Статті в журналах: "Identité neuronale"

1

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.

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2

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.

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3

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.

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4

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.

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5

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.

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6

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.

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7

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.

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The mesodiencephalic dopaminergic (mdDA) group of neurons comprises molecularly distinct subgroups, of which the substantia nigra (SN) and ventral tegmental area (VTA) are the best known, due to the selective degeneration of the SN during Parkinson’s disease. However, although significant research has been conducted on the molecular build-up of these subsets, much is still unknown about how these subsets develop and which factors are involved in this process. In this review, we aim to describe the life of an mdDA neuron, from specification in the floor plate to differentiation into the different subsets. All mdDA neurons are born in the mesodiencephalic floor plate under the influence of both SHH-signaling, important for floor plate patterning, and WNT-signaling, involved in establishing the progenitor pool and the start of the specification of mdDA neurons. Furthermore, transcription factors, like Ngn2, Ascl1, Lmx1a, and En1, and epigenetic factors, like Ezh2, are important in the correct specification of dopamine (DA) progenitors. Later during development, mdDA neurons are further subdivided into different molecular subsets by, amongst others, Otx2, involved in the specification of subsets in the VTA, and En1, Pitx3, Lmx1a, and WNT-signaling, involved in the specification of subsets in the SN. Interestingly, factors involved in early specification in the floor plate can serve a dual function and can also be involved in subset specification. Besides the mdDA group of neurons, other systems in the embryo contain different subsets, like the immune system. Interestingly, many factors involved in the development of mdDA neurons are similarly involved in immune system development and vice versa. This indicates that similar mechanisms are used in the development of these systems, and that knowledge about the development of the immune system may hold clues for the factors involved in the development of mdDA neurons, which may be used in culture protocols for cell replacement therapies.

8

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.

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The trigeminal and epibranchial placodes of vertebrate embryos form different types of sensory neurons. The trigeminal placodes form cutaneous sensory neurons that innervate the face and jaws, while the epibranchial placodes (geniculate, petrosal and nodose) form visceral sensory neurons that innervate taste buds and visceral organs. In the chick embryo, the ophthalmic trigeminal (opV) placode expresses the paired homeodomain transcription factor Pax3 from very early stages, while the epibranchial placodes express Pax2. Here, we show that Pax3 expression in explanted opV placode ectoderm correlates at the single cell level with neuronal specification and with commitment to an opV fate. When opV (trigeminal) ectoderm is grafted in place of the nodose (epibranchial) placode, Pax3-expressing cells form Pax3-positive neurons on the same schedule as in the opV placode. In contrast, Pax3-negative cells in the grafted ectoderm are induced to express the epibranchial placode marker Pax2 and form neurons in the nodose ganglion that express the epibranchial neuron marker Phox2a on the same schedule as host nodose neurons. They also project neurites along central and peripheral nodose neurite pathways and survive until well after the main period of cell death in the nodose ganglion. The older the opV ectoderm is at the time of grafting, the more Pax3-positive cells it contains and the more committed it is to an opV fate. Our results suggest that, within the neurogenic placodes, there does not appear to be a two-step induction of ‘generic’ neurons followed by specification of the neuron to a particular fate. Instead, there seems to be a one-step induction in which neuronal subtype identity is coupled to neuronal differentiation.

9

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.

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10

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.

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11

Yu, Hung-Hsiang, and Tzumin Lee. "Neuronal temporal identity in post-embryonic Drosophila brain." Trends in Neurosciences 30, no. 10 (October 2007): 520–26. http://dx.doi.org/10.1016/j.tins.2007.07.003.

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12

Allene, Camille, Joana Lourenço, and Alberto Bacci. "The neuronal identity bias behind neocortical GABAergic plasticity." Trends in Neurosciences 38, no. 9 (September 2015): 524–34. http://dx.doi.org/10.1016/j.tins.2015.07.008.

