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Journal articles on the topic 'Cellule neuronali'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

Ricquebourg, Rebekah, and Nikolaos Konstantinides. "Un mécanisme temporel pour la génération de la diversité neuronale." médecine/sciences 40, no. 3 (2024): 251–57. http://dx.doi.org/10.1051/medsci/2024012.

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L’un des plus grands défis des neurosciences est de comprendre comment une structure complexe, telle que le cerveau, se construit. L’encodage spatial et temporel des progéniteurs neuronaux permet la génération de l’essentiel de la diversité neuronale. Cette revue se concentre sur l’expression séquentielle de facteurs de transcription temporels, qui modifie la capacité des cellules souches à générer différents types de neurones et qui est conservée chez plusieurs espèces animales. Des publications récentes ont permis, en particulier, une compréhension fine de ce processus au cours du développem

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Benaïssa, Ibtissem. "Analogie du transport neuronal au transport électronique en nanotechnologie." Journal of Renewable Energies 12, no. 1 (2023): 9–28. http://dx.doi.org/10.54966/jreen.v12i1.115.

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Le système nerveux est formé de deux types de cellules: les cellules gliales et les neurones. Les astrocytes, comme la plupart des cellules gliales, ont longtemps été considérés essentiellement pour leur rôle de support et d’entretien du tissu nerveux. Mais, de plus en plus d’évidences plaident en faveur d’une implication beaucoup plus importante des astrocytes dans la communication nerveuse. Les astrocytes sont couplés les uns aux autres par des ‘gap-jonctions’ à travers lesquels peuvent circuler divers métabolites. C’est par ces jonctions que les astrocytes évacuent vers les capillaires, le

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3

VILETTE, D., and H. LAUDE. "Pathogenèse des Encéphalopathies Spongiformes Transmissibles : apports des modèles cellulaires." INRAE Productions Animales 17, HS (2004): 23–30. http://dx.doi.org/10.20870/productions-animales.2004.17.hs.3621.

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Malgré des efforts répétés et soutenus lors des 30 dernières années, le nombre de modèles permettant l’étude en culture cellulaire de la multiplication des prions était, jusqu’à récemment, extrêmement restreint. Il s’agissait, pour l’essentiel, de quelques lignées cellulaires, ne permettant la multiplication que de rares souches expérimentales de prions. Pour tenter de pallier ces insuffisances, un projet a été initié en vue d’établir des modèles capables notamment de permettre la multiplication et l’étude de souches naturelles de prions. Quatre nouveaux modèles cellulaires ont été obtenus. S’

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4

Ronzitti, Emiliano, Dimitrii Tanese, Alexis Picot, Benoît C. Forget, Valentina Emiliani, and Eirini Papagiakoumou. "Holographie numérique pour la photostimulation de circuits neuronaux." Photoniques, no. 92 (July 2018): 34–37. http://dx.doi.org/10.1051/photon/20189234.

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Le développement de techniques originales de manipulation de la lumière ont permis de grandes avancées dans le domaine de l’optogénétique. Elles permettent d’étudier et de stimuler la communication au sein des circuits neuronaux et du cerveau avec une précision spatiale et temporelle correspondant à l’activation d’une cellule unique au sein d’un circuit.

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5

Behar-Cohen, Francine, Emmanuelle Gelizé, Laurent Jonet, and Patricia Lassiaz. "Anatomie de la rétine." médecine/sciences 36, no. 6-7 (2020): 594–99. http://dx.doi.org/10.1051/medsci/2020094.

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La neurorétine est une unité fonctionnelle du système nerveux central assurant la conversion d’un signal lumineux en un influx nerveux. D’origine neuroectodermique, dérivée du diencéphale, la neurorétine est un tissu stratifié, composé de six types de cellules neuronales (deux types de photorécepteurs : les cônes et les bâtonnets ; les cellules horizontales, bipolaires, amacrines et ganglionnaires) et de trois types de cellules gliales (les cellules gliales de Müller, les astrocytes et les cellules microgliales). La neurorétine repose sur l’épithélium pigmentaire rétinien, l’ensemble constitua

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6

Lledo, Pierre-Marie. "Cellules souches neuronales." Morphologie 99, no. 327 (2015): 154. http://dx.doi.org/10.1016/j.morpho.2015.09.012.

