Articles de revues : « Cellule neuronali »

1

Lledo, Pierre-Marie. « Cellules souches neuronales ». Morphologie 99, n^o 327 (décembre 2015) : 154. http://dx.doi.org/10.1016/j.morpho.2015.09.012.

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Corner, M. A. « Neuronal and cellular oscillators ». Journal of the Neurological Sciences 92, n^o 2-3 (septembre 1989) : 349. http://dx.doi.org/10.1016/0022-510x(89)90150-0.

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Korn, H. « Neuronal and cellular oscillators ». Biochimie 72, n^o 5 (mai 1990) : 376. http://dx.doi.org/10.1016/0300-9084(90)90037-h.

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Young, Fraser I., Vsevolod Telezhkin, Sarah J. Youde, Martin S. Langley, Maria Stack, Paul J. Kemp, Rachel J. Waddington, Alastair J. Sloan et Bing Song. « Clonal Heterogeneity in the Neuronal and Glial Differentiation of Dental Pulp Stem/Progenitor Cells ». Stem Cells International 2016 (2016) : 1–10. http://dx.doi.org/10.1155/2016/1290561.

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Cellular heterogeneity presents an important challenge to the development of cell-based therapies where there is a fundamental requirement for predictable and reproducible outcomes. Transplanted Dental Pulp Stem/Progenitor Cells (DPSCs) have demonstrated early promise in experimental models of spinal cord injury and stroke, despite limited evidence of neuronal and glial-like differentiation after transplantation. Here, we report, for the first time, on the ability of single cell-derived clonal cultures of murine DPSCs to differentiatein vitrointo immature neuronal-like and oligodendrocyte-like cells. Importantly, only DPSC clones with high nestin mRNA expression levels were found to successfully differentiate into Map2 and NF-positive neuronal-like cells. Neuronally differentiated DPSCs possessed a membrane capacitance comparable with primary cultured striatal neurons and small inward voltage-activated K+but not outward Na+currents were recorded suggesting a functionally immature phenotype. Similarly, only high nestin-expressing clones demonstrated the ability to adopt Olig1, Olig2, and MBP-positive immature oligodendrocyte-like phenotype. Together, these results demonstrate that appropriate markers may be used to provide an early indication of the suitability of a cell population for purposes where differentiation into a specific lineage may be beneficial and highlight that further understanding of heterogeneity within mixed cellular populations is required.

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Wylie, Steven R., et Peter D. Chantler. « Myosin IIC : A Third Molecular Motor Driving Neuronal Dynamics ». Molecular Biology of the Cell 19, n^o 9 (septembre 2008) : 3956–68. http://dx.doi.org/10.1091/mbc.e07-08-0744.

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Neuronal dynamics result from the integration of forces developed by molecular motors, especially conventional myosins. Myosin IIC is a recently discovered nonsarcomeric conventional myosin motor, the function of which is poorly understood, particularly in relation to the separate but coupled activities of its close homologues, myosins IIA and IIB, which participate in neuronal adhesion, outgrowth and retraction. To determine myosin IIC function, we have applied a comparative functional knockdown approach by using isoform-specific antisense oligodeoxyribonucleotides to deplete expression within neuronally derived cells. Myosin IIC was found to be critical for driving neuronal process outgrowth, a function that it shares with myosin IIB. Additionally, myosin IIC modulates neuronal cell adhesion, a function that it shares with myosin IIA but not myosin IIB. Consistent with this role, myosin IIC knockdown caused a concomitant decrease in paxillin-phospho-Tyr118 immunofluorescence, similar to knockdown of myosin IIA but not myosin IIB. Myosin IIC depletion also created a distinctive phenotype with increased cell body diameter, increased vacuolization, and impaired responsiveness to triggered neurite collapse by lysophosphatidic acid. This novel combination of properties suggests that myosin IIC must participate in distinctive cellular roles and reinforces our view that closely related motor isoforms drive diverse functions within neuronal cells.

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Boulant, Jack A. « Cellular mechanisms of neuronal thermosensitivity ». Journal of Thermal Biology 24, n^o 5-6 (octobre 1999) : 333–38. http://dx.doi.org/10.1016/s0306-4565(99)00038-8.

