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Готові списки джерел за темами / Organotypic spinal cord slices

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Добірка наукової літератури з теми "Organotypic spinal cord slices"

Автор: Grafiati

Опубліковано: 10 березня 2023

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Статті в журналах з теми "Organotypic spinal cord slices"

1

Biancotti, Juan C., Kendal A. Walker, Guihua Jiang, Julie Di Bernardo, Lonnie D. Shea, and Shaun M. Kunisaki. "Hydrogel and neural progenitor cell delivery supports organotypic fetal spinal cord development in an ex vivo model of prenatal spina bifida repair." Journal of Tissue Engineering 11 (January 2020): 204173142094383. http://dx.doi.org/10.1177/2041731420943833.

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Studying how the fetal spinal cord regenerates in an ex vivo model of spina bifida repair may provide insights into the development of new tissue engineering treatment strategies to better optimize neurologic function in affected patients. Here, we developed hydrogel surgical patches designed for prenatal repair of myelomeningocele defects and demonstrated viability of both human and rat neural progenitor donor cells within this three-dimensional scaffold microenvironment. We then established an organotypic slice culture model using transverse lumbar spinal cord slices harvested from retinoic acid–exposed fetal rats to study the effect of fibrin hydrogel patches ex vivo. Based on histology, immunohistochemistry, gene expression, and enzyme-linked immunoabsorbent assays, these experiments demonstrate the biocompatibility of fibrin hydrogel patches on the fetal spinal cord and suggest this organotypic slice culture system as a useful platform for evaluating mechanisms of damage and repair in children with neural tube defects.

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2

Sypecka, Joanna, Sylwia Koniusz, Maria Kawalec, and Anna Sarnowska. "The Organotypic Longitudinal Spinal Cord Slice Culture for Stem Cell Study." Stem Cells International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/471216.

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The objective of this paper is to describe in detail the method of organotypic longitudinal spinal cord slice culture and the scientific basis for its potential utility. The technique is based on the interface method, which was described previously and thereafter was modified in our laboratory. The most important advantage of the presented model is the preservation of the intrinsic spinal cord fiber tract and the ventrodorsal polarity of the spinal cord. All the processes occurring during axonal growth, regeneration, synapse formation, and myelination could be visualized while being culturedin vitrofor up to 4-5 weeks after the slices had been isolated. Both pups and adult animals can undergo the same, equally efficient procedures when going by the protocol in question. The urgent need for an appropriatein vitromodel for spinal cord regeneration results from a greater number of clinical trials concerning regenerative medicine in the spinal cord injury and from still insufficient knowledge of the molecular mechanisms involved in the neuroreparative processes. The detailed method of organotypic longitudinal spinal cord slice culture is accompanied by examples of its application to studying biological processes to which both the CNS inhabiting and grafted cells are subjected.

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3

Haque, Azizul, Donald C. Shields, Arabinda Das, Abhay Varma, Russel J. Reiter, and Narendra L. Banik. "Melatonin receptor-mediated attenuation of excitotoxic cell death in cultured spinal cord slices." Melatonin Research 4, no. 2 (April 30, 2021): 336–47. http://dx.doi.org/10.32794/mr11250098.

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Recent studies suggest ex vivo modeling of neuronal injury is a robust approach for the mechanistic study of neurodegeneration. Melatonin, an indolamine, is a versatile molecule with antioxidative, antiapoptotic, neuroprotective, and anti-inflammatory properties. While melatonin has been studied as a therapeutic agent for spinal cord injury (SCI) related neuronal cell loss, its actions in organotypic slice cultures approximating SCI effects are less well understood. The actions of melatonin were therefore examined following exposure of cultured rat spinal cord slices to glutamate excitotoxicity. Exposure to glutamate (500 μM) for 4 hours induced neuronal degeneration that was prevented by 0.5 μM melatonin (applied immediately or 4 hours following glutamate exposure). Decreased internucleosomal DNA fragmentation, Bax:Bcl-2 and calpain:calpastatin ratios, caspase 8, 9 and 3 activities in slice cultures were measured following melatonin treatment. Melatonin receptor (MTR1, MTR2) mRNA levels were increased in the melatonin treated spinal cord slices. To confirm melatonin receptor-mediated protection, slice cultures were treated with 10 or 25 μM luzindole (melatonin receptor antagonist) at 0 and 4 hours, respectively, after glutamate exposure. Luzindole significantly decreased the ability of melatonin to prevent cell death in the sliced culture model. These results suggest melatonin receptors may provide a pathway for therapeutic applications to prevent penumbral neuron loss following SCI.

