Relevant bibliographies by topics / Neuronal signaling

Academic literature on the topic 'Neuronal signaling'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Neuronal signaling"

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Kurniawan, Shahdevi Nandar. "NEURONAL SIGNALING." MNJ (Malang Neurology Journal) 1, no. 2 (July 1, 2015): 85–95. http://dx.doi.org/10.21776/ub.mnj.2015.001.02.7.

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Berridge, Michael J. "Neuronal Calcium Signaling." Neuron 21, no. 1 (July 1998): 13–26. http://dx.doi.org/10.1016/s0896-6273(00)80510-3.

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Cosker, K. E., and R. A. Segal. "Neuronal Signaling through Endocytosis." Cold Spring Harbor Perspectives in Biology 6, no. 2 (February 1, 2014): a020669. http://dx.doi.org/10.1101/cshperspect.a020669.

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Fields, R. D. "Signaling by Neuronal Swelling." Science Signaling 4, no. 155 (January 4, 2011): tr1. http://dx.doi.org/10.1126/scisignal.4155tr1.

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Amato, Stephen, and Heng-Ye Man. "AMPK signaling in neuronal polarization." Communicative & Integrative Biology 5, no. 2 (March 2012): 152–55. http://dx.doi.org/10.4161/cib.18968.

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Zheng, James Q., and Mu-ming Poo. "Calcium Signaling in Neuronal Motility." Annual Review of Cell and Developmental Biology 23, no. 1 (November 2007): 375–404. http://dx.doi.org/10.1146/annurev.cellbio.23.090506.123221.

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Rosenberg, S. S., and N. C. Spitzer. "Calcium Signaling in Neuronal Development." Cold Spring Harbor Perspectives in Biology 3, no. 10 (July 5, 2011): a004259. http://dx.doi.org/10.1101/cshperspect.a004259.

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Dorans, Kirsten. "Glowing worms elucidate neuronal signaling." Lab Animal 38, no. 11 (November 2009): 340. http://dx.doi.org/10.1038/laban1109-340b.

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Sontheimer, Harald. "Glial Influences on Neuronal Signaling." Neuroscientist 1, no. 3 (May 1995): 123–26. http://dx.doi.org/10.1177/107385849500100302.

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Nakamura, Shun-ichi, Eri Fukai, Satoshi Miya, Henryk Jesko, and Taro Okada. "Sphingolipid signaling and neuronal function." Pharmacological Reports 63, no. 5 (September 2011): 1279–80. http://dx.doi.org/10.1016/s1734-1140(11)70665-x.

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Dissertations / Theses on the topic "Neuronal signaling"

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Sann, Sharon Bree. "Neuronal development roles of calcium signaling /." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3259060.

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Thesis (Ph. D.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed June 21, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
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Yang, Silei. "Rapid neuronal signaling cascades initiated by corticosterone." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-148762.

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O'Hare, Michael J. "Cell cycle related signaling in neuronal death." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/29368.

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Evidence indicates that neuronal loss in the course of neurodegenerative disease often occurs through programmed death processes. The development of effective therapeutic treatments for such diseases requires detailed knowledge of the intracellular signaling pathways controlling these death processes. Previous work has identified cyclin-dependent kinases, a family of kinases normally involved in the control of cell division, as potential regulators of death in neurons. For instance, a number of events that occur during the G1 to S transition in proliferating cells, such as cyclin D/cdk4 activation and phosphorylation of its target, pRb, have been detected in dying neurons and appear to be essential for death. In the cell cycle, pRb phosphorylation is followed by activation of the transcription factor E2F1. It is not known if E2F1 is also involved in neuronal death. I found that E2F1 expression in neurons induced apoptotic death dependent on Bax but independent of p53. Also, E2F1 mRNA and protein levels increase in neurons induced to die by exposure to low concentrations of K+, and neurons from E2F1 null mice are resistant to this death. These results are consistent with participation of endogenous E2F1 in neuronal death signaling. Cdk5 is a member of the cyclin-dependent kinase family which does not have a function in the cell cycle. Instead cdk5, together with its binding partners p35 and p39, is involved in a variety of neuronal functions. Cleavage of p35 into a smaller p25 form has been shown to convert cdk5 into a death promoting kinase. However, it is not yet clear under which circumstances cdk5 signals death, and there is also some contrasting evidence suggesting cdk5 is a pro-survival factor. By targeting dominant negative cdk5 expression to either the nuclear or cytoplasmic compartments I show that cdk5 performs a pro-death function within the nucleus but a pro-survival function within the cytoplasm. The nuclear pro-death signal is relevant only when p25 is produced early, as it is following glutamate induced death, and not when it is produced late as a result of caspase activation, as it is following DNA damage.
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Tornieri, Karine. "Signaling Mechanisms Regulating Neuronal Growth Cone Dynamics." Digital Archive @ GSU, 2008. http://digitalarchive.gsu.edu/biology_diss/48.