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13

Shirasaki, Ryuichi, and Samuel L. Pfaff. "Transcriptional Codes and the Control of Neuronal Identity." Annual Review of Neuroscience 25, no. 1 (March 2002): 251–81. http://dx.doi.org/10.1146/annurev.neuro.25.112701.142916.

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14

Brunet, Jean-François, and Alain Ghysen. "Deconstructing cell determination: proneural genes and neuronal identity." BioEssays 21, no. 4 (April 28, 1999): 313–18. http://dx.doi.org/10.1002/(sici)1521-1878(199904)21:4<313::aid-bies7>3.0.co;2-c.

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15

Tosches, Maria Antonietta, and Gilles Laurent. "Evolution of neuronal identity in the cerebral cortex." Current Opinion in Neurobiology 56 (June 2019): 199–208. http://dx.doi.org/10.1016/j.conb.2019.04.009.

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16

Barth, K. Anukampa, and Stephen W. Wilson. "Specification of neuronal identity in the embryonic CNS." Seminars in Developmental Biology 5, no. 6 (December 1994): 349–58. http://dx.doi.org/10.1006/sedb.1994.1045.

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17

Esmaeili, Behrooz, Jennifer M. Ross, Cara Neades, David M. Miller, and Julie Ahringer. "The C. elegans even-skipped homologue, vab-7, specifies DB motoneurone identity and axon trajectory." Development 129, no. 4 (February 15, 2002): 853–62. http://dx.doi.org/10.1242/dev.129.4.853.

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Locomotory activity is defined by the specification of motoneurone subtypes. In the nematode, C. elegans, DA and DB motoneurones innervate dorsal muscles and function to induce movement in the backwards or forwards direction, respectively. These two neurone classes express separate sets of genes and extend axons with oppositely directed trajectories; anterior (DA) versus posterior (DB). The DA-specific homeoprotein UNC-4 interacts with UNC-37/Groucho to repress the DB gene, acr-5 (nicotinic acetylcholine receptor subunit). We show that the C. elegans even-skipped-like homoedomain protein, VAB-7, coordinately regulates different aspects of the DB motoneurone fate, in part by repressing unc-4. Wild-type DB motoneurones express VAB-7, have posteriorly directed axons, express ACR-5 and lack expression of the homeodomain protein UNC-4. In a vab-7 mutant, ectopic UNC-4 represses acr-5 and induces an anteriorly directed DB axon trajectory. Thus, vab-7 indirectly promotes DB-specific gene expression and posteriorly directed axon outgrowth by preventing UNC-4 repression of DB differentiation. Ectopic expression of VAB-7 also induces DB traits in an unc-4-independent manner, suggesting that VAB-7 can act through a parallel pathway. This work supports a model in which a complementary pair of homeodomain transcription factors (VAB-7 and UNC-4) specifies differences between DA and DB neurones through inhibition of the alternative fates. The recent findings that Even-skipped transcriptional repressor activity specifies neurone identity and axon guidance in the mouse and Drosophila motoneurone circuit points to an ancient origin for homeoprotein-dependent mechanisms of neuronal differentiation in the metazoan nerve cord.

18

Kiefer, Alex B. "Psychophysical identity and free energy." Journal of The Royal Society Interface 17, no. 169 (August 2020): 20200370. http://dx.doi.org/10.1098/rsif.2020.0370.

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An approach to implementing variational Bayesian inference in biological systems is considered, under which the thermodynamic free energy of a system directly encodes its variational free energy. In the case of the brain, this assumption places constraints on the neuronal encoding of generative and recognition densities, in particular requiring a stochastic population code. The resulting relationship between thermodynamic and variational free energies is prefigured in mind–brain identity theses in philosophy and in the Gestalt hypothesis of psychophysical isomorphism.

19

RIVERA-ALVIDREZ, ZULEY, ICHI LIN, and CHARLES M. HIGGINS. "A neuronally based model of contrast gain adaptation in fly motion vision." Visual Neuroscience 28, no. 5 (August 22, 2011): 419–31. http://dx.doi.org/10.1017/s095252381100023x.