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7

Dumbacher, Michael, Dooren Tom Van, Katrien Princen та ін. "Modifying Rap1-signalling by targeting Pde6δ is neuroprotective in models of Alzheimer's disease". Molecular Neurodegeneration 13, № 1 (2018): 50. https://doi.org/10.1186/s13024-018-0283-3.

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<strong>Background: </strong>Neuronal Ca<sup>2+</sup> dyshomeostasis and hyperactivity play a central role in Alzheimer's disease pathology and progression. Amyloid-beta together with non-genetic risk-factors of Alzheimer's disease contributes to increased Ca<sup>2+</sup> influx and aberrant neuronal activity, which accelerates neurodegeneration in a feed-forward fashion. As such, identifying new targets and drugs to modulate excessive Ca<sup>2+</sup> signalling and neuronal hyperactivity, without overly suppressing them, has promising therapeutic potential.<strong>Methods: </strong>Here we sh

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8

Rakotobe, Malalaniaina, and Chiara Zurzolo. "Les tunneling nanotubes." médecine/sciences 40, no. 11 (2024): 829–36. https://doi.org/10.1051/medsci/2024152.

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Les tunneling nanotubes (TNT) sont des protrusions membranaires ouvertes permettant la communication directe entre cellules distantes. Des recherches récentes ont révélé leur importance biologique, notamment dans le système nerveux où leurs rôles pourraient être cruciaux. Observés dans le cerveau en développement, les TNT sont impliqués dans les maladies neurodégénératives, les cancers du cerveau et dans d’autres types de maladies, soulignant leur rôle physiopathologique. Leur découverte pourrait conduire à reconsidérer le cerveau comme un réseau neuronal physiquement connecté, complémentant a

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9

Baratas Díaz, Luis Alfredo. "Significación histórica de La rétine des Vertébrés de Santiago Ramón y Cajal: Síntesis de su primera etapa investigadora." Asclepio 46, no. 1 (1994): 243. http://dx.doi.org/10.3989/asclepio.1994.v46.1.482.

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La retina fue uno de los objetos de estudio preferentes en la primera etapa de la obra científica de Ramón y Cajal. Como culminación de sus trabajos previos, Cajal publicó en 1893 en La Cellule un artículo titulado «La rétine des Vertébrés», en el que se aprecian las influencias más significativas que pesaron sobre su obra. Este trabajo sobre la retina ilustra perfectamente su capacidad para el estudio sistemático de los tipos celulares de los centros nerviosos, su descripción morfológica y los contactos intercelulares, así como para formular interpretaciones fisiológicas coherentes con las ob

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10

Corner, M. A. "Neuronal and cellular oscillators." Journal of the Neurological Sciences 92, no. 2-3 (1989): 349. http://dx.doi.org/10.1016/0022-510x(89)90150-0.

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11

Korn, H. "Neuronal and cellular oscillators." Biochimie 72, no. 5 (1990): 376. http://dx.doi.org/10.1016/0300-9084(90)90037-h.

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12

Boulant, Jack A. "Cellular mechanisms of neuronal thermosensitivity." Journal of Thermal Biology 24, no. 5-6 (1999): 333–38. http://dx.doi.org/10.1016/s0306-4565(99)00038-8.

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13

Morant, Laura, Maria-Luise Petrovic-Erfurth, and Albena Jordanova. "An Adapted GeneSwitch Toolkit for Comparable Cellular and Animal Models: A Proof of Concept in Modeling Charcot-Marie-Tooth Neuropathy." International Journal of Molecular Sciences 24, no. 22 (2023): 16138. http://dx.doi.org/10.3390/ijms242216138.