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Agnati, Luigi F., Diego Guidolin, Chiara Carone, Mauro Dam, Susanna Genedani et Kjell Fuxe. « Understanding neuronal molecular networks builds on neuronal cellular network architecture ». Brain Research Reviews 58, n^o 2 (août 2008) : 379–99. http://dx.doi.org/10.1016/j.brainresrev.2007.11.002.

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Lillycrop, K. A., Y. Z. Liu, T. Theil, T. Möröy et D. S. Latchman. « Activation of the herpes simplex virus immediate-early gene promoters by neuronally expressed POU family transcription factors ». Biochemical Journal 307, n^o 2 (15 avril 1995) : 581–84. http://dx.doi.org/10.1042/bj3070581.

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Herpes simplex virus immediate-early (IE) promoters contain the TAATGARAT motif which acts as a target site for the cellular POU family transcription factors Oct-1 and Oct-2. Here we show that other members of the POU family that are expressed in sensory neurons can also affect IE promoter activity. In particular, two members of the Brn-3 family of POU proteins Brn-3a and Brn-3c can activate the IE-1 and IE-3 promoters when co-transfected into fibroblasts and neuronal cells whereas a third member Brn-3b represses IE promoter activity. In contrast, Brn-3 proteins cannot overcome the inhibitory effect of neuronal Oct-2 on IE promoter activity in co-transfections nor do they prevent transactivation of the IE promoters by the Oct-1-Vmw65 complex. The potential regulation of the IE promoters by several different neuronally expressed POU proteins during the initiation, maintenance and re-activation of latent infection in sensory neurons is discussed.

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Dale, Nicholas. « Neuronal and cellular oscillators (cellular clocks series, vol. 2) ». Trends in Neurosciences 12, n^o 12 (janvier 1989) : 521–22. http://dx.doi.org/10.1016/0166-2236(89)90114-8.

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Kristan,, William B. « Neuronal and Cellular Oscillators.Jon W. Jacklet ». Quarterly Review of Biology 65, n^o 1 (mars 1990) : 73–74. http://dx.doi.org/10.1086/416613.

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Bignami, F., P. Bevilacqua, S. Biagioni, A. De Jaco, F. Casamenti, A. Felsani et G. Augusti-Tocco. « Cellular Acetylcholine Content and Neuronal Differentiation ». Journal of Neurochemistry 69, n^o 4 (octobre 1997) : 1374–81. http://dx.doi.org/10.1046/j.1471-4159.1997.69041374.x.

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Powell, Sharon K., et Hynda K. Kleinman. « Neuronal laminins and their cellular receptors ». International Journal of Biochemistry & ; Cell Biology 29, n^o 3 (mars 1997) : 401–14. http://dx.doi.org/10.1016/s1357-2725(96)00110-0.

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Bowie, Derek, et David Attwell. « Coupling cellular metabolism to neuronal signalling ». Journal of Physiology 593, n^o 16 (14 août 2015) : 3413–15. http://dx.doi.org/10.1113/jp271075.

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Trube, G., et R. Netzer. « Dextromethorphan : Cellular Effects Reducing Neuronal Hyperactivity ». Epilepsia 35, s5 (octobre 1994) : S62—S67. http://dx.doi.org/10.1111/j.1528-1157.1994.tb05972.x.

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Wright, Kevin M., Michael W. Linhoff, Patrick Ryan Potts et Mohanish Deshmukh. « Decreased apoptosome activity with neuronal differentiation sets the threshold for strict IAP regulation of apoptosis ». Journal of Cell Biology 167, n^o 2 (25 octobre 2004) : 303–13. http://dx.doi.org/10.1083/jcb.200406073.

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Despite the potential of the inhibitor of apoptosis proteins (IAPs) to block cytochrome c–dependent caspase activation, the critical function of IAPs in regulating mammalian apoptosis remains unclear. We report that the ability of endogenous IAPs to effectively regulate caspase activation depends on the differentiation state of the cell. Despite being expressed at equivalent levels, endogenous IAPs afforded no protection against cytochrome c–induced apoptosis in naïve pheochromocytoma (PC12) cells, but were remarkably effective in doing so in neuronally differentiated cells. Neuronal differentiation was also accompanied with a marked reduction in Apaf-1, resulting in a significant decrease in apoptosome activity. Importantly, this decrease in Apaf-1 protein was directly linked to the increased ability of IAPs to stringently regulate apoptosis in neuronally differentiated PC12 and primary cells. These data illustrate specifically how the apoptotic pathway acquires increased regulation with cellular differentiation, and are the first to show that IAP function and apoptosome activity are coupled in cells.