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During the development of the nervous system, neurons migrate to their final location and extend neurites that navigate long distances in the extracellular environment to reach their synaptic targets. The proper functioning of the nervous system depends on correct connectivity, and mistakes in the wiring of the nervous system lead to brain abnormalities and mental illness. Growth cones are motile structures located at the tip of extending neurites that sense and respond to guidance cues encountered along the path toward their targets. Binding of these cues to receptors located on growth cone filopodia and lamellipodia triggers intracellular signaling pathways that regulate growth cone cytoskeletal dynamics. Although studies on extracellular cues and their effects on neuronal guidance are well documented, less is known about the intracellular signaling mechanisms that regulate growth cone motility. This dissertation focuses on two signaling pathways and describes how they might be involved in determining growth cone morphology during neuronal development. The specific aims of this work address: (1) the role of phosphatidylinositol-3-kinase (PI-3K) and its downstream signaling pathway in regulating growth cone motility, and (2) the effect of nitric oxide (NO) release from a single cell on growth cone morphology of neighboring neurons. This study employs defined neurons from the pond snail, Helisoma trivolvis, to demonstrate that inhibition of PI-3K induces a concomitant increase in filopodial length and a decrease in the rate at which neurites advance. These effects are mediated through the lipid and protein kinase activities of PI-3K, and filopodial elongation is due to an increase in the rate at which filopodia elongate and the time that individual filopodia spend extending. Additionally, this study demonstrates that NO release from a single cell can affect growth cone dynamics on neighboring neurons via soluble guanylyl cyclase (sGC), and that NO has a physiological effect up to a distance of 100 ìm. Overall this study provides new information on cellular mechanisms regulating growth cone motility, and suggests a potential role of PI-3K and NO in neuronal pathfinding in vivo.
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Rogoz, Katarzyna. "Signaling Mechanisms in the Neuronal Networks of Pain and Itch." Doctoral thesis, Uppsala universitet, Genetisk utvecklingsbiologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-183255.