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Investigating the impact of disease-causing mutations, their affected pathways, and/or potential therapeutic strategies using disease modeling often requires the generation of different in vivo and in cellulo models. To date, several approaches have been established to induce transgene expression in a controlled manner in different model systems. Several rounds of subcloning are, however, required, depending on the model organism used, thus bringing labor-intensive experiments into the technical approach and analysis comparison. The GeneSwitch™ technology is an adapted version of the classical

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14

Agnati, Luigi F., Diego Guidolin, Chiara Carone, Mauro Dam, Susanna Genedani, and Kjell Fuxe. "Understanding neuronal molecular networks builds on neuronal cellular network architecture." Brain Research Reviews 58, no. 2 (2008): 379–99. http://dx.doi.org/10.1016/j.brainresrev.2007.11.002.

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15

Dale, Nicholas. "Neuronal and cellular oscillators (cellular clocks series, vol. 2)." Trends in Neurosciences 12, no. 12 (1989): 521–22. http://dx.doi.org/10.1016/0166-2236(89)90114-8.

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16

NASRI, Ahmed. "Écotoxicité de l'exposition des larves du poisson zèbre au mélange EE2/A6: Un accent particulier sur la ligne latérale postérieure, PLL." Revue Marocaine des Sciences Agronomiques et Vétérinaires 12, no. 4 (2024): 301–5. https://doi.org/10.5281/zenodo.14582243.

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La ligne latérale postérieure ou PLL est un système mécano-sensoriel présent chez les poissons et les amphibiens, qui permet la détection des mouvements de l’eau dans l’environnement. La stimulation de ce système conduit à une réponse comportementale adaptée, telle que la nage contre le sens du courant, la parade sexuelle, la détection des proies et des prédateurs. Il a disparu chez les organismes terrestres, notamment chez la plupart des tétrapodes, où il a été remplac&e

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17

Kristan,, William B. "Neuronal and Cellular Oscillators.Jon W. Jacklet." Quarterly Review of Biology 65, no. 1 (1990): 73–74. http://dx.doi.org/10.1086/416613.

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18

Bignami, F., P. Bevilacqua, S. Biagioni, et al. "Cellular Acetylcholine Content and Neuronal Differentiation." Journal of Neurochemistry 69, no. 4 (1997): 1374–81. http://dx.doi.org/10.1046/j.1471-4159.1997.69041374.x.

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19

Powell, Sharon K., and Hynda K. Kleinman. "Neuronal laminins and their cellular receptors." International Journal of Biochemistry & Cell Biology 29, no. 3 (1997): 401–14. http://dx.doi.org/10.1016/s1357-2725(96)00110-0.

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20

Bowie, Derek, and David Attwell. "Coupling cellular metabolism to neuronal signalling." Journal of Physiology 593, no. 16 (2015): 3413–15. http://dx.doi.org/10.1113/jp271075.

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21

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

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22

Poncet, Anaïs F., Olivier Grunewald, Veronika Vaclavik, et al. "Contribution of Whole-Genome Sequencing and Transcript Analysis to Decipher Retinal Diseases Associated with MFSD8 Variants." International Journal of Molecular Sciences 23, no. 8 (2022): 4294. http://dx.doi.org/10.3390/ijms23084294.

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Biallelic gene defects in MFSD8 are not only a cause of the late-infantile form of neuronal ceroid lipofuscinosis, but also of rare isolated retinal degeneration. We report clinical and genetic data of seven patients compound heterozygous or homozygous for variants in MFSD8, issued from a French cohort with inherited retinal degeneration, and two additional patients retrieved from a Swiss cohort. Next-generation sequencing of large panels combined with whole-genome sequencing allowed for the identification of twelve variants from which seven were novel. Among them were one deep intronic varian

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23

Dupont, AC, D. Guilloteau, M. Kassiou, et al. "Radiopharmaceuticals for PET imaging of neuroinflammation - Les radiopharmaceutiques pour l’imagerie TEP de la neuroinflammation." Médecine Nucléaire 40, no. 1 (2016): 72–81. https://doi.org/10.1016/j.mednuc.2016.01.001.

