Academic literature on the topic 'Organotypic Brain Slice Co-Cultures'
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Journal articles on the topic "Organotypic Brain Slice Co-Cultures"
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Humpel, Christian. "Organotypic Brain Slice Cultures." Current Protocols in Immunology 123, no. 1 (October 12, 2018): e59. http://dx.doi.org/10.1002/cpim.59.
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Humpel, Christian. "Organotypic Brain Slices of ADULT Transgenic Mice: A Tool to Study Alzheimer’s Disease." Current Alzheimer Research 16, no. 2 (February 4, 2019): 172–81. http://dx.doi.org/10.2174/1567205016666181212153138.
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Transgenic mice have been extensively used to study the Alzheimer pathology. In order to reduce, refine and replace (3Rs) the number of animals, ex vivo cultures are used and optimized. Organotypic brain slices are the most potent ex vivo slice culture models, keeping the 3-dimensional structure of the brain and being closest to the in vivo situation. Organotypic brain slice cultures have been used for many decades but were mainly prepared from postnatal (day 8-10) old rats or mice. More recent work (including our lab) now aims to culture organotypic brain slices from adult mice including transgenic mice. Especially in Alzheimer´s disease research, brain slices from adult transgenic mice will be useful to study beta-amyloid plaques, tau pathology and glial activation. This review will summarize the studies using organotypic brain slice cultures from adult mice to mimic Alzheimer's disease and will highlight advantages and also pitfalls using this technique.
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Humpel, C. "Organotypic brain slice cultures: A review." Neuroscience 305 (October 2015): 86–98. http://dx.doi.org/10.1016/j.neuroscience.2015.07.086.
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Phillips, Wiktor S., Mikkel Herly, Christopher A. Del Negro, and Jens C. Rekling. "Organotypic slice cultures containing the preBötzinger complex generate respiratory-like rhythms." Journal of Neurophysiology 115, no. 2 (February 1, 2016): 1063–70. http://dx.doi.org/10.1152/jn.00904.2015.
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Study of acute brain stem slice preparations in vitro has advanced our understanding of the cellular and synaptic mechanisms of respiratory rhythm generation, but their inherent limitations preclude long-term manipulation and recording experiments. In the current study, we have developed an organotypic slice culture preparation containing the preBötzinger complex (preBötC), the core inspiratory rhythm generator of the ventrolateral brain stem. We measured bilateral synchronous network oscillations, using calcium-sensitive fluorescent dyes, in both ventrolateral (presumably the preBötC) and dorsomedial regions of slice cultures at 7–43 days in vitro. These calcium oscillations appear to be driven by periodic bursts of inspiratory neuronal activity, because whole cell recordings from ventrolateral neurons in culture revealed inspiratory-like drive potentials, and no oscillatory activity was detected from glial fibrillary associated protein-expressing astrocytes in cultures. Acute slices showed a burst frequency of 10.9 ± 4.2 bursts/min, which was not different from that of brain stem slice cultures (13.7 ± 10.6 bursts/min). However, slice cocultures that include two cerebellar explants placed along the dorsolateral border of the brainstem displayed up to 193% faster burst frequency (22.4 ± 8.3 bursts/min) and higher signal amplitude (340%) compared with acute slices. We conclude that preBötC-containing slice cultures retain inspiratory-like rhythmic function and therefore may facilitate lines of experimentation that involve extended incubation (e.g., genetic transfection or chronic drug exposure) while simultaneously being amenable to imaging and electrophysiology at cellular, synaptic, and network levels.
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Heine, Claudia, Katja Sygnecka, Nico Scherf, Marcus Grohmann, Annett Bräsigk, and Heike Franke. "P2Y1 receptor mediated neuronal fibre outgrowth in organotypic brain slice co-cultures." Neuropharmacology 93 (June 2015): 252–66. http://dx.doi.org/10.1016/j.neuropharm.2015.02.001.
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Joost, Sarah, Stefan Mikkat, Michael Wille, Antje Schümann, and Oliver Schmitt. "Membrane Protein Identification in Rodent Brain Tissue Samples and Acute Brain Slices." Cells 8, no. 5 (May 8, 2019): 423. http://dx.doi.org/10.3390/cells8050423.
