Academic literature on the topic 'Identité neuronale'
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Journal articles on the topic "Identité neuronale":
Hobert, Oliver, and Sacha Nelson. "Editorial overview: Neuronal Identity." Current Opinion in Neurobiology 56 (June 2019): iii—iv. http://dx.doi.org/10.1016/j.conb.2019.05.004.
Whalley, Katherine. "Relaying control of neuronal identity." Nature Reviews Neuroscience 18, no. 2 (January 5, 2017): 70. http://dx.doi.org/10.1038/nrn.2016.185.
Sousa, Erick, and Nuria Flames. "Transcriptional regulation of neuronal identity." European Journal of Neuroscience 55, no. 3 (January 18, 2022): 645–60. http://dx.doi.org/10.1111/ejn.15551.
Deneris, Evan S., and Oliver Hobert. "Maintenance of postmitotic neuronal cell identity." Nature Neuroscience 17, no. 7 (June 15, 2014): 899–907. http://dx.doi.org/10.1038/nn.3731.
Tsunemoto, Rachel, Sohyon Lee, Attila Szűcs, Pavel Chubukov, Irina Sokolova, Joel W. Blanchard, Kevin T. Eade, et al. "Diverse reprogramming codes for neuronal identity." Nature 557, no. 7705 (May 2018): 375–80. http://dx.doi.org/10.1038/s41586-018-0103-5.
Mall, Moritz, Michael S. Kareta, Soham Chanda, Henrik Ahlenius, Nicholas Perotti, Bo Zhou, Sarah D. Grieder, et al. "Myt1l safeguards neuronal identity by actively repressing many non-neuronal fates." Nature 544, no. 7649 (April 2017): 245–49. http://dx.doi.org/10.1038/nature21722.
Mesman, Simone, and Marten P. Smidt. "Acquisition of the Midbrain Dopaminergic Neuronal Identity." International Journal of Molecular Sciences 21, no. 13 (June 30, 2020): 4638. http://dx.doi.org/10.3390/ijms21134638.
Baker, C. V., and M. Bronner-Fraser. "Establishing neuronal identity in vertebrate neurogenic placodes." Development 127, no. 14 (July 15, 2000): 3045–56. http://dx.doi.org/10.1242/dev.127.14.3045.
Alcalà-Vida, Rafael, Ali Awada, Anne-Laurence Boutillier, and Karine Merienne. "Epigenetic mechanisms underlying enhancer modulation of neuronal identity, neuronal activity and neurodegeneration." Neurobiology of Disease 147 (January 2021): 105155. http://dx.doi.org/10.1016/j.nbd.2020.105155.
Kasthuri, Narayanan, and Jeff W. Lichtman. "The role of neuronal identity in synaptic competition." Nature 424, no. 6947 (July 2003): 426–30. http://dx.doi.org/10.1038/nature01836.
Dissertations / Theses on the topic "Identité neuronale":
Zimmer, Céline. "Spécification d'une identité neuronale : implication du gène à homéoboîte Cux2." Aix-Marseille 2, 2004. http://www.theses.fr/2004AIX22017.
Hache, Antoine. "Molecular basis of transcriptional dysregulations in the spinocerebellar ataxia type 7, a neurodegenerative polyglutamine disorder." Thesis, Strasbourg, 2020. http://www.theses.fr/2020STRAJ083.
SCA7 is a genetic disorder whose one of its main symptoms is a progressive loss of visual acuity which can ultimately lead to blindness. The mutation responsible for this disease is an unstable CAG expansion within ATXN7, a gene encoding a subunit of the SAGA complex, a co-activator of the RNA polymerase II. Previous studies performed on transgenic mouse models highlighted a neuronal identity loss of the photoreceptors at the morphological, functional and molecular levels. During my PhD a characterization of a new SCA7 knock-in mouse model was performed. This model, which expresses the mutated genes at endogenous level recapitulates the retinal impairments observed in transgenic models and in patients. A transcriptomic (RNA-seq) and epigenomic (ChIP-seq) analyses were performed on this model and highlight global acetylation defects on lysine 9 and 27 of histone H3 (H3K9ac and H3K27ac). Moreover, investigations on non-coding RNAs identified the presence of enhancer RNAs (eRNAs) on photoreceptor specific genes such as Rho. These eRNAs, which were never described before, undergo a downregulation in symptomatic SCA7 mice
Roque, Anne. "Détermination neurale et neuronale : implication des protéines de la superfamille Snail dans le lignage des soies mécanosensorielles chez la drosophile." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066559/document.