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AbstractMotion-sensitive neurons in the visual systems of many species, including humans, exhibit a depression of motion responses immediately after being exposed to rapidly moving images. This motion adaptation has been extensively studied in flies, but a neuronal mechanism that explains the most prominent component of adaptation, which occurs regardless of the direction of motion of the visual stimulus, has yet to be proposed. We identify a neuronal mechanism, namely frequency-dependent synaptic depression, which explains a number of the features of adaptation in mammalian motion-sensitive neurons and use it to model fly motion adaptation. While synaptic depression has been studied mainly in spiking cells, we use the same principles to develop a simple model for depression in a graded synapse. By incorporating this synaptic model into a neuronally based model for elementary motion detection, along with the implementation of a center-surround spatial band-pass filtering stage that mimics the interactions among a subset of visual neurons, we show that we can predict with remarkable success most of the qualitative features of adaptation observed in electrophysiological experiments. Our results support the idea that diverse species share common computational principles for processing visual motion and suggest that such principles could be neuronally implemented in very similar ways.

20

Russ, Jeffrey B., and Julia A. Kaltschmidt. "From induction to conduction: how intrinsic transcriptional priming of extrinsic neuronal connectivity shapes neuronal identity." Open Biology 4, no. 10 (October 2014): 140144. http://dx.doi.org/10.1098/rsob.140144.

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Every behaviour of an organism relies on an intricate and vastly diverse network of neurons whose identity and connectivity must be specified with extreme precision during development. Intrinsically, specification of neuronal identity depends heavily on the expression of powerful transcription factors that direct numerous features of neuronal identity, including especially properties of neuronal connectivity, such as dendritic morphology, axonal targeting or synaptic specificity, ultimately priming the neuron for incorporation into emerging circuitry. As the neuron's early connectivity is established, extrinsic signals from its pre- and postsynaptic partners feedback on the neuron to further refine its unique characteristics. As a result, disruption of one component of the circuitry during development can have vital consequences for the proper identity specification of its synaptic partners. Recent studies have begun to harness the power of various transcription factors that control neuronal cell fate, including those that specify a neuron's subtype-specific identity, seeking insight for future therapeutic strategies that aim to reconstitute damaged circuitry through neuronal reprogramming.

21

Li, Xuekun, and Peng Jin. "Roles of small regulatory RNAs in determining neuronal identity." Nature Reviews Neuroscience 11, no. 5 (March 31, 2010): 329–38. http://dx.doi.org/10.1038/nrn2739.

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22

Dubreuil, V., M. Hirsch, A. Pattyn, J. Brunet, and C. Goridis. "The Phox2b transcription factor coordinately regulates neuronal cell cycle exit and identity." Development 127, no. 23 (December 1, 2000): 5191–201. http://dx.doi.org/10.1242/dev.127.23.5191.

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In the vertebrate neural tube, cell cycle exit of neuronal progenitors is accompanied by the expression of transcription factors that define their generic and sub-type specific properties, but how the regulation of cell cycle withdrawal intersects with that of cell fate determination is poorly understood. Here we show by both loss- and gain-of-function experiments that the neuronal-subtype-specific homeodomain transcription factor Phox2b drives progenitor cells to become post-mitotic. In the absence of Phox2b, post-mitotic neuronal precursors are not generated in proper numbers. Conversely, forced expression of Phox2b in the embryonic chick spinal cord drives ventricular zone progenitors to become post-mitotic neurons and to relocate to the mantle layer. In the neurons thus generated, ectopic expression of Phox2b is sufficient to initiate a programme of motor neuronal differentiation characterised by expression of Islet1 and of the cholinergic transmitter phenotype, in line with our previous results showing that Phox2b is an essential determinant of cranial motor neurons. These results suggest that Phox2b coordinates quantitative and qualitative aspects of neurogenesis, thus ensuring that neurons of the correct phenotype are generated in proper numbers at the appropriate times and locations.