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Acute brain slices are a sample format for electrophysiology, disease modeling, and organotypic cultures. Proteome analyses based on mass spectrometric measurements are seldom used on acute slices, although they offer high-content protein analyses and explorative approaches. In neuroscience, membrane proteins are of special interest for proteome-based analysis as they are necessary for metabolic, electrical, and signaling functions, including myelin maintenance and regeneration. A previously published protocol for the enrichment of plasma membrane proteins based on aqueous two-phase polymer systems followed by mass spectrometric protein identification was adjusted to the small sample size of single acute murine slices from newborn animals and the reproducibility of the results was analyzed. For this, plasma membrane proteins of 12 acute slice samples from six animals were enriched and analyzed by liquid chromatography-mass spectrometry. A total of 1161 proteins were identified, of which 369 were assigned to membranes. Protein abundances showed high reproducibility between samples. The plasma membrane protein separation protocol can be applied to single acute slices despite the low sample size and offers a high yield of identifiable proteins. This is not only the prerequisite for proteome analysis of organotypic slice cultures but also allows for the analysis of small-sized isolated brain regions at the proteome level.
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Ucar, Buket, Sedef Yusufogullari, and Christian Humpel. "Collagen hydrogels loaded with fibroblast growth factor-2 as a bridge to repair brain vessels in organotypic brain slices." Experimental Brain Research 238, no. 11 (August 29, 2020): 2521–29. http://dx.doi.org/10.1007/s00221-020-05907-7.
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Abstract Vessel damage is a general pathological process in many neurodegenerative disorders, as well as spinal cord injury, stroke, or trauma. Biomaterials can present novel tools to repair and regenerate damaged vessels. The aim of the present study is to test collagen hydrogels loaded with different angiogenic factors to study vessel repair in organotypic brain slice cultures. In the experimental set up I, we made a cut on the organotypic brain slice and tested re-growth of laminin + vessels. In the experimental set up II, we cultured two half brain slices with a gap with a collagen hydrogel placed in between to study endothelial cell migration. In the experimental set up I, we showed that the number of vessels crossing the cut was tendencially increased with the addition of fibroblast growth factor-2 (FGF-2), vascular endothelial growth factor, or platelet-derived growth factor-BB compared to the control group. In the experimental set up II, we demonstrated that a collagen hydrogel loaded with FGF-2 resulted in a significantly increased number of migrated laminin + cells in the gap between the slices compared to the control hydrogel. Co-administration of several growth factors did not further potentiate the effects. Taken together, we show that organotypic brain slices are good models to study brain vessels and FGF-2 is a potent angiogenic factor for endothelial cell proliferation and migration. Our results provide evidence that the collagen hydrogels can be used as an extracellular matrix for the vascular endothelial cells.
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GIANINAZZI, C., M. SCHILD, N. MÜLLER, S. L. LEIB, F. SIMON, S. NUÑEZ, P. JOSS, and B. GOTTSTEIN. "Organotypic slice cultures from rat brain tissue: a new approach forNaegleria fowleriCNS infectionin vitro." Parasitology 132, no. 6 (September 13, 2005): 797–804. http://dx.doi.org/10.1017/s0031182005008619.
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The free-living amoebaNaegleria fowleriis the aetiological agent of primary amoebic meningoencephalitis (PAM), a disease leading to death in the vast majority of cases. In patients suffering from PAM, and in corresponding animal models, the brain undergoes a massive inflammatory response, followed by haemorrhage and severe tissue necrosis. Both,in vivoandin vitromodels are currently being used to study PAM infection. However, animal models may pose ethical issues, are dependent upon availability of specific infrastructural facilities, and are time-consuming and costly. Conversely, cell cultures lack the complex organ-specific morphology foundin vivo, and thus, findings obtainedin vitrodo not necessarily reflect the situationin vivo. The present study reports infection of organotypic slice cultures from rat brain withN. fowleriand compares the findings in this culture system within vivoinfection in a rat model of PAM, that proved complementary to that of mice. We found that brain morphology, as presentin vivo, is well retained in organotypic slice cultures, and that infection time-course including tissue damage parallels the observationsin vivoin the rat. Therefore, organotypic slice cultures from rat brain offer a newin vitroapproach to studyN. fowleriinfection in the context of PAM.