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Henley, Jeremy M., Tim J. Craig et Kevin A. Wilkinson. « Neuronal SUMOylation : Mechanisms, Physiology, and Roles in Neuronal Dysfunction ». Physiological Reviews 94, n^o 4 (octobre 2014) : 1249–85. http://dx.doi.org/10.1152/physrev.00008.2014.

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Protein SUMOylation is a critically important posttranslational protein modification that participates in nearly all aspects of cellular physiology. In the nearly 20 years since its discovery, SUMOylation has emerged as a major regulator of nuclear function, and more recently, it has become clear that SUMOylation has key roles in the regulation of protein trafficking and function outside of the nucleus. In neurons, SUMOylation participates in cellular processes ranging from neuronal differentiation and control of synapse formation to regulation of synaptic transmission and cell survival. It is a highly dynamic and usually transient modification that enhances or hinders interactions between proteins, and its consequences are extremely diverse. Hundreds of different proteins are SUMO substrates, and dysfunction of protein SUMOylation is implicated in a many different diseases. Here we briefly outline core aspects of the SUMO system and provide a detailed overview of the current understanding of the roles of SUMOylation in healthy and diseased neurons.

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Sweeney, Marva I., Wolfgang Waiz, Jerome Y. Yager et Bernhard Juurlink. « Cellular mechanisms involved in brain ischemia ». Canadian Journal of Physiology and Pharmacology 73, n^o 11 (1 novembre 1995) : 1525–35. http://dx.doi.org/10.1139/y95-211.

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Cellular mechanisms, both destructive and protective, that are associated with cerebral ischemia are reviewed in this paper. Central to understanding the evolution of stroke are the concepts of ischemic core and surrounding penumbral region damage, delayed neuronal death, and neuronal rescue. The role of spreading depression in the evolution of subsequent ATP depletion, ion shifts, glutamate release, activation of glutamate receptors, intracellular Ca2+ changes, and generation of reactive oxygen species in the penumbra in relationship to neuronal and glial cell damage are discussed. We conclude that the most fruitful areas for future stroke research include traditional approaches as well as novel approaches. Traditional approaches include stroke prevention and examination of the effects of combinations of proven and promising effective therapeutic interventions. Novel approaches include delineating mechanisms whereby growth factors and compounds such as deprenyl and staurosporine afford neuroprotection, ultimately leading to direct manipulation of the signal transduction pathways that lead to neuronal dysfunction and death. This includes determining which genes are activated and repressed in specific response to hypoxia–ischemia and determining how such alterations in gene expression affect survival and function of neurons. We also suggest that advantage be taken of the blood–brain barrier compromise during stroke in designing neuroprotective therapies.Key words: development and ageing, free radicals, neural protection, signal transduction, spreading depression, stroke.

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Bentley, Marvin, et Gary Banker. « The cellular mechanisms that maintain neuronal polarity ». Nature Reviews Neuroscience 17, n^o 10 (11 août 2016) : 611–22. http://dx.doi.org/10.1038/nrn.2016.100.

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Phiwchai, Isara, Watchareeporn Chariyarangsitham, Thipjutha Phatruengdet et Chalermchai Pilapong. « Ferric–Tannic Nanoparticles Increase Neuronal Cellular Clearance ». ACS Chemical Neuroscience 10, n^o 9 (29 juillet 2019) : 4136–44. http://dx.doi.org/10.1021/acschemneuro.9b00345.

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Duane, Gregory S. « A “cellular neuronal” approach to optimization problems ». Chaos : An Interdisciplinary Journal of Nonlinear Science 19, n^o 3 (septembre 2009) : 033114. http://dx.doi.org/10.1063/1.3184829.

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Ramdial, Kristina, Maria Clara Franco et Alvaro G. Estevez. « Cellular mechanisms of peroxynitrite-induced neuronal death ». Brain Research Bulletin 133 (juillet 2017) : 4–11. http://dx.doi.org/10.1016/j.brainresbull.2017.05.008.

