial Cells, ubiquitous throughout the developing CNS, guide radially migrating neurons and are the precursors of astrocytes. Recent evidence indicates that radial Glial Cells also generate neurons in the developing cerebral cortex. Here we investigated the role of the transcription factor Pax6 expressed in cortical radial glia. We showed that radial Glial Cells isolated from the cortex of Pax6 mutant mice have a reduced neurogenic potential, whereas the neurogenic potential of non-radial Glial precursors is not affected. Consistent with defects in only one neurogenic lineage, the number of neurons in the Pax6 mutant cortex in vivo is reduced by half. Conversely, retrovirally mediated Pax6 expression instructs neurogenesis even in astrocytes from postnatal cortex in vitro. These results demonstrated an important role of Pax6 as intrinsic fate determinant of the neurogenic potential of Glial Cells.
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isolation of radial Glial Cells by fluorescent activated cell sorting reveals a neuronal lineage
Development, 2000Co-Authors: Paolo Malatesta, Eva Hartfuss, Magdalena GötzAbstract:The developing central nervous system of vertebrates contains an abundant cell type designated radial Glial Cells. These Cells are known as guiding cables for migrating neurons, while their role as precursor Cells is less clear. Since radial Glial Cells express a variety of astroGlial characteristics and differentiate as astrocytes after completing their guidance function, they have been considered as part of the Glial lineage. Using fluorescence-activated cell sorting, we show here that radial Glial Cells also are neuronal precursors and only later, after neurogenesis, do they shift towards an exclusive generation of astrocytes. These results thus demonstrate a novel function for radial Glial Cells, namely their ability to generate two major cell types found in the nervous system, neurons and astrocytes.
Kalipada Pahan - One of the best experts on this subject based on the ideXlab platform.
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regulation of inducible nitric oxide synthase gene in Glial Cells
Antioxidants & Redox Signaling, 2006Co-Authors: Ramendra N Saha, Kalipada PahanAbstract:Elevated levels of NO produced within the central nervous system (CNS) are associated with the pathogenesis of neuroinflammatory and neurodegenerative human diseases such as multiple sclerosis, HIV dementia, brain ischemia, trauma, Parkinson's disease, and Alzheimer's disease. Resident Glial Cells in the CNS (astroglia and microglia) express inducible nitric oxide synthase (iNOS) and produce high levels of NO in response to a wide variety of proinflammatory and degenerative stimuli. Although pathways resulting in the expression of iNOS may vary in two different Glial Cells of different species, the intracellular signaling events required for the expression of iNOS in these Cells are slowly becoming clear. Various signaling cascades converge to activate several transcription factors that control the transcription of iNOS in Glial Cells. The present review summarizes different results and discusses current understandings about signaling mechanisms for the induction of iNOS expression in activated Glial cell...
Ramendra N Saha - One of the best experts on this subject based on the ideXlab platform.
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regulation of inducible nitric oxide synthase gene in Glial Cells
Antioxidants & Redox Signaling, 2006Co-Authors: Ramendra N Saha, Kalipada PahanAbstract:Elevated levels of NO produced within the central nervous system (CNS) are associated with the pathogenesis of neuroinflammatory and neurodegenerative human diseases such as multiple sclerosis, HIV dementia, brain ischemia, trauma, Parkinson's disease, and Alzheimer's disease. Resident Glial Cells in the CNS (astroglia and microglia) express inducible nitric oxide synthase (iNOS) and produce high levels of NO in response to a wide variety of proinflammatory and degenerative stimuli. Although pathways resulting in the expression of iNOS may vary in two different Glial Cells of different species, the intracellular signaling events required for the expression of iNOS in these Cells are slowly becoming clear. Various signaling cascades converge to activate several transcription factors that control the transcription of iNOS in Glial Cells. The present review summarizes different results and discusses current understandings about signaling mechanisms for the induction of iNOS expression in activated Glial cell...
Richard Robitaille - One of the best experts on this subject based on the ideXlab platform.
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gabaergic network activation of Glial Cells underlies hippocampal heterosynaptic depression
The Journal of Neuroscience, 2006Co-Authors: Alexandre Serrano, Nasser Haddjeri, Jeanclaude Lacaille, Richard RobitailleAbstract:Tetanus-induced heterosynaptic depression in the hippocampus is a key cellular mechanism in neural networks implicated in learning and memory. A growing body of evidence indicates that Glial Cells are important modulators of synaptic functions, but very little is known about their role in heterosynaptic plasticity. We examined the role of Glial Cells in heterosynaptic depression, knowing that tetanization and NMDA application caused depression of synaptic field responses (fEPSPs) and induced Ca 2+ rise in Glial Cells. Here we report that chelating Ca 2+ in a Glial syncytium interfered with heterosynaptic depression and NMDA-induced fEPSP depression, suggesting that Ca 2+ activation of Glial Cells is necessary for heterosynaptic depression. The NMDA-induced Ca 2+ rise in Glial Cells was sensitive to tetrodotoxin and reduced by the GABA B antagonist CGP55845. Both heterosynaptic depression and simultaneous Ca 2+ activation of Glial Cells were prevented by CGP55845, suggesting an involvement of the GABAergic network in Glial activation and heterosynaptic depression. Also, the GABA B agonist baclofen caused both a Ca 2+ rise in Glial Cells and fEPSP depression. Heterosynaptic depression, as well as NMDA- and baclofen-induced depression, were attenuated by an A 1 antagonist, cyclopentyl-theophylline, whereas Glial cell activation was not, indicating a role of adenosine downstream of Glial activation. Finally, heterosynaptic depression requires ATP degradation because ectonucleotidase inhibitors reduced this plasticity. Our work indicates that Ca 2+ activation of Glial Cells is necessary for heterosynaptic depression, which involves the sequential interaction of Schaffer collaterals, the GABAergic network, and glia. Thus, Glial and neuronal networks are functionally associated during the genesis of heterosynaptic plasticity at mammalian central excitatory synapses.
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Glial Cells in synaptic plasticity.
Journal of physiology Paris, 2006Co-Authors: Keith J Todd, Jeanclaude Lacaille, Alexandre Serrano, Richard RobitailleAbstract:Plasticity of synaptic transmission is believed to be the cellular basis for learning and memory, and depends upon different pre- and post-synaptic neuronal mechanisms. Recently, however, an increasing number of studies have implicated a third element in plasticity; the perisynaptic Glial cell. Originally Glial Cells were thought to be important for metabolic maintenance and support of the nervous system. However, work in the past decade has clearly demonstrated active involvement of glia in stability and overall nervous system function as well as synaptic plasticity. Through specific modulation of Glial cell function, a wide variety of roles for glia in synaptic plasticity have been uncovered. Furthermore, interesting circumstantial evidence suggests a Glial involvement in multiple other types of plasticity. We will discuss recent advances in neuron-Glial interactions that take place during synaptic plasticity and explore different plasticity phenomena in which Glial Cells may be involved.
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Glial Cells and neurotransmission an inclusive view of synaptic function
Neuron, 2003Co-Authors: Daniel S Auld, Richard RobitailleAbstract:Glial Cells throughout the nervous system are closely associated with synapses. Accompanying these anatomical couplings are intriguing functional interactions, including the capacity of certain Glial Cells to respond to and modulate neurotransmission. Glial Cells can also help establish, maintain, and reconstitute synapses. In this review, we discuss evidence indicating that Glial Cells make important contributions to synaptic function.