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Glutamate is the essential neurotransmitters in pain pathways. The discovery of the vesicular glutamate transporters (VGLUT1-3) has been a fundamental step on the way to describe glutamate-dependent pain pathways. We used the Cre-lox system to construct conditional knockouts with deficient Vglut2 transmission in specific neuronal populations. We generated a Vglut2f/f;Ht-Pa-Cre line to selectively delete Vglut2 from the peripheral nervous system. These Vglut2 deficient mice showed decreased acute nociceptive responses and were less prone to develop an inflammatory state. They did not develop cold allodynia, or heat hyperalgesia and were less hypersensitive to mechanical stimuli in the PSNL chronic pain model. Further analyses of genes with altered expression after nerve injury, revealed candidates for future studies of chronic pain biomarkers. Interestingly, the Vglut2f/f;Ht-Pa-Cre mice developed an elevated itch behavior. To investigate more specific neuronal populations, we analyzed mice lacking Vglut2 in the Nav1.8 population, as inflammatory hyperalgesia, cold pain, and noxious mechanosensation have been shown to depend upon Nav1.8Cre positive sensory neurons. We showed that deleting Vglut2 in Nav1.8Cre positive neurons abolished thermal hyperalgesia in persistent inflammatory models and responses to noxious mechanical stimuli. We also demonstrated that substance P and VGLUT2-dependent glutamatergic transmission are co-required for the development of formalin-induced inflammatory pain and heat hyperalgesia in persistent inflammatory states. Deletion of Vglut2 in a subpopulation of neurons overlapping with the vanilloid receptor (TRPV1) primary afferents in the dorsal root ganglia resulted in a dramatic increase in itch behavior accompanied by a reduced responsiveness to thermal pain. Substance P signaling and VGLUT2-mediated glutamatergic transmission in TRPV1 neurons was co-required for the development of inflammatory pain states. Analyses of an itch phenotype uncovered the pathway within TRPV1 neurons, with VGLUT2 playing a regulatory role and GRPR neurons, which are to plausible converge the itch signal in the spinal cord. These studies confirmed the essential role of VGLUT2-dependent glutamatergic transmission in acute and persistent pain states and identified the roles of specific subpopulations of primary afferent neurons. Additionally, a novel pain and itch transmission pathway in TRPV1/VGLUT2 positive neurons was identified, which could be part of the gate control of pain.
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Cui, Rui. "The role of Ryanodine receptors in neuronal calcium signaling." Scholarly Commons, 2008. https://scholarlycommons.pacific.edu/uop_etds/705.

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Calcium (Ca2+) is a universal second messenger controlling a wide variety of cellular reactions and adaptive responses. All the versatility of a Ca2+ signaling requires that the concentration of Ca2+ ions in the cytoplasm be highly regulated. Generation of Ca2+ mobilizing signals in cells involves regulation by multiple components controlling Ca2+ release from the internal stores, Ca2+ influx across the plasma membrane, elicitation of Ca2+ sensitive processes and finally the removal of Ca2+ from the cells. Inositol-1, 4, 5-trisphosphate receptors (IP3Rs) and ryandine receptors (RyRs) are the most studied Ca2+ release channels located on the internal stores. Previous studies have shown ryanodine receptors (RyRs) play a key role in the process of Ca2+ signaling participating in the oscillatory patterns of controlling the release of Ca2+ from ER and regulating the influx of Ca2+ by coupling with plasma Ca2+ channels. Although recent progress deciphered the behavior and function of RyRs in regulation of Ca2+ signal, it still remains mysterious in understanding the molecular mechanism of its regulation and its connection with plasma membrane Ca2+ channels in neuronal cells. Here this study aimed to utilized the most cutting-edge RNA interference techniques, along with well-characterized pharmacological regulators of RyRs, to better characterized the role of RyRs is our neuronal cell line model NG115-401L. Our first main goal of this project was to develop an effective protocol that could selectively knockout or knockdown expression levels of the RyR1 gene in NG115-401L cells. After testing different siRNA primers including their combination with different transfection reagent, the result shows a significant silencing effect to the RyR1 mRNA expression levels. In the second part of this study, we used a group of pharmacological agents with well-known regulatory actions on RyRs to characterize the functional roles of the RyRs expressed in NG115-401L cells. All four agonists which are ryanodine, caffeine, CMC and PCB 95 show their abilities to activate the RyRs, increase [Ca2+]iand induce the influx of Ca2+ via SOC. After transfected NG115-401L cells by siRNA, the Ca2+ release and influx signals were highly diminished suggesting RyR1 gene was successfully knocked down and the successfully knocked down and the Ca2+ mobilization mediated by RyR1 was decreased greatly. Finally in order to study the effects of the regulation of Ca2+ by RyR modulators and RyR gene knockdown on cell growth patterns and cell viability, the NG115-401L cells were exposed to various concentrations of RyR regulators and siRyR1 primer for different time periods. The siRNA transfection showed the least effect on cell growth, as compared with pharmacological agents that modulate RyR function. Considering we achieved high levels of gene knockdown and its low cytotoxity, our result suggests that siRNA silencing for RyRs may become a promising gene therapeutic target in the future.
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Guo, Jing. "Studying the signaling pathways in ROS-induced neuronal cell death /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202005%20GUO.