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Herzog, Nitzan, Mark Shein-Idelson et Yael Hanein. « Optical validation ofin vitroextra-cellular neuronal recordings ». Journal of Neural Engineering 8, n^o 5 (12 août 2011) : 056008. http://dx.doi.org/10.1088/1741-2560/8/5/056008.

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Greengard, Paul. « Neuronal phosphoproteins ». Molecular Neurobiology 1, n^o 1-2 (mars 1987) : 81–119. http://dx.doi.org/10.1007/bf02935265.

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Zott, Benedikt, Marc Aurel Busche, Reisa A. Sperling et Arthur Konnerth. « What Happens with the Circuit in Alzheimer's Disease in Mice and Humans ? » Annual Review of Neuroscience 41, n^o 1 (8 juillet 2018) : 277–97. http://dx.doi.org/10.1146/annurev-neuro-080317-061725.

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A major mystery of many types of neurological and psychiatric disorders, such as Alzheimer's disease (AD), remains the underlying, disease-specific neuronal damage. Because of the strong interconnectivity of neurons in the brain, neuronal dysfunction necessarily disrupts neuronal circuits. In this article, we review evidence for the disruption of large-scale networks from imaging studies of humans and relate it to studies of cellular dysfunction in mouse models of AD. The emerging picture is that some forms of early network dysfunctions can be explained by excessively increased levels of neuronal activity. The notion of such neuronal hyperactivity receives strong support from in vivo and in vitro cellular imaging and electrophysiological recordings in the mouse, which provide mechanistic insights underlying the change in neuronal excitability. Overall, some key aspects of AD-related neuronal dysfunctions in humans and mice are strikingly similar and support the continuation of such a translational strategy.

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Curiel, Julian, Guillermo Rodríguez Bey, Asako Takanohashi, Marianna Bugiani, Xiaoqin Fu, Nicole I. Wolf, Bruce Nmezi et al. « TUBB4A mutations result in specific neuronal and oligodendrocytic defects that closely match clinically distinct phenotypes ». Human Molecular Genetics 26, n^o 22 (29 août 2017) : 4506–18. http://dx.doi.org/10.1093/hmg/ddx338.

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Abstract Hypomyelinating leukodystrophies are heritable disorders defined by lack of development of brain myelin, but the cellular mechanisms of hypomyelination are often poorly understood. Mutations in TUBB4A, encoding the tubulin isoform tubulin beta class IVA (Tubb4a), result in the symptom complex of hypomyelination with atrophy of basal ganglia and cerebellum (H-ABC). Additionally, TUBB4A mutations are known to result in a broad phenotypic spectrum, ranging from primary dystonia (DYT4), isolated hypomyelination with spastic quadriplegia, and an infantile onset encephalopathy, suggesting multiple cell types may be involved. We present a study of the cellular effects of TUBB4A mutations responsible for H-ABC (p.Asp249Asn), DYT4 (p.Arg2Gly), a severe combined phenotype with hypomyelination and encephalopathy (p.Asn414Lys), as well as milder phenotypes causing isolated hypomyelination (p.Val255Ile and p.Arg282Pro). We used a combination of histopathological, biochemical and cellular approaches to determine how these different mutations may have variable cellular effects in neurons and/or oligodendrocytes. Our results demonstrate that specific mutations lead to either purely neuronal, combined neuronal and oligodendrocytic or purely oligodendrocytic defects that closely match their respective clinical phenotypes. Thus, the DYT4 mutation that leads to phenotypes attributable to neuronal dysfunction results in altered neuronal morphology, but with unchanged tubulin quantity and polymerization, with normal oligodendrocyte morphology and myelin gene expression. Conversely, mutations associated with isolated hypomyelination (p.Val255Ile and p.Arg282Pro) and the severe combined phenotype (p.Asn414Lys) resulted in normal neuronal morphology but were associated with altered oligodendrocyte morphology, myelin gene expression, and microtubule dysfunction. The H-ABC mutation (p.Asp249Asn) that exhibits a combined neuronal and myelin phenotype had overlapping cellular defects involving both neuronal and oligodendrocyte cell types in vitro. Only mutations causing hypomyelination phenotypes showed altered microtubule dynamics and acted through a dominant toxic gain of function mechanism. The DYT4 mutation had no impact on microtubule dynamics suggesting a distinct mechanism of action. In summary, the different clinical phenotypes associated with TUBB4A reflect the selective and specific cellular effects of the causative mutations. Cellular specificity of disease pathogenesis is relevant to developing targeted treatments for this disabling condition.

