Relevant bibliographies by topics / Cortical neuronal cultures

Academic literature on the topic 'Cortical neuronal cultures'

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Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Cortical neuronal cultures"

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Boespflug, Odile, and Kenneth F. Swaiman. "Neurotransmitter Changes during Development of Cortical Neuronal Cultures." Developmental Neuroscience 8, no. 2 (1986): 102–10. http://dx.doi.org/10.1159/000112245.

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Joo, Chul Hyun, Yoo Kyum Kim, Heuiran Lee, HeaNam Hong, Seung-Yong Yoon, and DongHou Kim. "Coxsackievirus B4-induced neuronal apoptosis in rat cortical cultures." Neuroscience Letters 326, no. 3 (July 2002): 175–78. http://dx.doi.org/10.1016/s0304-3940(02)00340-3.

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Lustig, Heather S., Kristine von B. Ahern, and David A. Greenberg. "ω-Agatoxin IVA and excitotoxicity in cortical neuronal cultures." Neuroscience Letters 213, no. 2 (August 1996): 142–44. http://dx.doi.org/10.1016/0304-3940(96)12849-4.

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JIA, L. C., C. R. HAN, PIK-YIN LAI, and C. K. CHAN. "CONNECTIVITY INDUCED SYNCHRONIZATION IN CORTICAL NEURONAL NETWORKS." International Journal of Modern Physics B 21, no. 23n24 (September 30, 2007): 4117–23. http://dx.doi.org/10.1142/s0217979207045293.

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Synchronization of cortical neural cultures is studied as a function of the effective network connectivity in the phenomenon of synchronized firing(SF). The synchronized bursting frequency (during SF) of the network is found to be much slower than the characteristic time scale of a neuron and increases with the network connectivity. The synchronized bursting frequency f is characterized by a critical age (tc) as: [Formula: see text]. Furthermore, tc is found to scale with the cell plating density ρ as tc ~ ρ−β with β ≃ 0.44 ± 0.08. Although some aspects of the observed SF is similar to the array enhanced synchronization, detailed comparison of measured spike statistics from synchronized and non-synchronized cultures suggests that the nature of synchronization during SF is different from that of the array-enhanced synchronization. In particular, electrophysiological measurements using double patch technique revel that even though the bursting frequencies are synchronized, the intra-burst spikes are not.
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Nguyen, Lan, Sarah Wright, Mike Lee, Zhao Ren, John-Michael Sauer, Wherly Hoffman, Wagner Zago, Gene G. Kinney, and Michael P. Bova. "Quantifying Amyloid Beta (Aβ)–Mediated Changes in Neuronal Morphology in Primary Cultures." Journal of Biomolecular Screening 17, no. 6 (April 2, 2012): 835–42. http://dx.doi.org/10.1177/1087057112441972.

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Alzheimer’s disease (AD) is a devastating neurodegenerative disease affecting millions of people. The amyloid hypothesis suggests that the pathogenesis of AD is related to the accumulation of amyloid beta (Aβ) in the brain. Herein, the authors quantify Aβ-mediated changes in neuronal morphology in primary cultures using the Cellomics neuronal profiling version 3.5 (NPv3.5) BioApplication. We observed that Aβ caused a 33% decrease in neurite length in primary human cortical cultures after 24 h of treatment compared with control-treated cultures. We also determined that quantifying changes of neuronal morphology was a more sensitive indicator of nonlethal cell injury than traditional cytotoxicity assays. Aβ-mediated neuronal deficits observed in human cortical cultures were also observed in primary rat hippocampal cultures, where we demonstrated that the integrin-blocking antibody, 17E6, completely abrogated Aβ-mediated cytotoxicity. Finally, we showed that Aβ challenge to 21 days in vitro rat hippocampal cultures reduced synapsin staining to 14% of control-treated cultures. These results are consistent with the finding that loss of presynaptic integrity is one of the initial deficits observed in AD. The implementation of phenotypic screens to identify compounds that block Aβ-mediated cytotoxicity in primary neuronal cultures may lead to the development of novel strategies to prevent AD.
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Guaraldi, Mary, Sangmook Lee, and Thomas B. Shea. "Synaptic Signals from Glutamate-Treated Neurons Induce Aberrant Post-Synaptic Signals in Untreated Neuronal Networks." Open Neurology Journal 14, no. 1 (August 24, 2020): 59–62. http://dx.doi.org/10.2174/1874205x02014010059.