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Suen, Ka-chun, and 孫嘉俊. "Molecular signaling of neuronal apoptosis in beta-amyloid peptide neurotoxicity." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31245961.

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Figueroa-Masot, Xavier Andres. "The role of JNK signaling and Bcl-2 in neuronal function : from apoptosis to neuron excitability /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/10647.

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Krjukova, Jelena. "Investigation on Pre- and Postsynaptic Ca2+ Signaling in Neuronal Model Systems." Doctoral thesis, Uppsala universitet, Institutionen för neurovetenskap, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4300.

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Communication between neuronal and non-neuronal is called volume transmission when the released neurotransmitter (NT) acts via diffusion and affects several target cells. Both the neurosecretory and postsynaptic cell responses are linked to [Ca2+]i elevations. In the present thesis the role of pre-and postsynaptic Ca2+ elevations has been investigated in the reconstituted "synapse" model comprised of NGF-differentiated PC12 and HEL cells as well as in SH-SY5Y neuroblastoma cells. In PC12 cells, both 70mM K+ and nicotine triggered NT release, which could be detected as a secondary [Ca2+]i increase in surrounding HEL cells. Both secretagogues shared the same voltage-dependent Ca2+ influx pathway as judged from the pharmacological profile blockers of voltage-gated Ca2+ channels. The coupling of electrical responses to the activation of Ca2+ signaling via muscarinic receptors in SH-SY5Y cells was also studied. These data revealed that depolarization caused a considerable potentiation of the muscarinic Ca2+ response. The potentiated Ca2+ increase was mainly dependent on the enhanced Ca2+ influx and to a lesser extent on [Ca2+]i release from intracellular stores. A phospholipase C (PLC) activator, m-3M3FBS was used to further study the role of G-protein coupled receptor (GPCR)-coupled Ca2+ signaling. However, it was found that m-3M3FBS instead triggered [Ca2+]i elevations independently of PLC activation. In conclusion, the results indicate that the magnitude of NT release from PC12 cells is sufficient to cause a robust activation of neighboring target cells. Postsynaptic muscarinic signaling is amplified due to integration of electrical excitation and GPCR signaling. The PLC activator, m-3M3FBS is not suitable for studies of PLC-mediated signals in intact cells.
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Books on the topic "Neuronal signaling"

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Hatton, Glenn I., and Vladimir Parpura, eds. Glial ⇔ Neuronal Signaling. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5.

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Tasker, Jeffrey G., Jaideep S. Bains, and Julie A. Chowen, eds. Glial-Neuronal Signaling in Neuroendocrine Systems. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62383-8.

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Wen, Joseph Yao Min. Neuronal-glial signaling involved in explant induced satellite cell proliferation in the adult trigeminal ganglia. Ottawa: National Library of Canada, 1993.

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Ron, Wallace. Membrane microdomain regulation of neuron signaling. New York: Nova Science Publishers, 2008.

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Membrane microdomain regulation of neuron signaling. New York: Nova Science Publishers, 2008.

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Chadwick, Derek J., and Jamie Goode, eds. Purinergic Signalling in Neuron-Glia Interactions. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/9780470032244.

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Derek, Chadwick, Goode Jamie, Novartis Foundation, and Symposium on Purinergic Signalling in Neuron-Glia Interactions (2005 : London, England), eds. Purinergic signalling in neuron-glia interactions. Chichester: John Wiley & Sons, 2006.

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N, Verkhratskiĭ A., ed. Calcium signalling in the nervous system. Chichester: Wiley, 1995.

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W, Arbuthnott Gordon, and Emson P. C, eds. Chemical signalling in the basal ganglia. Amsterdam: Elsevier, 1993.

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L, Iversen Leslie, Goodman E. C, and Neuroscience Research Centre (Merck Sharp & Dohme), eds. Fast and slow chemical signalling in the nervous system. Oxford: Oxford University Press, 1986.