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Xue, Bingzhong, Thomas Pulinilkunnil, Incoronata Murano, Kendra K. Bence, Huamei He, Yasuhiko Minokoshi, Kenji Asakura et al. « Neuronal Protein Tyrosine Phosphatase 1B Deficiency Results in Inhibition of Hypothalamic AMPK and Isoform-Specific Activation of AMPK in Peripheral Tissues ». Molecular and Cellular Biology 29, n^o 16 (15 juin 2009) : 4563–73. http://dx.doi.org/10.1128/mcb.01914-08.

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ABSTRACT PTP1B−/− mice are resistant to diet-induced obesity due to leptin hypersensitivity and consequent increased energy expenditure. We aimed to determine the cellular mechanisms underlying this metabolic state. AMPK is an important mediator of leptin's metabolic effects. We find that α1 and α2 AMPK activity are elevated and acetyl-coenzyme A carboxylase activity is decreased in the muscle and brown adipose tissue (BAT) of PTP1B−/− mice. The effects of PTP1B deficiency on α2, but not α1, AMPK activity in BAT and muscle are neuronally mediated, as they are present in neuron- but not muscle-specific PTP1B−/− mice. In addition, AMPK activity is decreased in the hypothalamic nuclei of neuronal and whole-body PTP1B−/− mice, accompanied by alterations in neuropeptide expression that are indicative of enhanced leptin sensitivity. Furthermore, AMPK target genes regulating mitochondrial biogenesis, fatty acid oxidation, and energy expenditure are induced with PTP1B inhibition, resulting in increased mitochondrial content in BAT and conversion to a more oxidative muscle fiber type. Thus, neuronal PTP1B inhibition results in decreased hypothalamic AMPK activity, isoform-specific AMPK activation in peripheral tissues, and downstream gene expression changes that promote leanness and increased energy expenditure. Therefore, the mechanism by which PTP1B regulates adiposity and leptin sensitivity likely involves the coordinated regulation of AMPK in hypothalamus and peripheral tissues.

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Anderson, Alexandra, et Rachel McMullan. « Neuronal and non-neuronal signals regulate Caernorhabditis elegans avoidance of contaminated food ». Philosophical Transactions of the Royal Society B : Biological Sciences 373, n^o 1751 (4 juin 2018) : 20170255. http://dx.doi.org/10.1098/rstb.2017.0255.

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One way in which animals minimize the risk of infection is to reduce their contact with contaminated food. Here, we establish a model of pathogen-contaminated food avoidance using the nematode worm Caernorhabditis elegans . We find that avoidance of pathogen-contaminated food protects C. elegans from the deleterious effects of infection and, using genetic approaches, demonstrate that multiple sensory neurons are required for this avoidance behaviour. In addition, our results reveal that the avoidance of contaminated food requires bacterial adherence to non-neuronal cells in the tail of C. elegans that are also required for the cellular immune response. Previous studies in C. elegans have contributed significantly to our understanding of molecular and cellular basis of host–pathogen interactions and our model provides a unique opportunity to gain basic insights into how animals avoid contaminated food. This article is part of the Theo Murphy meeting issue ‘Evolution of pathogen and parasite avoidance behaviours’.

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Won, Seok-Joon, Doo-Yeon Kim et Byoung-Joo Gwag. « Cellular and Molecular Pathways of Ischemic Neuronal Death ». BMB Reports 35, n^o 1 (31 janvier 2002) : 67–86. http://dx.doi.org/10.5483/bmbrep.2002.35.1.067.

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Stetler, R., Y. Gao, A. Signore, G. Cao et J. Chen. « HSP27 : Mechanisms of Cellular Protection Against Neuronal Injury ». Current Molecular Medicine 9, n^o 7 (1 septembre 2009) : 863–72. http://dx.doi.org/10.2174/156652409789105561.