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Background and Objective: Glutamate neurotoxicity is associated with a wide range of disorders and can impair synaptic function. Failure to clear extracellular glutamate fosters additional cycles and spread of regional hyperexcitation. Methods and Results: Using cultured murine cortical neurons, herein it is demonstrated that synaptic signals generated by cultures undergoing glutamate-induced hyperactivity can invoke similar effects in other cultures not exposed to elevated glutamate. Conclusion: Since sequential synaptic connectivity can encompass extensive cortical regions, this study presents a potential additional contributor to the spread of damage resulting from glutamate excitotoxicity and should be considered in attempts to mitigate neurodegeneration.
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Kim, Sun H., Seok J. Won, Seonghyang Sohn, Hyuk J. Kwon, Jee Y. Lee, Jong H. Park, and Byoung J. Gwag. "Brain-derived neurotrophic factor can act as a pronecrotic factor through transcriptional and translational activation of NADPH oxidase." Journal of Cell Biology 159, no. 5 (December 2, 2002): 821–31. http://dx.doi.org/10.1083/jcb.200112131.

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Several lines of evidence suggest that neurotrophins (NTs) potentiate or cause neuronal injury under various pathological conditions. Since NTs enhance survival and differentiation of cultured neurons in serum or defined media containing antioxidants, we set out experiments to delineate the patterns and underlying mechanisms of brain-derived neurotrophic factor (BDNF)–induced neuronal injury in mixed cortical cell cultures containing glia and neurons in serum-free media without antioxidants, where the three major routes of neuronal cell death, oxidative stress, excitotoxicity, and apoptosis, have been extensively studied. Rat cortical cell cultures, after prolonged exposure to NTs, underwent widespread neuronal necrosis. BDNF-induced neuronal necrosis was accompanied by reactive oxygen species (ROS) production and was dependent on the macromolecular synthesis. cDNA microarray analysis revealed that BDNF increased the expression of cytochrome b558, the plasma membrane-spanning subunit of NADPH oxidase. The expression and activation of NADPH oxidase were increased after exposure to BDNF. The selective inhibitors of NADPH oxidase prevented BDNF-induced ROS production and neuronal death without blocking antiapoptosis action of BDNF. The present study suggests that BDNF-induced expression and activation of NADPH oxidase cause oxidative neuronal necrosis and that the neurotrophic effects of NTs can be maximized under blockade of the pronecrotic action.
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Zhang, Junhui, Geoffrey Thomas Gibney, Peng Zhao, and Ying Xia. "Neuroprotective role of δ-opioid receptors in cortical neurons." American Journal of Physiology-Cell Physiology 282, no. 6 (June 1, 2002): C1225—C1234. http://dx.doi.org/10.1152/ajpcell.00226.2001.

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We recently demonstrated that δ-opioid receptor (DOR) activation protects cortical neurons against glutamate-induced injury. Because glutamate is a mediator of hypoxic injury in neurons, we hypothesized that DOR is involved in neuroprotection during O2 deprivation and that its activation/inhibition may alter neuronal susceptibility to hypoxic stress. In this work, we tested the effect of opioid receptor activation and inhibition on cultured cortical neurons in hypoxia (1% O2). Cell injury was assessed by lactate dehydrogenase release, morphology-based quantification, and live/dead staining. Our results show that 1) immature neurons ( days 4 and 6) were not significantly injured by hypoxia until 72 h of exposure, whereas day 8 neurons were injured after only 24-h hypoxia; 2) DOR inhibition (naltrindole) caused neuronal injury in both day 4 and day 8 normoxic cultures and further augmented hypoxic injury in these neurons; 3) DOR activation ([d-Ala2,d-Leu5]enkephalin) reduced neuronal injury in day 8 cultures after 24 h of normoxic or hypoxic exposure and attenuated naltrindole-induced injury with prolonged exposure; and 4) μ- or κ-opioid receptor inhibition (β-funaltrexamine or nor-binaltorphimine) had little effect on neurons in either normoxic or hypoxic conditions. Collectively, these data suggest that DOR plays a crucial role in neuroprotection in normoxic and hypoxic environments.
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C., L., C. R., C. H., M. T., Y. S., Pik-Yin Pik-Yin, and C. K. "Synchronized Bursting Induced by Network Connectivity in Cortical Neuronal Cultures." Journal of the Korean Physical Society 50, no. 91 (January 15, 2007): 207. http://dx.doi.org/10.3938/jkps.50.207.

