Journal articles: 'Organotypic cerebellar cultures'

1

Takács, J., and F. Metzger. "Morphological study of organotypic cerebellar cultures." Acta Biologica Hungarica 53, no. 1-2 (March 2002): 187–204. http://dx.doi.org/10.1556/abiol.53.2002.1-2.18.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Friedl, Gregor, Markus Hofer, Bernd Auber, Christian Sauder, Jürgen Hausmann, Peter Staeheli, and Axel Pagenstecher. "Borna Disease Virus Multiplication in Mouse Organotypic Slice Cultures Is Site-Specifically Inhibited by Gamma Interferon but Not by Interleukin-12." Journal of Virology 78, no. 3 (February 1, 2004): 1212–18. http://dx.doi.org/10.1128/jvi.78.3.1212-1218.2004.

Full text

Abstract:

ABSTRACT Borna disease virus (BDV) induces a nonpurulent CD4- and CD8-T-cell-dependent meningoencephalitis in susceptible animals. Upon intracerebral infection, BDV replicates in the mouse central nervous system (CNS), but only a few mouse strains develop neurological disorder. The antiviral T cells appear to suppress BDV replication by a noncytolytic mechanism. Since BDV does not replicate in standard mouse cell cultures, the putative role of gamma interferon (IFN-γ) in virus control could not be tested experimentally. Here, we report that mouse organotypic slice cultures can be used to elucidate the complex interactions of BDV, the CNS, and the immune system. We show that BDV replicated in various cell types of mouse cerebellar slice cultures in vitro. In infected slice cultures, a moderate upregulation of the chemokine genes CCL5 and CXCL10 was observed, while expression of various neural genes as well as other chemokine and cytokine genes was not altered. IFN-γ inhibited the multiplication of BDV in cerebellar and hippocampal slice cultures in a dose-dependent manner. However, while complete suppression of BDV was observed in cerebellar slice cultures, inhibition was incomplete in hippocampal slice cultures. Kinetic studies indicated that IFN-γ protects noninfected cells from infection rather than clearing the virus from infected cells. These results demonstrate that BDV can replicate in cultured neural cells of the mouse if organ integrity is well preserved. They further show that IFN-γ is a powerful inhibitor of BDV in the absence of blood-borne leukocytes in mouse cerebellar slice cultures.

APA, Harvard, Vancouver, ISO, and other styles

3

Egimendia, Ander, Susana Carregal-Romero, Iñaki Osorio-Querejeta, Daniel Padro, Jesús Ruiz-Cabello, David Otaegui, and Pedro Ramos-Cabrer. "Assessing the Potential of Molecular Imaging for Myelin Quantification in Organotypic Cultures." Pharmaceutics 13, no. 7 (June 28, 2021): 975. http://dx.doi.org/10.3390/pharmaceutics13070975.

Full text

Abstract:

Ex vivo models for the noninvasive study of myelin-related diseases represent an essential tool to understand the mechanisms of diseases and develop therapies against them. Herein, we assessed the potential of multimodal imaging traceable myelin-targeting liposomes to quantify myelin in organotypic cultures. Methods: MRI testing was used to image mouse cerebellar tissue sections and organotypic cultures. Demyelination was induced by lysolecithin treatment. Myelin-targeting liposomes were synthetized and characterized, and their capacity to quantify myelin was tested by fluorescence imaging. Results: Imaging of freshly excised tissue sections ranging from 300 µm to 1 mm in thickness was achieved with good contrast between white (WM) and gray matter (GM) using T2w MRI. The typical loss of stiffness, WM structures, and thickness of organotypic cultures required the use of diffusion-weighted methods. Designed myelin-targeting liposomes allowed for semiquantitative detection by fluorescence, but the specificity for myelin was not consistent between assays due to the unspecific binding of liposomes. Conclusions: With respect to the sensitivity, imaging of brain tissue sections and organotypic cultures by MRI is feasible, and myelin-targeting nanosystems are a promising solution to quantify myelin ex vivo. With respect to specificity, fine tuning of the probe is required. Lipid-based systems may not be suitable for this goal, due to unspecific binding to tissues.