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Morimune, Takao, Ayami Tano, Yuya Tanaka, Haruka Yukiue, Takefumi Yamamoto, Ikuo Tooyama, Yoshihiro Maruo, Masaki Nishimura et Masaki Mori. « Gm14230 controls Tbc1d24 cytoophidia and neuronal cellular juvenescence ». PLOS ONE 16, n^o 4 (22 avril 2021) : e0248517. http://dx.doi.org/10.1371/journal.pone.0248517.

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It is not fully understood how enzymes are regulated in the tiny reaction field of a cell. Several enzymatic proteins form cytoophidia, a cellular macrostructure to titrate enzymatic activities. Here, we show that the epileptic encephalopathy-associated protein Tbc1d24 forms cytoophidia in neuronal cells both in vitro and in vivo. The Tbc1d24 cytoophidia are distinct from previously reported cytoophidia consisting of inosine monophosphate dehydrogenase (Impdh) or cytidine-5’-triphosphate synthase (Ctps). Tbc1d24 cytoophidia is induced by loss of cellular juvenescence caused by depletion of Gm14230, a juvenility-associated lncRNA (JALNC) and zeocin treatment. Cytoophidia formation is associated with impaired enzymatic activity of Tbc1d24. Thus, our findings reveal the property of Tbc1d24 to form cytoophidia to maintain neuronal cellular juvenescence.

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Teichert, Russell W. « Investigating neuronal cell types through comparative cellular physiology ». Temperature 1, n^o 1 (24 juin 2014) : 22–23. http://dx.doi.org/10.4161/temp.29540.

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MOUILLET-RICHARD, S., B. SCHNEIDER, E. PRADINES, M. PIETRI, M. ERMONVAL, J. GRASSI, J. G. RICHARDS, V. MUTEL, J. M. LAUNAY et O. KELLERMANN. « Cellular Prion Protein Signaling in Serotonergic Neuronal Cells ». Annals of the New York Academy of Sciences 1096, n^o 1 (1 janvier 2007) : 106–19. http://dx.doi.org/10.1196/annals.1397.076.

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Bonzanni, Mattia, Nicolas Rouleau, Michael Levin et David L. Kaplan. « Optogenetically induced cellular habituation in non-neuronal cells ». PLOS ONE 15, n^o 1 (17 janvier 2020) : e0227230. http://dx.doi.org/10.1371/journal.pone.0227230.

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Kazantsev, A. G. « Cellular pathways leading to neuronal dysfunction and degeneration ». Drug News & ; Perspectives 20, n^o 8 (2007) : 501. http://dx.doi.org/10.1358/dnp.2007.20.8.1157616.

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Cannon, JingJing F., William H. Barnett et Gennady S. Cymbalyuk. « Cellular mechanisms generating bursting activity in neuronal networks ». BMC Neuroscience 15, Suppl 1 (2014) : P182. http://dx.doi.org/10.1186/1471-2202-15-s1-p182.

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Senior, Kathryn. « Discrete cellular entry points discovered in neuronal membrane ». Lancet Neurology 1, n^o 8 (décembre 2002) : 467. http://dx.doi.org/10.1016/s1474-4422(02)00251-x.

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MAIESE, KENNETH. « Neuronal Survival : Cellular and Molecular Pathways of Protection ». Annals of the New York Academy of Sciences 835, n^o 1 Frontiers of (décembre 1997) : 255–73. http://dx.doi.org/10.1111/j.1749-6632.1997.tb48636.x.

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Boulanger, Lisa M., Gene S. Huh et Carla J. Shatz. « Neuronal plasticity and cellular immunity : shared molecular mechanisms ». Current Opinion in Neurobiology 11, n^o 5 (octobre 2001) : 568–78. http://dx.doi.org/10.1016/s0959-4388(00)00251-8.

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Boulanger, Lisa M., Gene S. Huh et Carla J. Shatz. « Neuronal plasticity and cellular immunity : shared molecular mechanisms ». Current Opinion in Neurobiology 12, n^o 1 (février 2002) : 119. http://dx.doi.org/10.1016/s0959-4388(02)00300-8.

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Atasoy, Deniz, et Scott M. Sternson. « Chemogenetic Tools for Causal Cellular and Neuronal Biology ». Physiological Reviews 98, n^o 1 (1 janvier 2018) : 391–418. http://dx.doi.org/10.1152/physrev.00009.2017.