23

Kohyama, Jun, Tsukasa Sanosaka, Akinori Tokunaga, Eriko Takatsuka, Keita Tsujimura, Hideyuki Okano, and Kinichi Nakashima. "BMP-induced REST regulates the establishment and maintenance of astrocytic identity." Journal of Cell Biology 189, no. 1 (March 29, 2010): 159–70. http://dx.doi.org/10.1083/jcb.200908048.

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Once they have differentiated, cells retain their individual character and repress genes that are specifically expressed in other cell lineages, but how alternative fate choice is restricted during and/or after differentiation remains unclear. In the mammalian central nervous system, neurons, astrocytes, and oligodendrocytes are generated throughout life from common tripotent neural progenitor cells (NPCs). Bone morphogenetic proteins (BMPs) are well-known astrocyte-inducing cytokines. We show here that the expression of a transcriptional repressor, RE1 silencer of transcription (REST)/neuron-restrictive silencer factor (NRSF), is up-regulated and sustained by BMP signal activation in the course of astrocytic differentiation of NPCs, and restricts neuronal differentiation. We further show that, in differentiated astrocytes, endogenous REST/NRSF associates with various neuronal genes and that disruption of its function resulted in their derepression, thereby explaining how ectopic neuronal gene expression is prevented in cells with astrocytic traits. Collectively, our results suggest that REST/NRSF functions as a molecular regulator of the nonneuronal phenotype in astrocytes.

24

L.G, Khachatryan. "Clinical - genetic characteristics of neuronal ceroid lipofuscinosis type 2." Neuroscience and Neurological Surgery 6, no. 4 (September 7, 2020): 01–08. http://dx.doi.org/10.31579/2578-8868/129.

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The article is devoted to the issues of diagnosis and therapy of one of the most severe degenerative diseases in children - neuronal ceroid lipofuscinosis (NCL). This is a group of inherited neurodegenerative diseases related to lysosomal storage diseases characterized by regression of psychomotor development, resistant epileptic seizures, vision failure up to amaurosis. The morphological basis of NCL types is the accumulation of autofluorescence material in tissues (particularly in the brain), similar in structure to ceroids and lipofuscin, which are related to the “aging” and “wear-and-tear” pigments. To date, we know 14 variants of diseases associated with mutations in 13 genes (PPT1, TPP1, CLN3, CLN5, CLN6, MFSD8, CLN8, KPUR, DNAJC5, CTSF, ATP13A2, CTD7).The most common and deeply studied types of NCL are types 1,2,3. According to scientific data, neuronal ceroid lipofuscinosis is the most common neurodegenerative disease associated with epilepsy and an early fatal outcome. The article demonstrates a unique family case with this disease, reports a discussion of issues related to preclinical diagnosis through genetic verification and suggests a necessity for etiopathogenetic therapy. Here we present two children, from one family, a brother and sister. At the time of diagnosis the sister already had a complete clinical picture of the disease and was genetically verified as having NCL type 2. This fact enabled to identify the same disease in her younger brother at preclinical level and to begin his pathogenetic therapy in time. Currently, the treatment of these patients is conducted with the expensive preparation of Cerliponase - alpha (brineura), which is a purified human enzyme obtained through recombinant DNA technology. Brineura is a recombinant human tripeptidyl peptidase-1 (rhTPP1), the main function of which is the cleavage of the N-terminal tripeptides of a wide range of protein substrates. With the example of this family, the dynamics of clinical manifestations in a child with NCL has been demonstrated in detail, and the algorithm of the medical action aimed at leveling off the serious neurological deficit has been shown.

25

Fode, Carol, Qiufu Ma, Simona Casarosa, Siew-Lan Ang, David J. Anderson, and François Guillemot. "A role for neural determination genes in specifying the dorsoventral identity of telencephalic neurons." Genes & Development 14, no. 1 (January 1, 2000): 67–80. http://dx.doi.org/10.1101/gad.14.1.67.