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Book chapters on the topic "Neuronal signaling"

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Kettenmann, Helmut, and Carola G. Schipke. "Calcium signaling in glia." In Glial ⇔ Neuronal Signaling, 297–321. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5_12.

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Tekkök, Selva Baltan, and Bruce R. Ransom. "The glial-neuronal interactions and signaling: an introduction." In Glial ⇔ Neuronal Signaling, 1–20. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5_1.

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Deitmer, Joachim W. "pH regulation and acid/base-mediated transport in glial cells." In Glial ⇔ Neuronal Signaling, 263–77. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5_10.

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Brown, Angus M., Selva Baltan Tekkök, and Bruce R. Ransom. "Glial-neuronal interactions and brain energy metabolism." In Glial ⇔ Neuronal Signaling, 279–96. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5_11.

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Giaume, Christian, William Même, and Annette Koulakoff. "Astrocyte gap junctions and glutamate-induced neurotoxicity." In Glial ⇔ Neuronal Signaling, 323–48. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5_13.

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Arcuino, Gregory, Marisa Cotrina, and Maiken Nedergaard. "Mechanism and significance of astrocytic Ca2+ signaling." In Glial ⇔ Neuronal Signaling, 349–63. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5_14.

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Parpura, Vladimir. "Glutamate-mediated bi-directional signaling between neurons and astrocytes." In Glial ⇔ Neuronal Signaling, 365–95. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5_15.

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Evanko, Daniel S., Jai-Yoon Sul, Qi Zhang, and Philip G. Haydon. "The regulated release of transmitters from astrocytes." In Glial ⇔ Neuronal Signaling, 397–416. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5_16.

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Slezak, Michal, and Frank W. Pfrieger. "Role of astrocytes in the formation, maturation and maintenance of synapses." In Glial ⇔ Neuronal Signaling, 417–36. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5_17.

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Soustelle, Laurent, and Angela Giangrande. "Gene function in glial-neuronal interactions." In Glial ⇔ Neuronal Signaling, 21–52. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5_2.

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Conference papers on the topic "Neuronal signaling"

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Suzuki, Junichi, Pruet Boonma, and Dung H. Phan. "Neuronal signaling optimization for intrabody nanonetworks." In 2014 Fourth International Conference on Digital Information and Communication Technology and its Applications (DICTAP). IEEE, 2014. http://dx.doi.org/10.1109/dictap.2014.6821659.

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Roy, Jean-Pierre. "Neuronal mechanism for signaling the direction of self-motion." In Computational Vision Based on Neurobiology, edited by Teri B. Lawton. SPIE, 1994. http://dx.doi.org/10.1117/12.171137.

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Pagès, S., I. Veilleux, P. De Koninck, and D. Côté. "Multimodal optical microscopy for monitoring fast neuronal activity and signaling." In Biomedical Optics (BiOS) 2008, edited by Ammasi Periasamy and Peter T. C. So. SPIE, 2008. http://dx.doi.org/10.1117/12.764161.

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Ong, Taren, and David J. Solecki. "Abstract B02: Sonic hedgehog signaling in neuronal migration and tumorigenesis." In Abstracts: AACR Special Conference on Developmental Biology and Cancer; November 30 - December 3, 2015; Boston, Massachusetts. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.devbiolca15-b02.

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Ezell, Nicole, and Anna Ritz. "Reconstructing Neuronal Signaling Pathways With the Potential for Disruption in Schizophrenia." In BCB '16: ACM International Conference on Bioinformatics, Computational Biology, and Health Informatics. New York, NY, USA: ACM, 2016. http://dx.doi.org/10.1145/2975167.2985662.

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Ning Feng, Yong Yang, and Xiaoxiang Zheng. "Spatiotemporal Neuronal Signaling by Nitric Oxide: Diffusion-Reaction Modeling and Analysis." In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1615881.