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Wise-Faberowski, Lisa, Robert D. Pearlstein, and David S. Warner. "NMDA-induced Apoptosis in Mixed Neuronal/Glial Cortical Cell Cultures." Journal of Neurosurgical Anesthesiology 18, no. 4 (October 2006): 240–46. http://dx.doi.org/10.1097/00008506-200610000-00004.

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Dissertations / Theses on the topic "Cortical neuronal cultures"

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Boulos, Sherif. "Identification and characterisation of potential neuroprotective proteins induced by erythropoietin (EPO) preconditioning of cortical neuronal cultures." University of Western Australia. School of Biomedical and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0128.

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[Truncated abstract] Clinical therapeutic agents to directly inhibit ischaemic neuronal death are presently unavailable. One approach to developing therapeutics is based upon the identification of proteins up-regulated by 'preconditioning', a natural adaptive response utilised by the neural cells to counter damaging insults, such as ischaemia. Thus, my project aimed to firstly identify proteins differentially expressed following erythropoietin (EPO) mediated neuronal preconditioning and secondly to assess whether any of these proteins possessed neuroprotective activity using in vitro ischaemia like models. To achieve the first aim, it was shown that in vitro neuronal EPO preconditioning could: (i) induce cell signal changes in neuronal cultures, (ii) protect neurons against in vitro ischaemia and (iii) induce differential protein expression. Overall, 40 differentially expressed proteins were identified in cortical neuronal cultures following EPO preconditioning. In order to investigate the neuroprotective or neurodamaging activity of proteins induced by EPO preconditioning I developed an adenoviral expression system for use in neuronal cultures. To this end, I assessed the suitability of four promoters (cytomegalovirus [CMV], rous sarcoma virus [RSV], human synapsin 1 [hSYN1], rat synapsin 1 [rSYN1]) previously used to express proteins in neuronal cultures and demonstrated the superiority of the RSV promoter for this purpose. ... Finally, in order to validate this adenoviral expression system, I over-expressed the anti-apoptotic protein Bcl-XL in neuronal cultures and subsequently confirmed its neuroprotective activity in the in vitro ischaemia and oxidative stress models used in my project. Using this adenoviral vector system and the in vitro oxidative stress model I assessed a number of proteins up-regulated by EPO preconditioning. The results of this preliminary study indicated that cyclophilin A (CyPA), peroxiredoxin 2 (PRDX2) and superoxide dismutase 1 (SOD1) over-expression were neuroprotective. It was subsequently verified that adenoviral mediated over-expression of CyPA and PRDX2, v but not SOD1 in cortical neuronal cultures could protect neurons from in vitro ischaemia. I also confirmed that CyPA mRNA increased in the rat hippocampus in response to 3 minutes of global cerebral ischaemia. Interestingly, an increase in CyPA, PRDX2 or SOD1 protein was not observed in the same experimental paradigm. To investigate CyPA's mode of action I confirmed that cultured neurons, but not astrocytes, express the CyPA receptor, CD147. It was also demonstrated that administration of exogenous CyPA protein to neuronal cultures could protect neurons against oxidative and ischaemic injury. I further demonstrated that exogenous administration of CyPA induces a rapid and transient activation of the extracellular signal-regulated kinase (ERK) 1/2 pathway in neuronal cultures. From this observation, I have proposed that the extracellular mediated neuroprotective activity of CyPA occurs via CD147 receptor signalling and activation of ERK1/2 pro-survival pathways. Based on the findings reported in this thesis, the neuroprotective activities of PRDX2 and CyPA warrant further investigation as targets for the development of new therapies to treat cerebral ischaemia.
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Sattler, Rita. "Effects of moderate and profound hypothermia on excitatory amino acid-induced neuronal injury in cortical cell cultures." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ51597.pdf.