The commitment of cells to a given fate, or cell fate determination, is a key process in development. Cell type diversity arises from variations in this process. What are the mechanisms underlying cell determination and how is cell diversity achieved? In order to approach these questions, we use the Drosophila mechanosensory bristle lineage. In this lineage, cell diversity arises from the differential activation of the Notch pathway as well as the asymmetric segregation of cell fate determinants at each division. However, how does the repetition of the same mechanism trigger different cell fates? Other factors might be involved in cell fate commitment. In order to identify such factors, I focused my interest on the transcription factor of the Snail superfamily, known to be involved in cell determination during Drosophila development.Two members of this superfamily, escargot (esg) and scratch (scrt) are expressed in the bristle lineage, specifically in the inner neural cells and their precursor cells. Loss and gain of function analysis indicate that Esg and Scrt, acting redundantly, are necessary for the maintenance of the neural secondary precursor cell identity. A genetics interaction test showed that this role is achieved in interaction with the Notch pathway, probably through the repression of Notch target genes expression. Moreover, Esg, but not Scrt, has an additional role during the inner bristle cell formation. Loss of function of this factor induces a defect in neuronal differentiation, specifically axon growth and patterning. Moreover, the expression of genes involved in neuronal differentiation, such as elav and prospero, is impaired in this context. Altogether, these data suggests that Esg is involved in neuronal differentiation by regulating the expression of key neuronal genes.Together, my results showed that Esg and Scrt participate to the establishment of cell diversity in Drosophila bristle cell lineage
Stamataki, Despina. "Shh signalling and the specification of neuronal identity." Thesis, Open University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409850.
Carney, Travis. "Stem Cell Self-renewal and Neuronal Differentiation in the Drosophila Central Nervous System." Thesis, University of Oregon, 2013. http://hdl.handle.net/1794/13336.
Lischinsky, Julieta E. "Embryonic Transcription Factor Expression Predicts Neuronal Identity and Innate Behavioral Activation Patterns in the Limbic System." Thesis, The George Washington University, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10263849.
Instinctive behaviors such as mating and aggression are key for the survival and propagation of species. As innate behaviors manifest without prior training, there must be embryonic genetic mechanisms that specify these innate behavioral circuits. Focusing on the MeA and hypothalamus, both major integration centers of olfactory inputs, first, we sought to elucidate the link between embryonic transcription factor expression, neuronal identity and innate behavioral activation patterns in the MeA, and second, the link between embryonic transcription factor expression and instinctive behavioral activation patterns in hypothalamic subnuclei. Using mice as a model organism, we observed that the MeA progenitor niche in the preoptic area (POA) is comprised of distinct progenitor populations differentially marked by the transcription factors Dbx1 and Foxp2. Both embryonically and postnatally, Dbx1-derived and Foxp2+ subpopulations remain spatially segregated. We also observed that Dbx1-derived and Foxp2+ neurons differentially express sets of sex-steroid pathway proteins. Furthermore, both subpopulations differed in their intrinsic and extrinsic electrophysiological properties. Additionally, behavioral activation patterns were investigated in both subpopulations by determining the co-expression of the immediate early gene c-fos, an indirect marker of neuronal activity. During aggressive encounters, both Dbx1-derived and Foxp2+ neurons were activated in male and female mice; however, during mating cues, Dbx1-derived neurons in male and female mice were activated while only Foxp2+ neurons in male mice were activated and not in female mice. This denotes sex-specific differences in behavioral activation patterns in the MeA. Thus, parcellation of MeA neuronal subpopulations based on developmental genetics predicts molecular, electrophysiological, and behavioral specificity. Secondly, we were interested in determining whether embryonic transcription factor expression would be predictive of innate behavioral activation patterns in other limbic system structures implicated in the generation of innate behaviors such as the hypothalamus. Interestingly, we observed the presence of Dbx1-derived neurons in the lateral (LH), arcuate (Arc) and ventromedial (VMH) hypothalamic subnuclei. As Foxp2+ neurons are not present in the hypothalamus, we only analyzed Dbx1-derived neurons in these three hypothalamic regions. We show that Dbx1-derived neurons are activated in these structures during mating and aggression in both male and female mice. Thus, embryonic transcription factor expression in the hypothalamus is also linked to postnatal behavioral activation patterns. Taken together our findings indicate that embryonic transcription factor expression is predictive of behavioral activation patterns in the limbic system. We found that progenitor populations present in the same region but expressing distinct transcription factors, can generate MeA postnatal diversity based on molecular, electrophysiological and behavioral activation patterns. Furthermore, this can be generalized to other limbic system structures such as the hypothalamus, in which embryonic transcription factor expression of Dbx1 is also predictive of activation patterns during instinctive behavioral cues.