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Spahr-Schopfer, Isabelle, Lazlo Vutskits, Nicholas Toni, Pierre-Alain Buchs, Lorena Parisi, and Dominique Muller. "Differential Neurotoxic Effects of Propofol on Dissociated Cortical Cells and Organotypic Hippocampal Cultures." Anesthesiology 92, no. 5 (May 1, 2000): 1408–17. http://dx.doi.org/10.1097/00000542-200005000-00032.
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Background Propofol is a widely used anesthetic agent for adults and children. Although extensive clinical use has demonstrated its safety, neurologic dysfunctions have been described after the use of this agent. A recent study on a model of aggregating cell cultures reported that propofol might cause irreversible lesions of gamma-aminobutyric acid-mediated (GABAergic) neurons when administered at a critical phase of brain development. We investigated this issue by comparing the effects of long-term propofol treatment on two models of brain cultures: dissociated neonatal cortical cell cultures and organotypic slice cultures. Methods Survival of GABAergic neurons in dissociated cultures of newborn rat cortex (postnatal age, 1 day) treated for 3 days with different concentrations of propofol was assessed using histologic and cytochemical methods. For hippocampal organotypic slice cultures (postnatal age, 1 and 7 days), cell survival was assessed by measuring functional and morphologic parameters: extracellular and intracellular electrophysiology, propidium staining of dying cells, and light and electron microscopy. Results In dissociated neonatal cell cultures, propofol induced dose-dependent lesions of GABAergic neurons and of glial cells. In contrast, no evidence for neurotoxic effects of propofol were found after long-term treatment of organotypic slice cultures. Excitatory transmission was not affected by propofol, and inhibitory transmission was still functional. Histologic preparations showed no evidence for cell degeneration or death. Conclusion Although long-term applications of propofol to dissociated cortical cell cultures produced degeneration and death of GABAergic neurons and glial cells, no such lesions were found when using a model of postnatal organotypic slice cultures. This conclusion is based on both functional and morphologic tests.
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Croft, Cara L., and Wendy Noble. "Preparation of organotypic brain slice cultures for the study of Alzheimer’s disease." F1000Research 7 (May 15, 2018): 592. http://dx.doi.org/10.12688/f1000research.14500.1.
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Alzheimer's disease, the most common cause of dementia, is a progressive neurodegenerative disorder characterised by amyloid-beta deposits in extracellular plaques, intracellular neurofibrillary tangles of aggregated tau, synaptic dysfunction and neuronal death. There are no cures for AD and current medications only alleviate some disease symptoms. Transgenic rodent models to study Alzheimer’s mimic features of human disease such as age-dependent accumulation of abnormal beta-amyloid and tau, synaptic dysfunction, cognitive deficits and neurodegeneration. These models have proven vital for improving our understanding of the molecular mechanisms underlying AD and for identifying promising therapeutic approaches. However, modelling neurodegenerative disease in animals commonly involves aging animals until they develop harmful phenotypes, often coupled with invasive procedures. In vivo studies are also resource, labour, time and cost intensive. We have developed a novel organotypic brain slice culture model to study Alzheimer’ disease which brings the potential of substantially reducing the number of rodents used in dementia research from an estimated 20,000 per year. We obtain 36 brain slices from each mouse pup, considerably reducing the numbers of animals required to investigate multiple stages of disease. This tractable model also allows the opportunity to modulate multiple pathways in tissues from a single animal. We believe that this model will most benefit dementia researchers in the academic and drug discovery sectors. We validated the slice culture model against aged mice, showing that the molecular phenotype closely mimics that displayed in vivo, albeit in an accelerated timescale. We showed beneficial outcomes following treatment of slices with agents previously shown to have therapeutic effects in vivo, and we also identified new mechanisms of action of other compounds. Thus, organotypic brain slice cultures from transgenic mouse models expressing Alzheimer’s disease-related genes may provide a valid and sensitive replacement for in vivo studies that do not involve behavioural analysis.