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ANGELIKA, Dina, Risa ETIKA, and I. Dewa Gede UGRASENA. "Mechanism of necrotizing enterocolitis in preterm infants through the hypoxia signaling pathway, neuronal-glial signaling pathway, and intestinal fatty acid signaling pathway." In ICMHI 2022: 2022 6th International Conference on Medical and Health Informatics. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3545729.3545767.

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Liu, Mingli, Koichi Inoue, and Zhi-gang Xiong. "Abstract 4625: ASIC1 regulates neuronal differentiation of neuroblastoma through Notch signaling pathway." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4625.

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Lusardi, Theresa A., John Wolf, Douglas H. Smith, and David F. Meaney. "Strain and Strain Rate Dependent Changes in Cytosolic Calcium of Cultured Neurons Subjected to Mechanical Stretch." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0795.

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Abstract In this study, we examined the response of cultured neurons to mechanical stretch, varying the rate and magnitude of mechanical stretch to encompass both physiological and non-physiological levels. Fully differentiated NTera2 cells, a human-derived neuronal cell line, were cultured on a flexible substrate and a uniaxial strain was applied to the neurons at a specified magnitude and rate. Using rates representing non-physiologic (rapid onset time of 20ms and intermediate onset time of 85 ms), and physiologic levels (slow onset time of 1.5sec), we measured the intracellular calcium transient using the calcium indicator dye Fura-2. Immediately following the stretch, intracellular calcium concentration increased, then decreased as the cells attempted to restore pre-stretch cytosolic calcium levels. Statistical analysis using ANOVA showed that normalized peak [Ca+2]i immediately following stretch, average [Ca+2]i following the stimulation, and the final [Ca+2]i value at 4 minutes post-stretch had a significant (p < .0005) dependence on the rate and magnitude at which stretch was applied. At the physiologic rate cell response was minimal, while cell response was maximal at the severe onset rate. Unexpectedly, we observed an attenuation in the response in high stretch, high rate group. At the highest stretch rate studied, these data provide insight into the response of neurons to deformations associated with mechanical trauma. Since calcium is an important cation for processes that can remodel the cytoarchitecture, affect cell signaling, and influence gene expression, the changes associated with the high rates provide at least one pathway for influencing both acute and chronic changes in neuronal behavior following traumatic injury.
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Suzuki, Junichi, and Pruet Boonma. "Noise-aware evolutionary TDMA optimization for neuronal signaling in medical sensor-actuator networks." In GECCO '14: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2014. http://dx.doi.org/10.1145/2598394.2609854.

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Reports on the topic "Neuronal signaling"

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Liu, Ya F. Molecular Analysis of the Common Signaling Mechanism of Neuronal Death Induced by Glutamate and Mutated Huntington. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada393700.

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Elmann, Anat, Orly Lazarov, Joel Kashman, and Rivka Ofir. therapeutic potential of a desert plant and its active compounds for Alzheimer's Disease. United States Department of Agriculture, March 2015. http://dx.doi.org/10.32747/2015.7597913.bard.