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Mohandas, Bhavna. "The Effect of Exogenous Nitric Oxide on Neuronal Zn 2+ Homeostasis." Ohio : Ohio University, 2005. http://www.ohiolink.edu/etd/view.cgi?ohiou1126041116.

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Wu, Calvin. "In Vitro Cortical Networks for Disease Modeling and Drug Evaluation." Thesis, University of North Texas, 2013. https://digital.library.unt.edu/ark:/67531/metadc407860/.

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In translational research, disease models in preclinical studies are used as media for discovery of drugs or novel therapeutics. Development of in vitro models for various neurological diseases that enable efficient pharmacological or toxicological screening has been ongoing but challenging. Recognizing the potential benefit of in vitro disease models, dysfunctions in the cortical neuronal networks were induced to mimic the functional pathology of neurological symptoms using microelectrode arrays. Two different disease states – tinnitusand excitotoxicity – were investigated and discussed. In this model, pentylenetetrazol-induced increase in spontaneous firing rate and synchrony in the auditory cortical networks was used as correlate of tinnitus. Potential tinnitus treatment drugs from several different classes – including the novel class of potassium channel openers – were screened and quantified. The potentialtherapeutic values of these drugs were also discussed as the basis for drug repurposing. Functional excitotoxicity was induced by cisplatin (a cancer drug that causes neurological sideeffects) and glutamate (the major excitatory neurotransmitter). As proof-of-principle that the model may contribute to expediting the development of therapeutics, cisplatin excitotoxicity wasprevented by the antioxidant D-methionine, while glutamate excitotoxicity was prevented by ceftriaxone (a modulator of a glutamate reuptake transporter). In the latter part of the study, with results linking two of the screened drugs L-carnitine and D-methionine to GABAA receptor activation, it was demonstrated that this model not only served as an efficient drug-screening platform, but can be utilized to functionally investigate the underlying mechanism of drugs. Inaddition, several practical or conceptual directions for future studies to improve on this in vitro disease model are suggested.
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Qin, Yan. "Studies of Zinc Transport and Its Contribution to Zinc Homeostasis in Cultured Cortical Neurons." View abstract, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3339515.

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Honda, Kazuhiro. "Nongenomic antiapoptotic signal transduction by estrogen in cultured cortical neurons." Kyoto University, 2002. http://hdl.handle.net/2433/149665.

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Turina, Dean. "Propofol changes the cytoskeletal function in neurons : An experimental study in cortical cultures." Doctoral thesis, Linköpings universitet, Anestesiologi med intensivvård, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-77219.