Dissertations / Theses on the topic "Organotypic Brain Slice Co-Cultures"
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Sygnecka, Katja. "Organotypic brain slice co-cultures of the dopaminergic system - A model for the identification of neuroregenerative substances and cell populations." Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-188897.
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The development of new therapeutical approaches, devised to foster the regeneration of neuronal circuits after injury and/or in neurodegenerative diseases, is of great importance. The impairment of dopaminergic projections is especially severe, because these projections are involved in crucial brain functions such as motor control, reward and cognition. In the work presented here, organotypic brain slice co-cultures of (a) the mesostriatal and (b) the mesocortical dopaminergic projection systems consisting of tissue sections of the ventral tegmental area/substantia nigra (VTA/SN), in combination with the target regions of (a) the striatum (STR) or (b) the prefrontal cortex (PFC), respectively, were used to evaluate different approaches to stimulate neurite outgrowth: (i) inhibition of cAMP/cGMP turnover with 3’,5’ cyclic nucleotide phosphodiesterase inhibitors (PDE-Is), (ii) blockade of calcium currents with nimodipine, and (iii) the co-cultivation with bone marrow-derived mesenchymal stromal/stem cells (BM-MSCs). The neurite growth-promoting properties of the tested substances and cell populations were analyzed by neurite density quantification in the border region between the two brain slices, using biocytin tracing or tyrosine hydroxylase labeling and automated image processing procedures. In addition, toxicological tests and gene expression analyses were conducted.
(i) PDE-Is were applied to VTA/SN+STR rat co-cultures. The quantification of neurite density after both biocytin tracing and tyrosine hydroxylase labeling revealed a growth promoting effect of the PDE2A-Is BAY60-7550 and ND7001. The application of the PDE10-I MP-10 did not alter neurite density in comparison to the vehicle control.
(ii) The effects of nimodipine were evaluated in VTA/SN+PFC rat co-cultures. A neurite growth-promoting effect of 0.1 µM and 1 µM nimodipine was demonstrated in a projection system of the CNS. In contrast, the application of 10 µM nimodipine did not alter neurite density, compared to the vehicle control, but induced the activation of the apoptosis marker caspase 3. The expression levels of the investigated genes, including Ca2+ binding proteins (Pvalb, S100b), immediate early genes (Arc, Egr1, Egr2, Egr4, Fos and JunB), glial fibrillary acidic protein, and myelin components (Mal, Mog, Plp1) were not significantly changed (with the exception of Egr4) by the treatment with 0.1 µM and 1 µM nimodipine.
(iii) Bulk BM-MSCs that were classically isolated by plastic adhesion were compared to the subpopulation Sca-1+Lin-CD45--derived MSCs (SL45-MSCs). The neurite growth-promoting properties of both MSC populations were quantified in VTA/SN+PFC mouse co-cultures. For this purpose, the MSCs were seeded on glass slides that were placed underneath the co-cultures. A significantly enhanced neurite density within the co-cultures was induced by both bulk BM-MSCs and SL45-MSCs. SL45-MSCs increased neurite density to a higher degree. The characterization of both MSC populations revealed that the frequency of fibroblast colony forming units (CFU-f ) is 105-fold higher in SL45-MSCs. SL45-MSCs were morphologically more homogeneous and expressed higher levels of nestin, BDNF and FGF2 compared to bulk BM-MSCs.
Thus, this work emphasizes the vast potential for molecular targeting with respect to the development of therapeutic strategies in the enhancement of neurite regrowth.
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Rambani, Komal. "Thick brain slice cultures and a custom-fabricated multiphoton imaging system: progress towards development of a 3D hybrot model." Thesis, Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/22702.
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Development of a three dimensional (3D) HYBROT model with targeted in vivo like intact cellular circuitry in thick brain slices for multi-site stimulation and recording will provide a useful in vitro model to study neuronal dynamics at network level. In order to make this in vitro model feasible, we need to develop several associated technologies. These technologies include development of a thick organotypic brain slice culturing method, a three dimensional (3D) micro-fluidic multielectrode Neural Interface system (µNIS) and the associated electronic interfaces for stimulation and recording of/from tissue, development of targeted stimulation patterns for closed-loop interaction with a robotic body, and a deep-tissue non-invasive imaging system. To make progress towards this goal, I undertook two projects: (i) to develop a method to culture thick organotypic brain slices, and (ii) construct a multiphoton imaging system that allows long-term and deep-tissue imaging of two dimensional and three dimensional cultures.