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We chose to focus our investigations on the effect of the active forms, TTF and AcA, rather than the whole (crude) extract. 1. To establish cultivation program designed to develop lead cultivar/s (which will be selected from the different Af accessions) with the highest yield of the active compounds TTF and/or achillolide A (AcA). These cultivar/s will be the source for the purification of large amounts of the active compounds when needed in the future for functional foods/drug development. This task was completed. 2. To determine the effect of the Af extract, TTF and AcA on neuronal vulnerability to oxidative stress in cultured neurons expressing FAD-linked mutants.Compounds were tested in N2a neuroblastoma cell line. In addition, we have tested the effects of TTF and AcA on signaling events promoted by H₂O₂ in astrocytes and by β-amyloid in neuronal N2a cells. 3. To determine the effect of the Af extract, TTF and AcA on neuropathology (amyloidosis and tau phosphorylation) in cultured neurons expressing FAD-linked mutants. 4. To determine the effect of A¦ extract, AcA and TTF on FAD-linked neuropathology (amyloidosis, tau phosphorylation and inflammation) in transgenic mice. 5. To examine whether A¦ extract, TTF and AcA can reverse behavioral deficits in APPswe/PS1DE9 mice, and affect learning and memory and cognitive performance in these FAD-linked transgenic mice. Background to the topic.Neuroinflammation, oxidative stress, glutamate toxicity and amyloid beta (Ab) toxicity are involved in the pathogenesis of Alzheimer's diseases. We have previously purified from Achilleafragrantissimatwo active compounds: a protective flavonoid named 3,5,4’-trihydroxy-6,7,3’-trimethoxyflavone (TTF, Fl-72/2) and an anti-inflammatory sesquiterpenelactone named achillolide A (AcA). Major conclusions, solutions, achievements. In this study we could show that TTF and AcA protected cultured astrocytes from H₂O₂ –induced cell death via interference with cell signaling events. TTF inhibited SAPK/JNK, ERK1/2, MEK1 and CREBphosphorylation, while AcA inhibited only ERK1/2 and MEK1 phosphorylation. In addition to its protective activities, TTF had also anti-inflammatory activities, and inhibited the LPS-elicited secretion of the proinflammatorycytokinesInterleukin 6 (IL-6) and IL-1b from cultured microglial cells. Moreover, TTF and AcA protected neuronal cells from glutamate and Abcytotoxicity by reducing the glutamate and amyloid beta induced levels of intracellular reactive oxygen species (ROS) and via interference with cell signaling events induced by Ab. These compounds also reduced amyloid precursor protein net processing in vitro and in vivo in a mouse model for Alzheimer’s disease and improvedperformance in the novel object recognition learning and memory task. Conclusion: TTF and AcA are potential candidates to be developed as drugs or food additives to prevent, postpone or ameliorate Alzheimer’s disease. Implications, both scientific and agricultural.The synthesis ofAcA and TTF is very complicated. Thus, the plant itself will be the source for the isolation of these compounds or their precursors for synthesis. Therefore, Achilleafragrantissima could be developed into a new crop with industrial potential for the Arava-Negev area in Israel, and will generate more working places in this region.
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3

Li, Nianzhen. Nitric Oxide in Astrocyte-Neuron Signaling. Office of Scientific and Technical Information (OSTI), January 2002. http://dx.doi.org/10.2172/803739.

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Heidenreich, Kim, and Dan A. Linseman. Signaling Pathways that Mediate Neurotoxin-Induced Death of Dopamine Neurons. Fort Belvoir, VA: Defense Technical Information Center, November 2005. http://dx.doi.org/10.21236/ada447899.

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Heidenreich, Kim A. Signaling Pathways that Mediate Neurotoxin-Induced Death of Dopamine Neurons. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada429190.

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Lekhanya, Portia Keabetswe, and Kabelo Mokgalaboni. Exploring the effectiveness of vitamin B12 complex and alpha-lipoic acid as a treatment for diabetic neuropathy. Protocol for systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0167.

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Review question / Objective: Does Alpha-Lipoic acid increase the uptake of glucose for better glycaemic control? Does vitamin B12 and Alpha-Lipoic acid improve inflammation? The aim of the study is to explore the effectiveness of Vitamin B12 and Alpha-Lipoic Acid as a possible treatment for diabetic neuropathy with major emphasis on markers of inflammation and glucose metabolism. Condition being studied: Diabetic Neuropathy (DN) is a heterogeneous type of nerve damage associated with diabetes mellitus, the condition most often damages nerves in the legs and feet. It presents both clinically and sub-clinically affecting the peripheral nervous system as a result of an increase in glucose concentration which interferes with nerve signalling. After the discovery of insulin as a treatment for Diabetes Mellitus (DM), the prevalence of DN has since increased significantly due to DM patients having a longer life expectancy. It has been estimated that atleast 50% of DM patients will develop DN in their life, with approximately 20% of these patients experiencing neuropathic pain. Nerves are susceptible to changes in glucose concentrations and insulin makes it impossible for neurons to continue regulating glucose uptake.
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