APA, Harvard, Vancouver, ISO, and other styles

4

Falsig, Jeppe, Tiziana Sonati, Uli S. Herrmann, Dino Saban, Bei Li, Karina Arroyo, Boris Ballmer, Pawel P. Liberski, and Adriano Aguzzi. "Prion Pathogenesis Is Faithfully Reproduced in Cerebellar Organotypic Slice Cultures." PLoS Pathogens 8, no. 11 (November 1, 2012): e1002985. http://dx.doi.org/10.1371/journal.ppat.1002985.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Martin, Elodie, Marie-Stéphane Aigrot, Roland Grenningloh, Bruno Stankoff, Catherine Lubetzki, Ursula Boschert, and Bernard Zalc. "Bruton’s Tyrosine Kinase Inhibition Promotes Myelin Repair." Brain Plasticity 5, no. 2 (October 1, 2020): 123–33. http://dx.doi.org/10.3233/bpl-200100.

Full text

Abstract:

Background: Microglia are the resident macrophages of the central nervous system (CNS). In multiple sclerosis (MS) and related experimental models, microglia have either a pro-inflammatory or a pro-regenerative/pro-remyelinating function. Inhibition of Bruton’s tyrosine kinase (BTK), a member of the Tec family of kinases, has been shown to block differentiation of pro-inflammatory macrophages in response to granulocyte–macrophage colony-stimulating factor in vitro. However, the role of BTK in the CNS is unknown. Methods: Our aim was to investigate the effect of BTK inhibition on myelin repair in ex vivo and in vivo experimental models of demyelination and remyelination. The remyelination effect of a BTK inhibitor (BTKi; BTKi-1) was then investigated in LPC-induced demyelinated cerebellar organotypic slice cultures and metronidazole-induced demyelinated Xenopus MBP-GFP-NTR transgenic tadpoles. Results: Cellular detection of BTK and its activated form BTK-phospho-Y223 (p-BTK) was determined by immunohistochemistry in organotypic cerebellar slice cultures, before and after lysophosphatidylcholine (LPC)-induced demyelination. A low BTK signal detected by immunolabeling under normal conditions in cerebellar slices was in sharp contrast to an 8.5-fold increase in the number of BTK-positive cells observed in LPC-demyelinated slice cultures. Under both conditions, approximately 75% of cells expressing BTK and p-BTK were microglia and 25% were astrocytes. Compared with spontaneous recovery, treatment of demyelinated slice cultures and MTZ-demyelinated transgenic tadpoles with BTKi resulted in at least a 1.7-fold improvement of remyelination. Conclusion: Our data demonstrate that BTK inhibition is a promising therapeutic strategy for myelin repair.

APA, Harvard, Vancouver, ISO, and other styles

6

Nagata, Isao, and Norio Nakatsuji. "Migration Behavior of Granule Cell Neurons in Cerebellar Cultures I. A PKH26 Labeling Study in Microexplant and Organotypic Cultures. (mouse cerebellar granule cell/microexplant culture/organotypic explant culture/PKH26/migration)." Development, Growth and Differentiation 36, no. 1 (February 1994): 19–27. http://dx.doi.org/10.1111/j.1440-169x.1994.00019.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Dupont, Jean-Luc, Elodie Fourcaudot, Huguette Beekenkamp, Bernard Poulain, and Jean-Louis Bossu. "Synaptic organization of the mouse cerebellar cortex in organotypic slice cultures." Cerebellum 5, no. 4 (December 2006): 243–56. http://dx.doi.org/10.1080/14734220600905317.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Drake-Baumann, R., and F. J. Seil. "Electrophysiological differences between Purkinje cells in organotypic and granuloprival cerebellar cultures." Neuroscience 69, no. 2 (November 1995): 467–76. http://dx.doi.org/10.1016/0306-4522(95)00263-i.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Sherkhane, Pradeep, and Josef P. Kapfhammer. "The Plasma Membrane Ca2+-ATPase2 (PMCA2) Is Involved in the Regulation of Purkinje Cell Dendritic Growth in Cerebellar Organotypic Slice Cultures." Neural Plasticity 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/321685.

Full text

Abstract:

Purkinje cells are the principal neurons of the cerebellar cortex and have an extensive and elaborate dendritic tree. Chronic activation of type I metabotropic glutamate receptors inhibits Purkinje cell dendritic growth in organotypic cerebellar slice cultures. This effect is mediated by calcium influx through P/Q-type and T-type Ca2+channels. We have now studied the role of the plasma membrane Ca2+-ATPase2 (PMCA2), a major calcium extrusion pump, for Purkinje cell dendritic development. We found that PMCA2 is strongly expressed in the plasma membrane and dendritic spines of Purkinje cells in organotypic slice cultures compatible with a role for controlling the local dendritic calcium equilibrium. Inhibition of PMCA2 activity by carboxyeosin resulted in a moderate reduction of Purkinje cell dendritic tree size indicating that the extrusion of calcium by PMCA2 is important for maintaining the dendritic calcium concentration and controlling dendritic growth. When inhibition of PMCA2 was combined with stimulation of type I metabotropic glutamate receptors, it partially rescued dendritic morphology. This protection can be explained by a compensatory inactivation of voltage-gated calcium channels in Purkinje cells after PMCA2 inhibition. Our results demonstrate that PMCA2 activity is an important regulator of the dendritic calcium equilibrium controlling Purkinje cell dendritic growth.