Organotypic brain slices preserve cytoarchitecture of the brain. Therefore, they make more a realistic reduced model for various network level investigations. However, current culturing methods are not successful for culturing thick brain slices due to limited supply of nutrients and oxygen to inner layers of the culture. We developed a forced-convection based perfusion method to culture viable 700µm thick brain slices.
Multiphoton microscopy is ideal for imaging living 2D or 3D cultures at submicron resolution. We successfully fabricated a custom-designed high efficiency multiphoton microscope that has the desired flexibility to perform experiments using multiple technologies simultaneously. This microscope was used successfully for 3D and time-lapse imaging.
Together these projects have contributed towards the progress of development of a 3D HYBROT.
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3D Hybrot: A hybrid system of a brain slice culture embodied with a robotic body.
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Sygnecka, Katja [Verfasser], Andrea [Akademischer Betreuer] Robitzki, Andrea [Gutachter] Robitzki, and Bernd [Gutachter] Heimrich. "Organotypic brain slice co-cultures of the dopaminergic system - A model for the identification of neuroregenerative substances and cell populations / Katja Sygnecka ; Gutachter: Andrea Robitzki, Bernd Heimrich ; Betreuer: Andrea Robitzki." Leipzig : Universitätsbibliothek Leipzig, 2015. http://d-nb.info/1239740050/34.
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Henning, Karen [Verfasser]. "Adeno-associated viral gene transfer to prevent the cellular phenotype of cortical organotypic brain-slice cultures derived from Gaucher’s disease type II mice. / Karen Henning." Berlin : Freie Universität Berlin, 2014. http://d-nb.info/1050978242/34.
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Dias, Francisco Filipe Terra Silveira Schäller. "Organotypic brain slice cultures as a model to study supressors of amyloid-β toxicity relevant in Alzheimer’s disease." Master's thesis, 2020. http://hdl.handle.net/10451/48714.
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Tese de mestrado, Bioquímica (Bioquímica Médica) Universidade de Lisboa, Faculdade de Ciências, 2021The accumulation of the amyloid-β peptide and its subsequent aggregation is followed by an initial neuroinflammatory response, thought as one of the driving processes leading to neurodegeneration in AD. Rising evidence describe this disease as an evolving two-stage inflammatory process, where early stages involve glial ability to regulate AD related mechanisms, maintaining an homeostatic environment prior to plaque formation, whilst late stages are characterized by an amyloid plaque-associated exacerbated neuroinflammation and consequent neurodegeneration. The proinflammatory protein S100B is one of the glial response alarmins upregulated in AD, thought to play an important, although unclear role during the early stages of the disease. S100B has been known for its role as an inflammatory inducer in other neurodegenerative disorders, yet recent in vitro approaches established a new chaperone-like function for this protein, as a suppressor of Aβ aggregation. Therefore, we here investigated whether S100B plays a neuroprotective or disease-aggravating role against Aβ induced toxicity in a hippocampal organotypic slice culture model. First, S100B and Aβ42 were recombinantly purified in E. coli. Then, tissue slices were incubated with the recombinant proteins to mimic the AD environment and explore the dual role of S100B. In these conditions, our results suggest that in the dentate gyrus region, S100B is able to partially prevent microglia reactivity induced by Aβ42. Also, it seems to regulate the Aβ42 induced expression of inflammatory genes, such as IL-1β, without affecting neuronal death. Although these initial studies suggest that S100B might play a neuroprotective role against Aβ-induced neuroinflammation, further studies are needed to better ascertain whether the interplay between these two biomolecules can be used as potential therapeutic approach to ameliorate AD pathology.