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Neurogenin1 (Ngn1), Neurogenin2(Ngn2), and Mash1 encode bHLH transcription factors with neuronal determination functions. In the telencephalon, theNgns and Mash1 are expressed at high levels in complementary dorsal and ventral domains, respectively. We found thatNgn function is required to maintain these two separate expression domains, as Mash1 expression is up-regulated in the dorsal telencephalon of Ngn mutant embryos. We have taken advantage of the replacement of the Ngns by Mash1 in dorsal progenitors to address the role of the neural determination genes in neuronal-type specification in the telencephalon. InNgn2 single and Ngn1; Ngn2 double mutants, a population of early born cortical neurons lose expression of dorsal-specific markers and ectopically express a subset of ventral telencephalic-specific markers. Analysis of Mash1; Ngn2double mutant embryos and of embryos carrying a Ngn2 toMash1 replacement mutation demonstrated that ectopic expression of Mash1 is required and sufficient to confer these ventral characteristics to cortical neurons. Our results indicate that in addition to acting as neuronal determinants, Mash1 andNgns play a role in the specification of dorsal-ventral neuronal identity, directly linking pathways of neurogenesis and regional patterning in the forebrain.

26

Wurtz, Robert H. "Using perturbations to identify the brain circuits underlying active vision." Philosophical Transactions of the Royal Society B: Biological Sciences 370, no. 1677 (September 19, 2015): 20140205. http://dx.doi.org/10.1098/rstb.2014.0205.

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The visual and oculomotor systems in the brain have been studied extensively in the primate. Together, they can be regarded as a single brain system that underlies active vision—the normal vision that begins with visual processing in the retina and extends through the brain to the generation of eye movement by the brainstem. The system is probably one of the most thoroughly studied brain systems in the primate, and it offers an ideal opportunity to evaluate the advantages and disadvantages of the series of perturbation techniques that have been used to study it. The perturbations have been critical in moving from correlations between neuronal activity and behaviour closer to a causal relation between neuronal activity and behaviour. The same perturbation techniques have also been used to tease out neuronal circuits that are related to active vision that in turn are driving behaviour. The evolution of perturbation techniques includes ablation of both cortical and subcortical targets, punctate chemical lesions, reversible inactivations, electrical stimulation, and finally the expanding optogenetic techniques. The evolution of perturbation techniques has supported progressively stronger conclusions about what neuronal circuits in the brain underlie active vision and how the circuits themselves might be organized.

27

Lee, Seunghee, Bora Lee, Kaumudi Joshi, Samuel L. Pfaff, Jae W. Lee, and Soo-Kyung Lee. "A regulatory network to segregate the identity of neuronal subtypes." Developmental Biology 319, no. 2 (July 2008): 574. http://dx.doi.org/10.1016/j.ydbio.2008.05.379.

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28

Toma, Ken-ichi, Ken-ichi Mizutani, Yuko Gonda, and Carina Hanashima. "Molecular identity of temporal neuronal precursors in the mouse neocortex." Neuroscience Research 68 (January 2010): e245. http://dx.doi.org/10.1016/j.neures.2010.07.1085.

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29

Lee, Soo-Kyung, and Samuel L. Pfaff. "Transcriptional networks regulating neuronal identity in the developing spinal cord." Nature Neuroscience 4, S11 (October 29, 2001): 1183–91. http://dx.doi.org/10.1038/nn750.

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30

Paoli, Marco, Angela Albi, Mirko Zanon, Damiano Zanini, Renzo Antolini, and Albrecht Haase. "Neuronal Response Latencies Encode First Odor Identity Information across Subjects." Journal of Neuroscience 38, no. 43 (September 10, 2018): 9240–51. http://dx.doi.org/10.1523/jneurosci.0453-18.2018.

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31

Li, Xuekun, and Peng Jin. "Erratum: Roles of small regulatory RNAs in determining neuronal identity." Nature Reviews Neuroscience 11, no. 6 (June 2010): 449. http://dx.doi.org/10.1038/nrn2853.

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32

Hobert, Oliver. "A map of terminal regulators of neuronal identity inCaenorhabditis elegans." Wiley Interdisciplinary Reviews: Developmental Biology 5, no. 4 (May 2, 2016): 474–98. http://dx.doi.org/10.1002/wdev.233.