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Every day, general anaesthetics are given to a large number of patients around the world but the cellular mechanisms of how anaesthetics act are still not clear. General anaesthetics cause the intended unconsciousness, amnesia and immobility in patients, but also side effects such as a decrease in mean arterial pressure and arrhythmia, both of which contribute to complications such as heart damage and stroke. With more knowledge of the mechanism of anaesthetic drugs, these complications could be reduced. It has been shown that anaesthetics cause a disruption of the thalamocortical connectivity and brain network connectivity. How the network communication is disrupted however is not known. Propofol and thiopental are both intravenous anaesthetic drugs used widely in clinical anaesthesia. They bind to the GABAA receptor and enhance its function. The cytoskeleton helps the cell to maintain its shape and participate in cellular movement and transport. Cellular transport to and from a neuron’s cell body and periphery is performed by motor proteins that move vesicles, organelles and proteins along cytoskeletal tracks. We have previously shown that propofol causes a reorganisation of the cytoskeleton protein actin in neurons, but we were further interested to study the effects of propofol and thiopental on the cytoskeletal function of cultured cortical rat neurons. Our results show that propofol and thiopental cause neurite (axon and dendrite) retraction. Propofol’s effects were time- and dose-dependent, and can be reversed when propofol is removed. We were able to inhibit propofolinduced neurite retraction if we stabilised actin by blocking either the motor protein myosin II or the GABAA receptor. We have previously shown that a small GTP-binding protein, RhoA, inhibits propofol-caused actin reorganisation. Propofol-induced neurite retraction was mediated via a downstream effector of RhoA, ROK, which induces phosphorylation of the myosin light chain and increases contractility. Furthermore, we have shown that propofol causes a switch from anterograde to retrograde transport and increases the average velocity of the moving vesicles in neurites. The propofol induced retrograde vesicle transport was GABAA receptor-mediated. Orexin A is a neuropeptide which regulates the sleep/awake cycle and has also been shown to reduce anaesthesia in animals when given intracerebroventricularly. We found that orexin A reverses propofol and thiopental-induced neurite retraction and actin reorganisation. Moreover, we have shown that the orexin A inhibition of propofol-induced neurite retraction is mediated via the PLD/PKC intracellular signalling pathway. Propofol and thiopental decreased the tyrosine phosphorilation of the intermediate cytoskeletal protein vimentin which is reversed by orexin A. Taken together, these results suggest that propofol causes a time- and dose-dependent, reversible and GABAAreceptor-mediated neurite retraction in cultured cortical rat neurons. Propofol also causes a switch from anterograde to retrograde vesicle transport in neurites. Orexin A reverses propofol and thiopental-induced neurite retraction and cytoskeletal reorganisation. Orexin A inhibits propofol-induced neurite retraction via the PLD/PKC intracellular signalling pathway.
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Durant, Stormy R. "In Vitro Exploration of Functional Acrolein Toxicity with Cortical Neuronal Networks." Thesis, University of North Texas, 2018. https://digital.library.unt.edu/ark:/67531/metadc1157516/.

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Acrolein is produced endogenously after traumatic brain injury (TBI) and is considered a primary mechanism for secondary damage occurring after TBI. We are using frontal cortex networks derived from mouse embryos and grown on microelectrode arrays in vitro to monitor the spontaneous activity of networks and the changes that occur after acrolein application. Networks exposed to acrolein exhibit a biphasic response profile. An initial increase in network activity, followed by a decrease to 100% activity loss in applications ≥ 50 µM. In applications below 50 µM, acrolein was not toxic but generated activity instability with coordinated but irregular population busts lasting for up to 6 days. The increase in activity preceding toxicity may be linked to a decrease in free spermine, a free radical scavenger that modulates Na+, K+, Ca+ channels as well as NMDA, Kainate, and AMPA receptors. Action potential wave shape analysis after 20 and 30 µM acrolein application revealed a concentration-dependent 15-33% increase in peak to peak amplitude within minutes after exposure. For the same concentrations of acrolein (50 µM), the time required to reach 100% activity loss (IT100) was longer in serum-free medium than in medium with 5% serum, in which IT100 values were reduced by a factor of 4. The greater toxicity in the presence of serum may be explained by acrolein adducts on serum proteins. These reaction products have been shown by other labs to be toxic in cell culture. This in vitro system could be used to expand biochemical analyses such as acrolein-induced spermine depletion and may provide an effective platform for investigating cell culture correlates of secondary TBI damage.
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Lavergne, Pauline, and Pauline Lavergne. "Caractérisation des réponses de neurones corticaux de rat en culture suite à des stimulations glutamatergiques grâce à la microscopie holographique numérique : vers une mesure de la balance excitation/inhibition." Master's thesis, Université Laval, 2020. http://hdl.handle.net/20.500.11794/38153.