Etheredge, Jack. "Transcriptional profiling of Drosophila larval ventral nervous system hemilineages." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/270548.
Natinsky, Ari Simon. "Psychotherapy and the Embodiment of the Neuronal Identity: A Hermeneutic Study of Louis Cozolino's (2010) The Neuroscience of Psychotherapy: Healing the Social Brain." Antioch University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=antioch1399924216.
Atlan, Henri. "Spinoza et la biologie actuelle." Thesis, Paris 1, 2017. http://www.theses.fr/2017PA01H232.
Old philosophical problems are raised in renewed ways by advances in biology of today. Most obvious are the problems of relationship between living and non-living, mind and body, error en truth. Spinoza's philosophy, although from 17th century, offers solutions to these problems more relevant than most more recent philosophies. In return, present knowledge from physical and biological sciences, especially cognitive neurosciences, can provide a new look at some specifically Spinozist notions such as his "little physics", Nature as cause of itself, the notion of matter, the essence of a thing, kinds of knowledge, which gain all the more interest from a present day point of view
Pagliaro, Sarah Beatriz De Oliveira. "Transcriptional control induced by bcr-abl and its role in leukemic stem cell heterogeneity. Single-Cell Transcriptome in Chronic Myeloid Leukemia: Pseudotime Analysis Reveals Evidence of Embryonic and Transitional Stem Cell States Single Cell Transcriptome in Chronic Myeloid Leukemia (CML): Pseudotime Analysis Reveals a Rare Population with Embryonic Stem Cell Features and Druggable Intricated Transitional Stem Cell States A novel neuronal organoid model mimicking glioblastoma (GBM) features from induced pluripotent stem cells (iPSC) Experimental and integrative analyses identify an ETS1 network downstream of BCR-ABL in chronic myeloid leukemia (CML)." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASQ032.
Chronic myeloid leukemia is a clonal hematopoietic malignancy, characterized by the acquisition of the t (9;22) translocation leading to Ph1 chromosome and its counterpart BCR-ABL oncogene, in a very primitive hematopoietic stem cell. CML is a model of targeted therapies as the proof of concept of the feasibility of targeting the tyrosine kinase (TK) activity BCR-ABL using TK inhibitors (TKI) has been shown to lead to major responses and remissions. However, the current problems encountered in these therapies are primitive leukemic stem cells resistance and their persistence which is thought to be related to the heterogeneity of the stem cells at diagnosis leading to clonal selection of cells resisting to TKI therapies. I have applied the technology of single cell transcriptome analysis to CML cells using a panel of genes involved in different pathways combined with trajectory inference analysis to the gene expression pattern. The results showed a transitional stem cell states including embryonic genes identified in CML cells at diagnosis which could contribute to LSC resistance and persistence. Furthermore, the oncoprotein Bcr-Abl is the constitutively active tyrosine kinase produced by the chimeric BCR-ABL gene in chronic myeloid leukemia (CML). The transcriptional targets of Bcr-Abl in leukemic cells have not been extensively studied. A transcriptome experiment using the hematopoietic UT7 cell line expressing BCR-ABL, has identified the overexpression of eukaryotic elongation factor kinase 2 (eEF2K) which plays a major role in the survival of cells upon nutrient deprivation. Overall, the data suggest that overexpression of eEF2K in CML is associated with an increased sensitivity to nutrient-deprivation
Books on the topic "Identité neuronale":
Marty, Shankland, and Macagno Eduardo R, eds. Determinants of neuronal identity. San Diego: Academic Press, 1992.