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Chemogenetic technologies enable selective pharmacological control of specific cell populations. An increasing number of approaches have been developed that modulate different signaling pathways. Selective pharmacological control over G protein-coupled receptor signaling, ion channel conductances, protein association, protein stability, and small molecule targeting allows modulation of cellular processes in distinct cell types. Here, we review these chemogenetic technologies and instances of their applications in complex tissues in vivo and ex vivo.

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Hinshaw, Daniel B., Mary T. Miller, Geneva M. Omann, Theodore F. Beals et Paul A. Hyslop. « A cellular model of oxidant-mediated neuronal injury ». Brain Research 615, n^o 1 (juin 1993) : 13–26. http://dx.doi.org/10.1016/0006-8993(93)91110-e.

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Barral, Yves, et Isabelle M. Mansuy. « Septins : Cellular and Functional Barriers of Neuronal Activity ». Current Biology 17, n^o 22 (novembre 2007) : R961—R963. http://dx.doi.org/10.1016/j.cub.2007.10.001.

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Wang, Yan, et Zheng-hong Qin. « Molecular and cellular mechanisms of excitotoxic neuronal death ». Apoptosis 15, n^o 11 (6 mars 2010) : 1382–402. http://dx.doi.org/10.1007/s10495-010-0481-0.

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Dowson, J. H. « Neuronal Lipopigment : A Marker for Cognitive Impairment and Long-Term Effects of Psychotropic Drugs ». British Journal of Psychiatry 155, n^o 1 (juillet 1989) : 1–11. http://dx.doi.org/10.1192/bjp.155.1.1.

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Lipopigment, identifiable in the fluorescence microscope, is thought to be cellular debris partly derived from free-radical-induced peroxidation of cellular constituents. The volume of neuronal lipopigment has been positively correlated with advancing age, Alzheimer dementia, and the neuronal ceroidoses, while various changes in neuronal lipopigment have been reported in association with the chronic administration of dihydroergotoxine, ethanol, phenytoin, centrophenoxine, and chlorpromazine. An increase in the volume of neuronal lipopigment may indicate increased functional activity of the cell, impaired removal of pigment or anoxia. Chronic administration of agents which can be correlated with decreased neuronal lipopigment in animal models might protect neuronal function against any adverse effects associated with (but not necessarily resulting from) lipopigment accumulation in normal ageing, anoxia, or certain degenerative diseases. Long-term studies of the prophylactic use of such agents, or of drugs which neutralise free radicals, may be indicated. Other clinical applications of such drugs may include protection against the effects of free radicals formed during periods of oxygen deprivation.

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Pfaender, Stefanie, Karl Föhr, Anne-Kathrin Lutz, Stefan Putz, Kevin Achberger, Leonhard Linta, Stefan Liebau, Tobias M. Boeckers et Andreas M. Grabrucker. « Cellular Zinc Homeostasis Contributes to Neuronal Differentiation in Human Induced Pluripotent Stem Cells ». Neural Plasticity 2016 (2016) : 1–15. http://dx.doi.org/10.1155/2016/3760702.

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Disturbances in neuronal differentiation and function are an underlying factor of many brain disorders. Zinc homeostasis and signaling are important mediators for a normal brain development and function, given that zinc deficiency was shown to result in cognitive and emotional deficits in animal models that might be associated with neurodevelopmental disorders. One underlying mechanism of the observed detrimental effects of zinc deficiency on the brain might be impaired proliferation and differentiation of stem cells participating in neurogenesis. Thus, to examine the molecular mechanisms regulating zinc metabolism and signaling in differentiating neurons, using a protocol for motor neuron differentiation, we characterized the expression of zinc homeostasis genes during neurogenesis using human induced pluripotent stem cells (hiPSCs) and evaluated the influence of altered zinc levels on the expression of zinc homeostasis genes, cell survival, cell fate, and neuronal function. Our results show that zinc transporters are highly regulated genes during neuronal differentiation and that low zinc levels are associated with decreased cell survival, altered neuronal differentiation, and, in particular, synaptic function. We conclude that zinc deficiency in a critical time window during brain development might influence brain function by modulating neuronal differentiation.