Os eventos que levam à acumulação do péptido Beta Amiloide (Aβ) e à sua subsequente agregação são seguidos por uma resposta neuro inflamatória, num estágio inicial da doença de Alzheimer (AD), que se pensa ser um dos principais processos conducentes à neurodegeneração observada nesta doença. De facto, descobertas recentes descrevem esta doença como um processo neuroinflamatório bifásico em constante evolução, cujos estados iniciais são caracterizados pela regulação de processos relacionados com AD pelas células gliais, mantendo assim um ambiente homeostático precedente à formação de placas amiloides, enquanto estados mais tardios são caracterizados por uma exacerbada neuroinflamação relacionada com estas placas, conduzindo assim à neurodegeneração característica desta doença. A proteína pró-inflamatória S100B é uma das alarminas provenientes desta resposta glial aumentada em AD, que se pensa ter um papel importante, embora pouco claro, durante os estados iniciais da doença. Esta proteína tem vindo a ser conhecida pela sua função como indutora inflamatória noutras doenças neurodegenerativas, contudo uma recente abordagem in vitro estabeleceu uma nova função para esta proteína, semelhante a uma chaperona, capaz de suprimir a agregação do péptido Aβ. Deste modo, foi investigado neste projeto se a S100B assume uma função neuro protetora ou agravadora da toxicidade imposta pelo péptido Aβ no modelo de culturas organotípicas de hipocampo. Primeiramente, a proteína S100B e o péptido Aβ42 foram purificados de forma recombinante a partir de E. coli. De seguida, as culturas organotípicas foram incubadas com ambas as proteínas de forma a mimetizar o ambiente proteico de AD e para explorar esta dupla função da S100B. Nestas condições, os resultados obtidos sugerem que na região do Dentate Gyrus, a S100B consegue prevenir, de forma parcial, a reatividade da microglia induzida pelo péptido Aβ42. Além disso, parece regular a expressão inflamatória de genes induzida pelo Aβ42, como por exemplo a expressão da citocina IL-1β, sem afetar a viabilidade neuronal. Embora estes resultados preliminares possam indicar que a S100B desempenha uma função neuro protetora face à neuroinflamação induzida pelo péptido Aβ, estudos adicionais são necessários para melhor confirmar se a interação entre estas duas biomoléculas pode ser usada como uma eventual abordagem terapêutica para melhorar a patologia de Alzheimer.
Book chapters on the topic "Organotypic Brain Slice Co-Cultures"
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Pringle, A. K., J. Self, and Fausto Iannotti. "Reducing Conditions Produce a Loss of Neuroprotective Efficacy of Competitive but not non-Competitive Antagonists in a Model of NMDA-Mediated Excitotoxicity in Organotypic Hippocampal Slice Cultures." In Brain Edema XI, 79–80. Vienna: Springer Vienna, 2000. http://dx.doi.org/10.1007/978-3-7091-6346-7_16.
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Kasri, Nael Nadif, Eve‐Ellen Govek, and Linda Van Aelst. "Characterization of Oligophrenin‐1, a RhoGAP Lost in Patients Affected with Mental Retardation: Lentiviral Injection in Organotypic Brain Slice Cultures." In Methods in Enzymology, 255–66. Elsevier, 2008. http://dx.doi.org/10.1016/s0076-6879(07)00419-3.
Full textConference papers on the topic "Organotypic Brain Slice Co-Cultures"
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Yu, Zhe, Woo Hyeun Kang, and Barclay Morrison. "Toward a Functional Tolerance Criterion for the Hippocampus Developed From Organotypic Slice Cultures." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19622.
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Approximately 1.5 million traumatic brain injuries (TBI) occur each year which result in 50,000 deaths, and about 80,000 people are left with a permanent disability. The annual cost associated with these injures is estimated to be $60 billion. Because there is no pharmacological treatment for TBI, engineering strategies to prevent these injuries enabled through an improved understanding of injury biomechanics is crucial. To this end, finite element models play a central role for predicting brain deformation induced by various loading scenarios such as falls or motor vehicle accidents. Novel protection strategies can then be tested in silico before the start of physical testing. However, in their current form, finite element models predict only mechanical responses and cannot predict the biological response of the brain tissue to the imposed deformation.