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33

Sellers, Katherine, Verena Zyka, Andrew G. Lumsden, and Alessio Delogu. "Transcriptional control of GABAergic neuronal subtype identity in the thalamus." Neural Development 9, no. 1 (2014): 14. http://dx.doi.org/10.1186/1749-8104-9-14.

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34

Conaco, Cecilia, Stefanie Otto, Jong-Jin Han, and Gail Mandel. "Reciprocal actions of REST and a microRNA promote neuronal identity." Proceedings of the National Academy of Sciences 103, no. 7 (February 6, 2006): 2422–27. http://dx.doi.org/10.1073/pnas.0511041103.

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35

Lee, Seunghee, Bora Lee, Kaumudi Joshi, Samuel L. Pfaff, Jae W. Lee, and Soo-Kyung Lee. "A Regulatory Network to Segregate the Identity of Neuronal Subtypes." Developmental Cell 14, no. 6 (June 2008): 877–89. http://dx.doi.org/10.1016/j.devcel.2008.03.021.

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36

McConnell, S. K. "The specification of neuronal identity in the mammalian cerebral cortex." Experientia 46, no. 9 (September 1990): 922–29. http://dx.doi.org/10.1007/bf01939385.

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37

McConnell, Susan K. "The control of neuronal identity in the developing cerebral cortex." Current Opinion in Neurobiology 2, no. 1 (February 1992): 23–27. http://dx.doi.org/10.1016/0959-4388(92)90156-f.

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38

Jacob, John, Jennifer Kong, Steven Moore, Christopher Milton, Noriaki Sasai, Rosa Gonzalez-Quevedo, Javier Terriente, et al. "Retinoid Acid Specifies Neuronal Identity through Graded Expression of Ascl1." Current Biology 23, no. 5 (March 2013): 412–18. http://dx.doi.org/10.1016/j.cub.2013.01.046.

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39

Jacob, John, Jennifer Kong, Steven Moore, Christopher Milton, Noriaki Sasai, Rosa Gonzalez-Quevedo, Javier Terriente, et al. "Retinoid Acid Specifies Neuronal Identity through Graded Expression of Ascl1." Current Biology 23, no. 7 (April 2013): 632. http://dx.doi.org/10.1016/j.cub.2013.03.017.

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40

Briscoe, James, and Johan Ericson. "The specification of neuronal identity by graded sonic hedgehog signalling." Seminars in Cell & Developmental Biology 10, no. 3 (June 1999): 353–62. http://dx.doi.org/10.1006/scdb.1999.0295.

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41

Lo, L., M. C. Tiveron, and D. J. Anderson. "MASH1 activates expression of the paired homeodomain transcription factor Phox2a, and couples pan-neuronal and subtype-specific components of autonomic neuronal identity." Development 125, no. 4 (February 15, 1998): 609–20. http://dx.doi.org/10.1242/dev.125.4.609.

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We have investigated the genetic circuitry underlying the determination of neuronal identity, using mammalian peripheral autonomic neurons as a model system. Previously, we showed that treatment of neural crest stem cells (NCSCs) with bone morphogenetic protein-2 (BMP-2) leads to an induction of MASH1 expression and consequent autonomic neuronal differentiation. We now show that BMP2 also induces expression of the paired homeodomain transcription factor Phox2a, and the GDNF/NTN signalling receptor tyrosine kinase c-RET. Constitutive expression of MASH1 in NCSCs from a retroviral vector, in the absence of exogenous BMP2, induces expression of both Phox2a and c-RET in a large fraction of infected colonies, and also promotes morphological neuronal differentiation and expression of pan-neuronal markers. In vivo, expression of Phox2a in autonomic ganglia is strongly reduced in Mash1 −/− embryos. These loss- and gain-of-function data suggest that MASH1 positively regulates expression of Phox2a, either directly or indirectly. Constitutive expression of Phox2a, by contrast to MASH1, fails to induce expression of neuronal markers or a neuronal morphology, but does induce expression of c-RET. These data suggest that MASH1 couples expression of pan-neuronal and subtype-specific components of autonomic neuronal identity, and support the general idea that identity is established by combining subprograms involving cascades of transcription factors, which specify distinct components of neuronal phenotype.