Determinants of Neuronal Identity. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-12-638280-8.x5001-2.
Rager, Günter, Josef Quitterer, and Edmund Runggaldier. Unser Selbst. Identität im Wandel der neuronalen Prozesse. Schöningh, 2003.
Cohen, Marlene R., and John H. R. Maunsell. Neuronal Mechanisms of Spatial Attention in Visual Cerebral Cortex. Edited by Anna C. (Kia) Nobre and Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.007.
Martin, Rebecca E., and Ross D. MacPherson. Pathophysiology and assessment of pain. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0356.
Sprigings, David. Coma. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0040.
McShane, Tony, Peter Clayton, Michael Donaghy, and Robert Surtees. Neurometabolic disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0213.
Book chapters on the topic "Identité neuronale":
Appel, Bruce, and Ajay Chitnis. "Neurogenesis and Specification of Neuronal Identity." In Results and Problems in Cell Differentiation, 237–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-540-46041-1_12.
Marcus, Donald M. "The Use of Antibodies to Identify Glycosphingolipids and to Localize Them in Tissues." In Gangliosides and Neuronal Plasticity, 77–82. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4757-5309-7_6.
Xavier, André Machado, and Isaias Glezer. "CD36 Neuronal Identity in the Olfactory Epithelium." In Methods in Molecular Biology, 1–19. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8609-5_1.
Natinsky, Ari. "Psychotherapy and the Embodiment of Neuronal Identity." In Hermeneutic Approaches to Interpretive Research, 48–62. New York: Routledge, 2021. http://dx.doi.org/10.4324/9781003140177-4.
Kim, Chiho, and Young J. Oh. "A Novel 2-DE-Based Proteomic Analysis to Identify Multiple Substrates for Specific Protease in Neuronal Cells." In Methods in Molecular Biology, 229–45. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6952-4_10.
Pecchinenda, Gianfranco. "The neuronal identity." In Postmortal Society, 138–55. Routledge, 2017. http://dx.doi.org/10.4324/9781315601700-8.
"Front Matter." In Determinants of Neuronal Identity, iii. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-12-638280-8.50001-1.
"Copyright." In Determinants of Neuronal Identity, iv. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-12-638280-8.50002-3.
Shankland, Marty, and Eduardo R. Macagno. "Preface." In Determinants of Neuronal Identity, xv—xvi. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-12-638280-8.50004-7.
Sternberg, Paul W., Katharine Liu, and Helen M. Chamberlin. "Specification of Neuronal Identity in Caenorhabditis elegans." In Determinants of Neuronal Identity, 1–43. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-12-638280-8.50005-9.
Conference papers on the topic "Identité neuronale":
Jabalameli, Amirhossein, and Aman Behal. "A constrained linear approach to identify a multi-timescale adaptive threshold neuronal model." In 2015 IEEE 5th International Conference on Computational Advances in Bio and Medical Sciences (ICCABS). IEEE, 2015. http://dx.doi.org/10.1109/iccabs.2015.7344704.
Zhang, H., N. Ye, J. He, A. Roontiva, and J. Aguayo. "Two-way ANOVA to identify impacts of multiple interactive behavioral factors on the neuronal population dependency during the reaching motion." In 2008 30th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2008. http://dx.doi.org/10.1109/iembs.2008.4649411.
Shukla, Amit, Ashutosh Mani, Amit Bhattacharya, and Fredy Revilla. "Classification of Postural Response in Parkinson’s Patients Using Support Vector Machines." In ASME 2013 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/dscc2013-3888.
Morales, Juan, Jorge G. Pen˜a, Jaime Ferna´ndez, and Angel Rodri´guez. "Towards a Scalable ESPINA for Neuroscience Data Analysis." In ASME 2011 World Conference on Innovative Virtual Reality. ASMEDC, 2011. http://dx.doi.org/10.1115/winvr2011-5553.
Rizzi, Liara, and Marcio Balthazar. "THE SUSPECTED NON-ALZHEIMER’S DISEASE PATHOPHYSIOLOGY." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda070.
Reports on the topic "Identité neuronale":
Library, Spring. The Cycle of Learning, Memorizing, and Forgetting. Spring Library, December 2020. http://dx.doi.org/10.47496/sl.blog.17.