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Friedman, Gabriel N., Mohsen Jamali, Firas Bounni et Ziv Williams. « 344 Studying the Single-cellular Substrates of Autism in a Mouse Model ». Neurosurgery 64, CN_suppl_1 (24 août 2017) : 277–78. http://dx.doi.org/10.1093/neuros/nyx417.344.

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Abstract INTRODUCTION Social dysfunction is among the most prominent features of autism spectrum disorder (ASD) as well as many other developmental and neuropsychiatric conditions. What precise neuronal mechanisms are disrupted in ASD, however, are unknown. The goal of this study is to provide a basic cellular-level understanding and treatment model for ASD. METHODS We developed an alternating appetitive/aversive paradigm in which socially-paired mice experienced both acute stress and food reward while we simultaneously recorded neuronal activity from medial prefrontal cortex. We compared WT to SHANK3 -/+ mice as a model of ASD, to explore the neuronal correlates socially relevant information and its dysfunction. RESULTS >Individual medial prefrontal neurons in SHANK3 -/+ mice displayed markedly different response profiles compared to that of WT. Specifically, neurons in SHANK3 -/+ mice demonstrated little differential response when presented with another unfamiliar mouse or nonsocial totem undergoing the same condition. However, in trials where the recorded mouse and a familiar mouse both receive a negative (painful) stimulus, SHANK3 -/+ mice demonstrated a significantly attenuated firing rate in response to the conspecific mouse, while the WT mice did not show any such differences. This attenuation was not observed when the other mice received positive (rewarding) stimuli. CONCLUSION Our study reveals some of the basic neuronal coding mechanisms that are disrupted in ASD. In particular, they demonstrate that, at the cellular level, autistic mice lack the neuronal-equivalent of an “empathic” response compared to wild-type. This neuronal response may provide a foundational mechanism for egocentric behavioral often found in ASD and suggests a basic model for testing neurobiologically plausible treatments for individuals with autism.

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Candadai, Amritha A., Fang Liu, Arti Verma, Mir S. Adil, Moaddey Alfarhan, Susan C. Fagan, Payaningal R. Somanath et S. Priya Narayanan. « Neuroprotective Effects of Fingolimod in a Cellular Model of Optic Neuritis ». Cells 10, n^o 11 (28 octobre 2021) : 2938. http://dx.doi.org/10.3390/cells10112938.

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Visual dysfunction resulting from optic neuritis (ON) is one of the most common clinical manifestations of multiple sclerosis (MS), characterized by loss of retinal ganglion cells, thinning of the nerve fiber layer, and inflammation to the optic nerve. Current treatments available for ON or MS are only partially effective, specifically target the inflammatory phase, and have limited effects on long-term disability. Fingolimod (FTY) is an FDA-approved immunomodulatory agent for MS therapy. The objective of the current study was to evaluate the neuroprotective properties of FTY in the cellular model of ON-associated neuronal damage. R28 retinal neuronal cell damage was induced through treatment with tumor necrosis factor-α (TNFα). In our cell viability analysis, FTY treatment showed significantly reduced TNFα-induced neuronal death. Treatment with FTY attenuated the TNFα-induced changes in cell survival and cell stress signaling molecules. Furthermore, immunofluorescence studies performed using various markers indicated that FTY treatment protects the R28 cells against the TNFα-induced neurodegenerative changes by suppressing reactive oxygen species generation and promoting the expression of neuronal markers. In conclusion, our study suggests neuroprotective effects of FTY in an in vitro model of optic neuritis.

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Priestly, J. V. « Neuronal Cholecystokinin ». Neurochemistry International 9, n^o 4 (janvier 1986) : 563–64. http://dx.doi.org/10.1016/0197-0186(86)90152-x.

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Streit, Wolfgang J. « Microglial—Neuronal interactions ». Journal of Chemical Neuroanatomy 6, n^o 4 (juillet 1993) : 261–66. http://dx.doi.org/10.1016/0891-0618(93)90047-8.

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Prunell, Giselle F., et Carol M. Troy. « Balancing neuronal death ». Journal of Neuroscience Research 78, n^o 1 (2004) : 1–6. http://dx.doi.org/10.1002/jnr.20252.

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Articles de revues sur le sujet « Cellule neuronali »

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