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De nouvelles preuves suggèrent que les dysfonctionnements des circuits sous-jacents aux symptômes et aux déficits cognitifs des maladies psychiatriques pourraient être causés par une altération des paramètres d'équilibre d’excitation/inhibition (E/I). Cependant, les preuves physiologiques directes de cette hypothèse à partir de données électrophysiologiques et de neuro-imagerie non invasives sont jusqu'à présent rares. Pour apporter un soutien supplémentaire à l’hypothèse de l’équilibre E/I, la présente étude a appliqué une approche avancée de microscopie holographique numérique (MHN) pour examiner la dynamique des systèmes excitateurs/inhibiteurs suite à une stimulation glutamatergique dans des réseaux de neurones à différents stades de maturation neuronale. Cette approche fournissant une mesure approximative très précise des variations de mouvement de l’eau dans les cellules permet d’étudier certains processus physiologiques, tels que ceux reliés à l’activité neuronale. Cette étude a ainsi permis d’améliorer les connaissances sur la dynamique de la réponse neuronale induite par le glutamate, notamment en la caractérisant dans des cultures de neurones corticaux primaires de rats postnataux. L’activation des neurones engendrée par le glutamate, le principal neurotransmetteur excitateur, a révélé des changements plus ou moins persistants de la morphologie et des propriétés intracellulaires des neurones. De plus, les différentes réponses obtenues indiquent que le glutamate engendre des mécanismes d’activation et des processus de régulation du volume neuronal distincts d’un neurone à l’autre, probablement dépendant de l’état d’excitabilité de ce dernier qui résulte de l’interaction complexe des neurones inhibiteurs et excitateurs. Ainsi, la régulation de l’équilibre E/I de réseaux neuronaux pourrait potentiellement être reflétée par la proportion des différentes réponses de phase induites lors de stimulation de réseaux neuronaux au glutamate.
De nouvelles preuves suggèrent que les dysfonctionnements des circuits sous-jacents aux symptômes et aux déficits cognitifs des maladies psychiatriques pourraient être causés par une altération des paramètres d'équilibre d’excitation/inhibition (E/I). Cependant, les preuves physiologiques directes de cette hypothèse à partir de données électrophysiologiques et de neuro-imagerie non invasives sont jusqu'à présent rares. Pour apporter un soutien supplémentaire à l’hypothèse de l’équilibre E/I, la présente étude a appliqué une approche avancée de microscopie holographique numérique (MHN) pour examiner la dynamique des systèmes excitateurs/inhibiteurs suite à une stimulation glutamatergique dans des réseaux de neurones à différents stades de maturation neuronale. Cette approche fournissant une mesure approximative très précise des variations de mouvement de l’eau dans les cellules permet d’étudier certains processus physiologiques, tels que ceux reliés à l’activité neuronale. Cette étude a ainsi permis d’améliorer les connaissances sur la dynamique de la réponse neuronale induite par le glutamate, notamment en la caractérisant dans des cultures de neurones corticaux primaires de rats postnataux. L’activation des neurones engendrée par le glutamate, le principal neurotransmetteur excitateur, a révélé des changements plus ou moins persistants de la morphologie et des propriétés intracellulaires des neurones. De plus, les différentes réponses obtenues indiquent que le glutamate engendre des mécanismes d’activation et des processus de régulation du volume neuronal distincts d’un neurone à l’autre, probablement dépendant de l’état d’excitabilité de ce dernier qui résulte de l’interaction complexe des neurones inhibiteurs et excitateurs. Ainsi, la régulation de l’équilibre E/I de réseaux neuronaux pourrait potentiellement être reflétée par la proportion des différentes réponses de phase induites lors de stimulation de réseaux neuronaux au glutamate.
New evidences suggest that circuit dysfunctions underlying symptoms and cognitive deficits of psychiatric disorders may be caused by impaired excitation/inhibition equilibrium parameters (E/I). However, direct physiological evidences supporting this hypothesis from non-invasive electrophysiological and neuroimaging remain scarce. To provide additional support concerning the E/I balance hypothesis, this study uses an advanced digital holographic microscopy (DHM) approach to explore the dynamics of excitatory/inhibitory systems following glutamatergic stimulation in neural networks at different stages of neuronal maturation. This approach provides a very accurate approximate measurement of the water movement variations in cells allowing to study certain specific physiological processes, such as those related to neuronal activity. This study improves the knowledge regarding the dynamics of the glutamate-induced neuronal response, especially by characterizing it in cultures of primary cortical neurons of postnatal rats. The activation of neurons induced by glutamate, which is the main excitatory neurotransmitter, revealed more or less permanent changes in the morphology and intracellular properties of neurons. Moreover, the various responses obtained indicate that glutamate generates different neuronal activation mechanisms and neuronal volume regulation processes from a neuron to another, probably depending to the excitability state of the neuron that results from the complex interaction of inhibitory and excitatory neurons. Thus, the E/I balance regulation of neural networks could potentially be reflected by the proportion of different phase responses induced during glutamate neural network stimulation.
New evidences suggest that circuit dysfunctions underlying symptoms and cognitive deficits of psychiatric disorders may be caused by impaired excitation/inhibition equilibrium parameters (E/I). However, direct physiological evidences supporting this hypothesis from non-invasive electrophysiological and neuroimaging remain scarce. To provide additional support concerning the E/I balance hypothesis, this study uses an advanced digital holographic microscopy (DHM) approach to explore the dynamics of excitatory/inhibitory systems following glutamatergic stimulation in neural networks at different stages of neuronal maturation. This approach provides a very accurate approximate measurement of the water movement variations in cells allowing to study certain specific physiological processes, such as those related to neuronal activity. This study improves the knowledge regarding the dynamics of the glutamate-induced neuronal response, especially by characterizing it in cultures of primary cortical neurons of postnatal rats. The activation of neurons induced by glutamate, which is the main excitatory neurotransmitter, revealed more or less permanent changes in the morphology and intracellular properties of neurons. Moreover, the various responses obtained indicate that glutamate generates different neuronal activation mechanisms and neuronal volume regulation processes from a neuron to another, probably depending to the excitability state of the neuron that results from the complex interaction of inhibitory and excitatory neurons. Thus, the E/I balance regulation of neural networks could potentially be reflected by the proportion of different phase responses induced during glutamate neural network stimulation.
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Hetsch, Florian Jan Alexander [Verfasser]. "Induction of Synapses by Agrin in Cultured Cortical Neurons / Florian Jan Alexander Hetsch." Berlin : Freie Universität Berlin, 2015. http://d-nb.info/1072622262/34.