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4

Shahar, A., S. Lustig, Y. Akov, Y. David, P. Schneider, and R. Levin. "Different pathogenicity of encephalitic togaviruses in organotypic cultures of spinal cord slices." Journal of Neuroscience Research 25, no. 3 (March 1990): 345–52. http://dx.doi.org/10.1002/jnr.490250311.

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5

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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6

Liu, Jing-Jie, Xiao-Yan Ding, Li Xiang, Feng Zhao, and Sheng-Li Huang. "A novel method for oxygen glucose deprivation model in organotypic spinal cord slices." Brain Research Bulletin 135 (October 2017): 163–69. http://dx.doi.org/10.1016/j.brainresbull.2017.10.010.

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7

Rybachuk, O. A., Yu A. Lazarenko, V. V. Krotov, and N. V. Voitenko. "Structural/Functional Characteristics of Organotypic Spinal Cord Slices under Conditions of Long-Lasting Culturing." Neurophysiology 49, no. 2 (April 2017): 162–64. http://dx.doi.org/10.1007/s11062-017-9647-5.

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8

Phelps, P. E., R. P. Barber, and J. E. Vaughn. "Nonradial migration of interneurons can be experimentally altered in spinal cord slice cultures." Development 122, no. 7 (July 1, 1996): 2013–22. http://dx.doi.org/10.1242/dev.122.7.2013.

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During development, many migrating neurons are thought to guide on radially oriented glia to reach their adult locations. However, members of the ‘U-shaped’ group of cholinergic interneurons in embryonic rat spinal cord appeared to migrate in a direction perpendicular to the orientation of radial glia. This ‘U-shaped’ group of cells was located around the ventral ventricular zone on embryonic day 16 and, during the next two days, the constituent cells dispersed into the dorsal horn or around the central canal. During this period, these cells could be identified with either ChAT immunocytochemistry or NADPH-diaphorase histochemistry and they appeared to be aligned along commissural axons, suggesting that such processes, rather than radial glia, might guide their migration. An organotypic spinal cord slice preparation was developed and utilized for three different experimental approaches to studying this migration. In the first experiments, slices of embryonic day 16 cervical spinal cord were cultured for one, two or three days, and a relatively histotypic dorsal migration of ‘U-derived’ cells could be inferred from these sequential cultures. A second set of experiments focused on the direct observation of dorsally directed migration in living spinal cord cultures. Embryonic day 16 slices were injected with a lipophilic fluorescent label near the dorsal boundary of the ‘U-shaped’ cell group and the dorsal movement of labeled cells was observed using confocal microscopy. These experiments confirmed the dorsal migratory pattern inferred from sequentially fixed specimens. A third experimental approach was to transect embryonic day 16 slice cultures microsurgically in order to disturb the migration of ‘U-derived’ cells. Depending upon the amount of ventral spinal cord removed, the source of cells was excised and/or their guidance pathway was perturbed. The number and position of ‘U-derived’ cells varied with the amount of ventral cord excised. If more than 400 microns was removed, no ‘U-derived’ diaphorase-labeled cells were present, whereas if only 200–300 microns was removed, the cultures contained such cells. However, in this instance, many of the ‘U-derived’ neurons did not move as far dorsally, nor did they display their characteristic dorsoventral orientation. When results from these three experiments are taken together, they provide strong evidence that nonradial neuronal migration occurs in developing spinal cord and that the ‘U-derived’ neurons utilize such a migration to move from their ventral generation sites to their dorsal adult locations.

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9

Ravikumar, Madhumitha, Seema Jain, Robert H. Miller, Jeffrey R. Capadona, and Stephen M. Selkirk. "An organotypic spinal cord slice culture model to quantify neurodegeneration." Journal of Neuroscience Methods 211, no. 2 (November 2012): 280–88. http://dx.doi.org/10.1016/j.jneumeth.2012.09.004.

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10

Patar, Azim, Peter Dockery, Siobhan McMahon, and Linda Howard. "Ex Vivo Rat Transected Spinal Cord Slices as a Model to Assess Lentiviral Vector Delivery of Neurotrophin-3 and Short Hairpin RNA against NG2." Biology 9, no. 3 (March 15, 2020): 54. http://dx.doi.org/10.3390/biology9030054.