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Constantine, Godwin Roger. "The Biological Basis of Performativity of Identity - Linking Scientific Evidence to Social Theory." Journal of Ethnic and Cultural Studies 4, no. 2 (December 29, 2017): 88. http://dx.doi.org/10.29333/ejecs/82.

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Identity is the essence of performance and performance is the essence of identity. Without identity our performance does not assume any cultural significance. Our relative identity allows our performance to be located in the socio-cultural space. Our identity forms the foundation for the discursive significance of our performance. However, our identity is not unique, it is established by performing a pre-existing script. The biological basis of identity can be understood by applying learning theories and by analyzing how these leant behavior is embedded in our neuronal network in the brain and how these behavior patterns are controlled by psychological factors to result in the identity we observe. Recent developments in the fields of neuroscience and functional neuro imaging have enabled us to study objectively the process of neural mechanisms and map areas of brain that are involved in learning various behavior patterns. These neuronal networks and the neuro transmitters play a key role in memory and behavior of animals. Aby studying the particular pattern of behavior and the brain area that mediates that behavior it will be possible to determine neuronal networks that control core identity characteristics and that control other less important characteristics. With the emergence of studies in neuroplasticity the possibility of relearning behaviors through new neuronal pathways may open new avenues to treat conditions that affect identity. Understanding the biological basis of identity will lead to widening of research area and better understanding of the concept.

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O’Toole, Sean M., Monica M. Ferrer, Jennifer Mekonnen, Haihan Zhang, Yasuyuki Shima, David R. Ladle, and Sacha B. Nelson. "Dicer maintains the identity and function of proprioceptive sensory neurons." Journal of Neurophysiology 117, no. 3 (March 1, 2017): 1057–69. http://dx.doi.org/10.1152/jn.00763.2016.

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Neuronal cell identity is established during development and must be maintained throughout an animal’s life (Fishell G, Heintz N. Neuron 80: 602–612, 2013). Transcription factors critical for establishing neuronal identity can be required for maintaining it (Deneris ES, Hobert O. Nat Neurosci 17: 899–907, 2014). Posttranscriptional regulation also plays an important role in neuronal differentiation (Bian S, Sun T. Mol Neurobiol 44: 359–373, 2011), but its role in maintaining cell identity is less established. To better understand how posttranscriptional regulation might contribute to cell identity, we examined the proprioceptive neurons in the dorsal root ganglion (DRG), a highly specialized sensory neuron class, with well-established properties that distinguish them from other neurons in the ganglion. By conditionally ablating Dicer in mice, using parvalbumin (Pvalb)-driven Cre recombinase, we impaired posttranscriptional regulation in the proprioceptive sensory neuron population. Knockout (KO) animals display a progressive form of ataxia at the beginning of the fourth postnatal week that is accompanied by a cell death within the DRG. Before cell loss, expression profiling shows a reduction of proprioceptor specific genes and an increased expression of nonproprioceptive genes normally enriched in other ganglion neurons. Furthermore, although central connections of these neurons are intact, the peripheral connections to the muscle are functionally impaired. Posttranscriptional regulation is therefore necessary to retain the transcriptional identity and support functional specialization of the proprioceptive sensory neurons. NEW & NOTEWORTHY We have demonstrated that selectively impairing Dicer in parvalbumin-positive neurons, which include the proprioceptors, triggers behavioral changes, a lack of muscle connectivity, and a loss of transcriptional identity as observed through RNA sequencing. These results suggest that Dicer and, most likely by extension, microRNAs are crucially important for maintaining proprioception. Additionally, this study hints at the larger question of how neurons maintain their functional and molecular specificity.