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Abstract Recently, accumulating evidence has revealed that neuroinflammation appears to be the cornerstone of many neurological diseases including stroke, multiple sclerosis, Alzheimer's disease or Parkinson's disease. Neuroinflammation causes neuronal damages by activation of numerous cells and molecular mediators in diseases involving the inflammatory process. In this article, we focus on noninvasive molecular imaging of radioligands that target inflammatory cells and molecules involved in neuroinflammation. PET is in fact one of the most promising imaging techniques to visualize and

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24

Talmont, Franck, Anastassia Hatzoglou, and Olivier Cuvillier. "La sclérose en plaques et les médicaments immuno-modulateurs des récepteurs de la sphingosine 1-phosphate." médecine/sciences 36, no. 3 (2020): 243–52. http://dx.doi.org/10.1051/medsci/2020026.

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La sclérose en plaques (SEP) est une maladie du système nerveux central à composante inflammatoire, très invalidante qui atteint généralement de jeunes adultes (20 à 40 ans). Cette maladie se caractérise par la destruction progressive, par les cellules du système immunitaire, de la gaine de myéline des axones, ce qui aboutit à une dégénérescence neuronale. Les lymphocytes T et B sont les acteurs principaux de cette maladie qui peut être rémittente ou progressive. Parmi les médicaments utilisés dans le cadre de son traitement, le fingolimod, un immunosuppresseur dont les cibles sont les récepte

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25

Sweeney, Marva I., Wolfgang Waiz, Jerome Y. Yager, and Bernhard Juurlink. "Cellular mechanisms involved in brain ischemia." Canadian Journal of Physiology and Pharmacology 73, no. 11 (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 conclud

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26

Bentley, Marvin, and Gary Banker. "The cellular mechanisms that maintain neuronal polarity." Nature Reviews Neuroscience 17, no. 10 (2016): 611–22. http://dx.doi.org/10.1038/nrn.2016.100.

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27

Phiwchai, Isara, Watchareeporn Chariyarangsitham, Thipjutha Phatruengdet, and Chalermchai Pilapong. "Ferric–Tannic Nanoparticles Increase Neuronal Cellular Clearance." ACS Chemical Neuroscience 10, no. 9 (2019): 4136–44. http://dx.doi.org/10.1021/acschemneuro.9b00345.

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28

Duane, Gregory S. "A “cellular neuronal” approach to optimization problems." Chaos: An Interdisciplinary Journal of Nonlinear Science 19, no. 3 (2009): 033114. http://dx.doi.org/10.1063/1.3184829.

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29

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

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30

Herzog, Nitzan, Mark Shein-Idelson, and Yael Hanein. "Optical validation ofin vitroextra-cellular neuronal recordings." Journal of Neural Engineering 8, no. 5 (2011): 056008. http://dx.doi.org/10.1088/1741-2560/8/5/056008.

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31

Deniz, MN, E. Sezer, A. Tetik, and S. Ulukaya. "Evaluation of the Brain Cellular Damage during Liver Transplantations." Nigerian Journal of Clinical Practice 26, no. 8 (2023): 1063–68. http://dx.doi.org/10.4103/njcp.njcp_332_22.

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ABSTRACT Background: Neuroinflammation in patients undergoing major surgery can lead to neuronal damage, and neuronal damage can be detected through the measurement of biochemical markers of brain damage. S100 beta (S100 β), neuron-specific enolase (NSE), and glial fibrillary acidic protein (GFAP) levels are considered good biomarkers to detect brain damage that emerged with neurotoxicity. Aim: To evaluate neuronal damage during liver transplantations. Materials and Methods: After approval of the ethics committee and patient consents, preoperative and postoperative cognitive functions of 33 pa

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32

Greengard, Paul. "Neuronal phosphoproteins." Molecular Neurobiology 1, no. 1-2 (1987): 81–119. http://dx.doi.org/10.1007/bf02935265.

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33

Won, Seok-Joon, Doo-Yeon Kim, and Byoung-Joo Gwag. "Cellular and Molecular Pathways of Ischemic Neuronal Death." BMB Reports 35, no. 1 (2002): 67–86. http://dx.doi.org/10.5483/bmbrep.2002.35.1.067.

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34

Stetler, R., Y. Gao, A. Signore, G. Cao, and J. Chen. "HSP27: Mechanisms of Cellular Protection Against Neuronal Injury." Current Molecular Medicine 9, no. 7 (2009): 863–72. http://dx.doi.org/10.2174/156652409789105561.