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The failure of the spinal cord to regenerate can be attributed both to a lack of trophic support for regenerating axons and to upregulation of inhibitory factors such as chondroitin sulphate proteoglycans including NG2 following injury. Lentiviral vector-mediated gene therapy is a possible strategy for treating spinal cord injury (SCI). This study investigated the effect of lentiviral vectors expressing Neurotrophin-3 (NT-3) and short-hairpin RNA against NG2 (NG2 sh) to enhance neurite outgrowth in in vitro and ex vivo transection injury models. Conditioned medium from cells transduced with NT-3 or shNG2 lentiviruses caused a significant increase in neurite length of primary dorsal root ganglia neurons compared to the control group in vitro. In an ex vivo organotypic slice culture (OSC) transduction with Lenti-NT-3 promoted axonal growth. Transducing OSCs with a combination of Lenti-NT-3/NG2 sh lead to a further increase in axonal growth but only in injured slices and only within the region adjacent to the site of injury. These findings suggest that the combination of lentiviral NT-3 and NG2 sh reduced NG2 levels and provided a more favourable microenvironment for neuronal regeneration after SCI. This study also shows that OSCs may be a useful platform for studying glial scarring and potential SCI treatments.

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Більше джерел

Дисертації з теми "Organotypic spinal cord slices"

1

Rioult-Pedotti, Marc Guy. "Optical multisite recording of neural activity patterns in organotypic spinal cord tissue cultures /." [S.l.] : [s.n.], 1991. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=9393.

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2

Cocchi, M. A. "THE MELATONIN PROTECTIVE ROLE IN AN ORGANOTYPIC MODEL OF SPINAL CORD INJURY SECONDARY DAMAGE." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/351674.

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Spinal cord injury (SCI) is characterized to be a two-step process composed by the primary lesion consisting of the initial trauma and the secondary damage, characterized by multiple processes including inflammation, oxidative stress and cell death that lead to a significant expansion of the original damage and to an increase of the functional deficit. Among the aforementioned processes, the oxidative stress plays a significant role in pathophysiology of SCI. In this study, we evaluated the role of melatonin, potent antioxidant and immunomodulator indoleamin, on the oxidative stress, the tissue viability and the neuritic plasticity deriving from the gray matter in an experimental model of organotypic cultures. These cultures consisted of Sprague Dawley rat spinal cord slice treated with hydrogen peroxide (H2O2). In five experimental groups, A) Control Group (CTR) – Organotypic spinal cord slice culture (350μm); B) Stressed Group (H2O2) – Organotypic spinal cord slice culture (350μm) exposed to H2O2 (50 μM); C) Control Group treated with melatonin (10-5M) of 24 hours (CTR+MEL) – Organotypic spinal cord slice culture (350μm) treated with melatonin for 24 hours; D) Treated Group (H2O2+MEL-POST) – Organotypic spinal cord slice culture (350μm) exposed to H2O2 (50 μM) and treated after 24 hours with melatonin (10-5M) for 24 hours; E) Treated Group (H2O2+MEL-PRE) – Organotypic spinal cord slice culture (350μm) pre-treated with melatonin (10-5M) for 24 hours (50 μM) and exposed to H2O2 for other 24 hours. We investigated the slice cellular death by propidium iodide (PI) assay, the slice vitality by MTT assay, the superoxide dismutase (SOD) and total thiols (SH) levels for the contrast to the oxidative stress, the neuronal (NeuN) and the synaptophysin (Syp) immunopositivity. Melatonin significantly decreased the number of dead cells, increased slice vitality, mainly in slices treated before H2O2 exposition. Melatonin enhanced SOD immunopositivity, contrasted total thiols decrease, attenuated Syp reduction and increased NeuN immunopositivity. Overall, these findings suggest that melatonin may exert a potentially beneficial effect upon the progression of SCI secondary damage, protecting the tissue from a further degeneration.

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3

Abdoun, Oussama. "Analyse spatiotemporelle de données MEA pour l'étude de la dynamique de l'activité de la moelle épinière et du tronc cérébral immatures chez la souris." Thesis, Bordeaux 1, 2012. http://www.theses.fr/2012BOR15266/document.