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Northcutt, Adam J., Daniel R. Kick, Adriane G. Otopalik, Benjamin M. Goetz, Rayna M. Harris, Joseph M. Santin, Hans A. Hofmann, Eve Marder, and David J. Schulz. "Molecular profiling of single neurons of known identity in two ganglia from the crabCancer borealis." Proceedings of the National Academy of Sciences 116, no. 52 (December 5, 2019): 26980–90. http://dx.doi.org/10.1073/pnas.1911413116.

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Understanding circuit organization depends on identification of cell types. Recent advances in transcriptional profiling methods have enabled classification of cell types by their gene expression. While exceptionally powerful and high throughput, the ground-truth validation of these methods is difficult: If cell type is unknown, how does one assess whether a given analysis accurately captures neuronal identity? To shed light on the capabilities and limitations of solely using transcriptional profiling for cell-type classification, we performed 2 forms of transcriptional profiling—RNA-seq and quantitative RT-PCR, in single, unambiguously identified neurons from 2 small crustacean neuronal networks: The stomatogastric and cardiac ganglia. We then combined our knowledge of cell type with unbiased clustering analyses and supervised machine learning to determine how accurately functionally defined neuron types can be classified by expression profile alone. The results demonstrate that expression profile is able to capture neuronal identity most accurately when combined with multimodal information that allows for post hoc grouping, so analysis can proceed from a supervised perspective. Solely unsupervised clustering can lead to misidentification and an inability to distinguish between 2 or more cell types. Therefore, this study supports the general utility of cell identification by transcriptional profiling, but adds a caution: It is difficult or impossible to know under what conditions transcriptional profiling alone is capable of assigning cell identity. Only by combining multiple modalities of information such as physiology, morphology, or innervation target can neuronal identity be unambiguously determined.

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Ferrera, Loretta, Antonella Caputo, and Luis J. V. Galietta. "TMEM16A Protein: A New Identity for Ca2+-Dependent Cl− Channels." Physiology 25, no. 6 (December 2010): 357–63. http://dx.doi.org/10.1152/physiol.00030.2010.

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Ca+-dependent Cl− channels (CaCCs) play a variety of physiological roles in different organs and tissues, including transepithelial Cl− secretion, smooth muscle contraction, regulation of neuronal excitability, and transduction of sensory stimuli. The recent identification of TMEM16A protein as an important component of CaCCs should allow a better understanding of their physiological role, structure-function relationship, and regulatory mechanisms.

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Akamatsu, W., H. Fujihara, T. Mitsuhashi, M. Yano, S. Shibata, Y. Hayakawa, H. J. Okano, et al. "The RNA-binding protein HuD regulates neuronal cell identity and maturation." Proceedings of the National Academy of Sciences 102, no. 12 (March 11, 2005): 4625–30. http://dx.doi.org/10.1073/pnas.0407523102.

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Cho, Yong Ku. "Genetically Encoded Tools: Bridging the Gap between Neuronal Identity and Function." ACS Chemical Neuroscience 6, no. 1 (January 9, 2015): 14–15. http://dx.doi.org/10.1021/acschemneuro.5b00008.

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Scholpp, S., A. Delogu, J. Gilthorpe, D. Peukert, S. Schindler, and A. Lumsden. "Her6 regulates the neurogenetic gradient and neuronal identity in the thalamus." Proceedings of the National Academy of Sciences 106, no. 47 (November 10, 2009): 19895–900. http://dx.doi.org/10.1073/pnas.0910894106.

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Mizutani, Ken-ichi, and Carina Hanashima. "Characterization of temporal identity of neuronal progenitor cells in the neocortex." Neuroscience Research 65 (January 2009): S157. http://dx.doi.org/10.1016/j.neures.2009.09.803.

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Schmucker, Dietmar. "Molecular diversity of Dscam: recognition of molecular identity in neuronal wiring." Nature Reviews Neuroscience 8, no. 12 (December 2007): 915–20. http://dx.doi.org/10.1038/nrn2256.

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