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Books on the topic "Cortical neuronal cultures"

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Sattler, Rita. Effects of moderate and profound hypothermia on excitatory amino-acid-induced neuronal injury in cortical cell cultures. Ottawa: National Library of Canada, 1996.

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Massimini, Marcello, and Giulio Tononi. Sizing up Consciousness. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198728443.001.0001.

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Sizing up Consciousness explores, at an introductory level, the potential practical, clinical, and ethical implications of a general principle about the nature of consciousness. Using information integration theory (IIT) as a guiding principle, the book takes the reader along a scientific trajectory to face fundamental questions about the relationships between matter and experience. What is so special about a piece of flesh that can host a subject who sees light or experiences darkness? Why is the brain associated with a capacity for consciousness, but not the liver or the heart, as previous cultures believed? Why the thalamocortical system, but not other complicated neural structures? Why does consciousness fade during deep sleep, while cortical neurons remain active? Why does it recover, vivid, and intense, when the brain is disconnected from the external world during a dream? Can unresponsive patients with a functional island of cortex surrounded by widespread damage be conscious? Is a parrot that talks, or an octopus that learns and plays conscious? Can computers be conscious? Could a system behave like us and yet be devoid of consciousness—a zombie? The authors take on these basic questions by translating theoretical principles into anatomical observations, novel empirical measurements—such as an index of brain complexity that can be applied at the bedside of brain-injured patients—and thought experiments. The aim of the book is to describe, in an accessible way, a preliminary attempt to identify a general rule to size up the capacity for consciousness within the human skull and beyond.
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Book chapters on the topic "Cortical neuronal cultures"

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Choi, Dennis W., Hannelore Monyer, Rona G. Giffard, Mark P. Goldberg, and Chadwick W. Christine. "Acute Brain Injury, NMDA Receptors, and Hydrogen Ions: Observations in Cortical Cell Cultures." In Excitatory Amino Acids and Neuronal Plasticity, 501–4. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5769-8_55.