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Tous les réseaux de neurones immatures génèrent une activité dite « spontanée »qui persiste même en l’absence de toute afférence et est impliquée dans de nombreux processus développementaux. Cette activité apparaît in vitro sous formes de vagues calciques ou électriques pouvant se propager sur de grandes distances et embraser toute la préparation. Toutefois, sa dynamique a été assez peu étudiée jusqu’à présent. En vue de combler quelque peu cette lacune, nous avons utilisé des matrices de microélectrodes (MEA) pour caractériser l’activité rythmique spontanée dans la moelle épinière embryonnaire de souris, sur des préparations aigues et en culture incluant également le tronc cérébral.Les enregistrements MEA produisent des volumes de données très importants qui nécessitent des outils d’analyse performants et adaptés à l’information que l’on souhaite extraire. Nous avons donc développé des méthodes pour la détection, la classification et la cartographie des patrons spatiotemporels d’activité dans les données multicanaux. Notre approche cartographique utilise l’interpolation par splines et est orientée vers la production de cartes multimodales combinant l’activité électrique et des données anatomiques ou biochimiques (marquages). Ces méthodes d’analyse nous ont permis de décrire très précisément l’évolution de l’activité spontanée aux stades précoces (E12.5–E15.5). Nous avons également montré que, à E14.5, l’activité est initiée dans le bulbe, plus précisément dans une région riche en neurones 5-HT, suggérant un nouveau rôle des voies sérotoninergiques descendantes dans la maturation des réseaux spinaux.Enfin, nous avons analysé les mouvements embryonnaires à E14.5 et avons découvert des caractéristiques analogues à la dynamiques spatiotemporelle des activités intraspinales
Immature neural networks generate a peculiar type of activity that persists even in the absence of electrical inputs and was termed for this reason “endogenous”or “spontaneous”. This activity is ubiquitous and was found involved in a wide range of developmental events. In vitro, it can be observed as calcium or electrical waves propagating over great distances, often invading the whole preparation,but its dynamics remain poorly described. In order to somewhat fill this gap,we used multielectrode arrays (MEAs) to characterise the spontaneous rhythmic activity in the mouse developing spinal cord, in both acute and cultured isolated hindbrain-spinal cord preparations.To extract relevant information from the massive amounts of data yielded by MEA recordings, adapted analysis tools are needed. Thus, we have developedmethods for the detection, classification and mapping of spatiotemporal patternsof activity in multichannel data. Our mapping approach is based on the thin plates pline interpolation and includes the possibility to combine maps of activity with anatomical or stained data for multimodal imaging.These methods allowed us to analyse in great detail the evolution of spontaneousactivity at early stages (E12.5–E15.5). In addition, we have localised theinitiation site of E14.5 activity in the medulla and shown that it matches a densemidline population of serotoninergic neurons, suggesting a new role for 5-HTpathways in the maturation of spinal networks. Finally, we have recorded andtracked spontaneous limb movements of E14.5 embryos and found that features of motility were consistent with patterns of spinal activity

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4

Parisio, Carmen. "VEGF-A/VEGFRs system in neuropathies: a crossroad between pain and neuroprotection." Doctoral thesis, 2022. http://hdl.handle.net/2158/1259994.