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35

Morimune, Takao, Ayami Tano, Yuya Tanaka, et al. "Gm14230 controls Tbc1d24 cytoophidia and neuronal cellular juvenescence." PLOS ONE 16, no. 4 (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 Gm1

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36

Teichert, Russell W. "Investigating neuronal cell types through comparative cellular physiology." Temperature 1, no. 1 (2014): 22–23. http://dx.doi.org/10.4161/temp.29540.

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37

MOUILLET-RICHARD, S., B. SCHNEIDER, E. PRADINES, et al. "Cellular Prion Protein Signaling in Serotonergic Neuronal Cells." Annals of the New York Academy of Sciences 1096, no. 1 (2007): 106–19. http://dx.doi.org/10.1196/annals.1397.076.

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38

Bonzanni, Mattia, Nicolas Rouleau, Michael Levin, and David L. Kaplan. "Optogenetically induced cellular habituation in non-neuronal cells." PLOS ONE 15, no. 1 (2020): e0227230. http://dx.doi.org/10.1371/journal.pone.0227230.

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39

Kazantsev, A. G. "Cellular pathways leading to neuronal dysfunction and degeneration." Drug News & Perspectives 20, no. 8 (2007): 501. http://dx.doi.org/10.1358/dnp.2007.20.8.1157616.

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40

Cannon, JingJing F., William H. Barnett, and 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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41

Senior, Kathryn. "Discrete cellular entry points discovered in neuronal membrane." Lancet Neurology 1, no. 8 (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, no. 1 Frontiers of (1997): 255–73. http://dx.doi.org/10.1111/j.1749-6632.1997.tb48636.x.

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43

Boulanger, Lisa M., Gene S. Huh, and Carla J. Shatz. "Neuronal plasticity and cellular immunity: shared molecular mechanisms." Current Opinion in Neurobiology 11, no. 5 (2001): 568–78. http://dx.doi.org/10.1016/s0959-4388(00)00251-8.

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Boulanger, Lisa M., Gene S. Huh, and Carla J. Shatz. "Neuronal plasticity and cellular immunity: shared molecular mechanisms." Current Opinion in Neurobiology 12, no. 1 (2002): 119. http://dx.doi.org/10.1016/s0959-4388(02)00300-8.

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45

Atasoy, Deniz, and Scott M. Sternson. "Chemogenetic Tools for Causal Cellular and Neuronal Biology." Physiological Reviews 98, no. 1 (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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46

Hinshaw, Daniel B., Mary T. Miller, Geneva M. Omann, Theodore F. Beals, and Paul A. Hyslop. "A cellular model of oxidant-mediated neuronal injury." Brain Research 615, no. 1 (1993): 13–26. http://dx.doi.org/10.1016/0006-8993(93)91110-e.

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47

Barral, Yves, and Isabelle M. Mansuy. "Septins: Cellular and Functional Barriers of Neuronal Activity." Current Biology 17, no. 22 (2007): R961—R963. http://dx.doi.org/10.1016/j.cub.2007.10.001.

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48

Wang, Yan, and Zheng-hong Qin. "Molecular and cellular mechanisms of excitotoxic neuronal death." Apoptosis 15, no. 11 (2010): 1382–402. http://dx.doi.org/10.1007/s10495-010-0481-0.

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49

McNearney, Terry A., and Karin N. Westlund. "Pluripotential GluN1 (NMDA NR1): Functional Significance in Cellular Nuclei in Pain/Nociception." International Journal of Molecular Sciences 24, no. 17 (2023): 13196. http://dx.doi.org/10.3390/ijms241713196.

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The N-methyl-D-aspartate (NMDA) glutamate receptors function as plasma membrane ionic channels and take part in very tightly controlled cellular processes activating neurogenic and inflammatory pathways. In particular, the NR1 subunit (new terminology: GluN1) is required for many neuronal and non-neuronal cell functions, including plasticity, survival, and differentiation. Physiologic levels of glutamate agonists and NMDA receptor activation are required for normal neuronal functions such as neuronal development, learning, and memory. When glutamate receptor agonists are present in excess, bin

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50

Pfaender, Stefanie, Karl Föhr, Anne-Kathrin Lutz, et al. "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 regu

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