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Kvist, Giedre. "Derivation of Adult Human Cortical Organotypic Slice Cultures for Coculture with Reprogrammed Neuronal Cells." In Methods in Molecular Biology, 253–59. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1601-7_17.

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Lau, Anthony C., Hong Cui, and Michael Tymianski. "The Use of Propidium Iodide to Assess Excitotoxic Neuronal Death in Primary Mixed Cortical Cultures." In Methods in Molecular Biology, 15–29. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-504-6_2.

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Darbinyan, Armine, Rafal Kaminski, Martyn K. White, Nune Darbinian, and Kamel Khalili. "Isolation and Propagation of Primary Human and Rodent Embryonic Neural Progenitor Cells and Cortical Neurons." In Neuronal Cell Culture, 45–54. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-640-5_5.

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Choi, D. W. "Excitotoxicity on Cultured Cortical Neurons." In Research and Perspectives in Neurosciences, 125–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84526-0_11.

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Facci, Laura, and Stephen D. Skaper. "Culture of Rodent Cortical and Hippocampal Neurons." In Neurotrophic Factors, 49–56. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-536-7_5.

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Facci, Laura, and Stephen D. Skaper. "Culture of Rodent Cortical, Hippocampal, and Striatal Neurons." In Neurotrophic Factors, 39–47. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7571-6_3.

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Gonthier, Bertrand, C�cile Nasarre, Tina R�diger, and Dominique Bagnard. "Protocol for the Primary Culture of Cortical Neurons." In New Methods for Culturing Cells from Nervous Tissues, 12–22. Basel: KARGER, 2005. http://dx.doi.org/10.1159/000083430.

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Facci, Laura, and Stephen D. Skaper. "Amyloid β-Peptide Neurotoxicity Assay Using Cultured Rat Cortical Neurons." In Neurotrophic Factors, 57–65. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-536-7_6.

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Yamamoto, Seiji, Y. Matsumoto, Y. Suzuki, T. Tsuboi, S. Terakawa, N. Ohashi, and K. Umemura. "An Na+/H+ exchanger inhibitor suppresses cellular swelling and neuronal death induced by glutamate in cultured cortical neurons." In Brain Edema XII, 223–26. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0651-8_48.

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Conference papers on the topic "Cortical neuronal cultures"

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Gritsun, T., J. Stegenga, J. le Feber, and W. L. C. Rutten. "Network bursts in cortical neuronal cultures ‘Noise- versus pacemaker’- driven neural network simulations." In 2009 4th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2009. http://dx.doi.org/10.1109/ner.2009.5109374.

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le Feber, Joost, Jaap van Pelt, and Wim Rutten. "Latency dependent development of related firing patterns of cultured cortical neurons." In 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4352960.

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He, Jun, Hui Gong, Shaoqun Zeng, Yanling Li, and Qingming Luo. "Enhancement of synaptic transmission induced by BDNF in cultured cortical neurons." In Biomedical Optics 2005, edited by Valery V. Tuchin. SPIE, 2005. http://dx.doi.org/10.1117/12.592072.

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Zorina, Inna, Irina Zakharova, Lubov Bayunova, Ekaterina Fokina, Alexander Shpakov, and Natalia Avrova. "MECHANISMS OF NEUROPROTECTIVE EFFECT OF INSULIN AND α-TOCOPHEROL AT THEIR JOINT ACTION ON BRAIN CORTICAL NEURONS IN CULTURE UNDER CONDITIONS OF H2O2-INDUCED OXIDATIVE STRESS." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2133.sudak.ns2021-17/157-158.

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You might also be interested in the extended bibliographies on the topic 'Cortical neuronal cultures' for particular source types:
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