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Vascular Endothelial Growth Factor (VEGF) is a family of signal proteins produced by different cells, that stimulates the formation of blood vessels. VEGF-A is the most studied member of its family. In addition to its well-known pro-angiogenic properties, it also directly influences neuronal and glial biological processes, exerting trophic and signaling functions in nervous tissue. In recent years, the involvement of the VEGF family in pain signaling is emerging, highlighting the opportunity of a new possible pharmacological target and making urgent the knowledge of its role in the pathophysiological mechanisms of algic sensitivity. For these reasons, the purpose of this thesis was to investigate the involvement of VEGF-A and its receptors VEGFR-1 and VEGFR-2 in pain perception, and the possible role of this growth factor in neuroprotection. In naïve mice, intrathecal infusion of VEGF165b (3- 10 and 30 ng/5 µL- a most representative member of VEGF-A) induced dose-dependent noxious hypersensitivity, assessed by pain threshold measurement, mediated by its VEGFR-1. The involvement of VEGFR-1 was confirmed by both using selective ligands (PlGF and VEGF-E that bind VEGFR-1 and VEGFR-2 respectively) and receptor blockers (mAb D16F7 specific for VEGFR-1 and DC101 for VEGFR-2), and from the silencing of the two VEGFRs by siRNAs in the lumbar spinal cord. In addition, to deepen the molecular mechanism underlying the painful action of VEGF-A, the immunofluorescence analysis showed that VEGFR-1 is more expressed on neuronal rather than astrocytic cells. Consequentially, in the electrophysiological study, VEGF165b stimulated the activity of spinal nociceptive neurons via VEGFR-1. Furthermore, in the dorsal horn of the spinal cord, immunofluorescence analysis revealed that VEGF-A increased in astrocytes from animals with oxaliplatin-induced neuropathy, compared to microglia and neurons, suggesting that this cell population is the source of the effective pain mediator. In addition, confocal microscopy confirmed the expression of VEGF-A in astrocytes, separately from its vascular component. To investigate the relevance of this result, we selectively silenced astrocytic VEGF-A via shRNAmir in spinal cord of neuropathic animals, resulting in a block of the development of chemotherapy-induced neuropathic pain. In addition, anti-VEGFR-1 mAb D16F7 effectively relieved neuropathic pain induced by various chemotherapeutic agents. Following these data, to further investigate the mechanisms of pain modulation and to study the neuroprotective component of VEGF-A in nervous tissue, we used the organotypic spinal cord slice. After fourteen days of cultivation, the slices were analyzed by immunofluorescence analysis with GFAP and NeuN markers to confirm the maintenance of cell morphology and structural organization of the spinal cord; in addition, using RECA-1 as endothelial marker, we highlighted a significant reduction of the normal vascular network. At this point, we focused our attention on three "key" factors that play important role in the development and maintenance of pain: Calcitonin gene-related peptide (CGRP), widely distributed in peripheral and central nervous system and its receptors are expressed in pain pathways; Substance P, involved in the onset and modulation of different types of pain; Glutamate, that showed a pivotal role in pain sensation and transmission. Treatment with both oxaliplatin (10 µM) and VEGF65b (100 ng/mL) enhanced the release of CGRP and Substance P in the culture medium of the slices compared to control; co-treatment with D16F7 (300 ng/mL), but not with DC101 (10 ng/mL), prevented the release of both two pro-algic factors. Measuring the mRNA of EAAT1 and EAAT2, the reduction in gene expression of the two glutamate transporters caused by VEGF165b, as well as by oxaliplatin, was improved by VEGFR-1 blocker. From the toxicity studies, we observed that oxaliplatin causes a dose-dependent neurotoxicity and alteration of neurons morphology expressed as a reduction in fluorescence intensity and in the number of NeuN+ cells, after 24 hours incubation. Moreover, activation of astrocytes (evaluated by immunoﬂuorescence staining) was observed. The co-treatment with VEGF165b showed neuroprotection of the nervous tissue assessed by PI ﬂuorescence, reduction of astrogliosis and neuronal alterations caused by oxaliplatin. To investigate the molecular mechanism underlying this neuroprotective eﬀect, we analyzed the role of VEGFR-1 and VEGFR-2 by using PlGF and VEGF-E as their speciﬁc ligand and also D16F7 and DC101 as receptor blockers. Quantitative analysis of PI fluorescence showed that VEGFR-2 is involved in VEGF-A-mediated neuroprotection. Ultimately, since the existence of astrocytic VEGF-A is reported in the literature, as confirmed by our in vivo results, we treated the slices with fluorocitrate, a glial metabolism blocker, to evaluate its effect in physiological and pathological conditions. Our results showed that fluoricitrate (80 µM) was able to reduce both VEGF-A baseline release and that induced by oxaliplatin treatment. Moreover, the astrocytic inhibition caused an increase in PI fluorescence at all times considered, as expected, worsening the toxicity due to oxaliplatin after three hours of treatment. The addition of exogenous VEGF165b reduces the toxicity caused by oxaliplatin and fluorocitrate after 24 hours of treatment. In conclusion, this thesis highlighted that VEGF-A released by astrocytes is a new actor in the complex neuron-glia network that oversees physiological and pathological pain, and mAb D16F7 exerts a potent painkiller action in different models of chemotherapy-induced neuropathic pain. Furthermore, the use of organotypic slices of the spinal cord has allowed to deepen the dichotomy between the proalgic and neuroprotective action of VEGF-A, highlighting that VEGFR-1 could be a promising therapeutic target in the modulation of chemotherapy-induced neuropathic pain, without blocking the protective component of the growth factor.

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5

Pettersson, Jennie. "Neuroprotective effects of hyaluronic acid hydrogel on organotypic spinal cord cultures." Thesis, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-205222.

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6

Xie, Huiwen. "Differentiation of motoneuron electrical properties in organotypic culture of rat spinal cord." 1994. http://catalog.hathitrust.org/api/volumes/oclc/32440401.html.

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7

Morais, Hermes Manuel Medina. "Development of secretome-based therapy by motor neuron modulation of miRNA-124 in ALS mouse models." Master's thesis, 2020. http://hdl.handle.net/10362/111128.

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Amyotrophic Lateral Sclerosis (ALS) is a fatal disease characterized by the degeneration of upper (cortical) and lower (spinal cord, SC) motor neurons (MNs) and aberrancy of glial cells. Results from our group point to a close connection between increased levels of miRNA-124 and the acquisition of pathological characteristics in MNs, astrocytes and microglia in ALS. Our main aim was to validate if the downregulation of the elevated levels of miR-124 in hSOD1G93A (mSOD1) MNs toward normal levels was preventive over neurodegeneration, astrocyte aberrancies and microglia activation in the mSOD1 mice at the early onset of the disease (10-12 weeks). Two ALS models were used: the NSC-34 MN-like cell line expressing mSOD1 (transgenic, TG) or not (wild-type, WT); and the SC organotypic cultures (OCs) from WT and TG mice. Pathological differences between TG and WT SCOCs were investigated. Relatively to the MN models, we used the modulation with pre-miR-124 (only in WT) and that of anti-miR-124 (only in the TG). The isolated secretomes were incubated in WT and TG SCOCs to assess harmful and/or neuroprotective properties. In TG SCOCs we observed: (i) increased necrotic cell death; (ii) disturbed inflammatory-associated miRNAs (increase in miR-21/miR-146a); (iii) and dysregulated neuronal and glial genes (increased CX3CR1, IL-1β, IL-10, SYP, DRP1, GLT-1 and downregulation of iNOS, HMGB1, Dlg4, CX3CL1 and GFAP). WT-MN secretome counteracted pathological markers in TG SCOCs. In contrast, TG MN secretome induced deleterious effects in WT SCOCs. Secretome from miR-124-enriched WT MNs incubated in WT SCOCs led to a profile of miRNAs and protein-coding genes similar to that caused by the TG MN secretome. On the contrary, the secretome from TG MNs depleted in miR-124 restored a deactivated profile in TG SCOCs. Our data reveals MN upregulation of miR-124 as a key player in ALS pathological processes.
Casa da Misericórdia de Lisboa (SCML), project ref. ALSResearch Grant ELA-2015-002

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Частини книг з теми "Organotypic spinal cord slices"

1

Deng, Ping, and Zao C. Xu. "Whole-Cell Patch-Clamp Recordings on Spinal Cord Slices." In Methods in Molecular Biology, 65–72. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-561-9_4.

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2

Biggs, James E., Van B. Lu, Helena J. Kim, Aaron Lai, Kathryn G. Todd, Klaus Ballanyi, William F. Colmers, and Peter A. Smith. "Defined Medium Organotypic Cultures of Spinal Cord Put ‘Pain in a Dish’." In Isolated Central Nervous System Circuits, 405–36. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-020-5_14.

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3

Pehl, U., H. A. Schmid, and E. Simon. "Lamina-Specific Effects of Nitric Oxide on Temperature Sensitive Neurons in Rat Spinal Cord Slices." In Thermal Balance in Health and Disease, 45–51. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7429-8_6.

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4

Nishi, S., M. Yoshimura, and C. Polosa. "Effect of Noradrenaline on the Electrical Activities of Lateral Horn Cells in Cat Spinal Cord Slices." In Histochemistry and Cell Biology of Autonomic Neurons and Paraganglia, 345–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72749-8_60.

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Murase, K., H. Ikeda, S. Terao, and T. Asai. "Slow Intrinsic Optical Signals in Rat Spinal Cord Slices and Their Modulation by Low-Frequency Stimulation." In Slow Synaptic Responses and Modulation, 429–35. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-66973-9_59.

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Allerton, C. A., P. R. Boden, and R. G. Hill. "In Vitro Studies on Neurones of the Superficial Dorsal Horn in Slices of 9–16 Day Old Rat Spinal Cord." In Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord, 395–98. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0825-6_38.

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Shahar, A., S. Lustig, Y. Akov, Y. David, P. Schneider, and R. Levin. "Spinal Cord Slices with Attached Dorsal Root Ganglia: A Culture Model for the Study of Pathogenicity of Encephalitic Viruses." In Plasticity and Regeneration of the Nervous System, 111–19. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-8047-4_12.

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Crain, Stanley M. "Neuropharmacological Analyses in Organotypic Cultures of Spinal Cord and Dorsal Root Ganglia." In Cell Culture, 75–86. Elsevier, 1990. http://dx.doi.org/10.1016/b978-0-12-185254-2.50010-3.

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