APA, Harvard, Vancouver, ISO, and other styles

10

Rakotomamonjy, Jennifer, and Abdel Ghoumari. "Brain-Derived Neurotrophic Factor Is Required for the Neuroprotective Effect of Mifepristone on Immature Purkinje Cells in Cerebellar Slice Culture." International Journal of Molecular Sciences 20, no. 2 (January 12, 2019): 285. http://dx.doi.org/10.3390/ijms20020285.

Full text

Abstract:

Endogenous γ-aminobutyric acid (GABA)-dependent activity induces death of developing Purkinje neurons in mouse organotypic cerebellar cultures and the synthetic steroid mifepristone blocks this effect. Here, using brain-derived neurotrophic factor (BDNF) heterozygous mice, we show that BDNF plays no role in immature Purkinje cell death. However, interestingly, BDNF haploinsufficiency impairs neuronal survival induced by mifepristone and GABAA-receptors antagonist (bicuculline) treatments, indicating that the underlying neuroprotective mechanism requires the neurotrophin full expression.

APA, Harvard, Vancouver, ISO, and other styles

11

Kunimoto, Manabu, and Tsuguyoshi Suzuki. "Migration of granule neurons in cerebellar organotypic cultures is impaired by methylmercury." Neuroscience Letters 226, no. 3 (May 1997): 183–86. http://dx.doi.org/10.1016/s0304-3940(97)00273-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Doussau, Frédéric, Jean-Luc Dupont, Dorine Neel, Aline Schneider, Bernard Poulain, and Jean Louis Bossu. "Organotypic cultures of cerebellar slices as a model to investigate demyelinating disorders." Expert Opinion on Drug Discovery 12, no. 10 (July 20, 2017): 1011–22. http://dx.doi.org/10.1080/17460441.2017.1356285.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Andersen, M. D., D. H. Szarowski, J. N. Turner, and W. Shain. "Visualization of individual astrocytes in three-dimensional cerebellar tissues using green fluorescent protein." Proceedings, annual meeting, Electron Microscopy Society of America 54 (August 11, 1996): 908–9. http://dx.doi.org/10.1017/s0424820100167007.

Full text

Abstract:

The central nervous system is a complex structure traditionally studied through selective stains and two-dimensional images of fixed tissues. A long term goal of this laboratory is the study of dynamic cellular interactions in three dimensional tissues such as organotypic cultures. Due to the large volume of tissue, traditional microscopy methods contain excessive out-of-focus data making it difficult to observe clearly specific cellular interactions. The visualization of morphological changes in specific cells in living, three-dimensional tissues is commonly done with vital dyes. An alternate approach is labeling individual astrocytes with Green Fluorescent Protein (GFP) and injecting them into organotypic cultures.GFP is a naturally fluorescent protein originally isolated from the jellyfish Aequorea victorea. To label individual astrocytes, LRM55 astroglial cells were transfected with GFP using calcium phosphate. The percentage of stable transfectants was low (< 1%) resulting in expression of varying amounts of GFP, as seen in Figs 5 and 6.

APA, Harvard, Vancouver, ISO, and other styles

14

Seil, Fredrick J. "Cerebellar Culture Models of Dendritic Spine Proliferation After Transplantation of Glia." Journal of Neural Transplantation and Plasticity 6, no. 1 (1997): 1–10. http://dx.doi.org/10.1155/np.1997.1.

Full text

Abstract:

Studies of Purkinje cell dendritic spine proliferation after transplantation of cytosine arabinoside (Ara C) treated organotypic cerebellar cultures with glia and granule cells, either separately and in combination, were reviewed. Exposure of cerebellar explants to Ara C for the first 5 days in vitro results in the destruction of granule cells, the only excitatory cortical neurons, and oligodendroglia, and functionally compromises surviving astrocytes so that they do not appose neuronal membranes. In the absence of granule cells, there is a sprouting of Purkinje cell recurrent axon collaterals, the terminals of which project to and form heterotypical synapses with Purkinje cell dendritic spines, which are usually occupied by terminals of granule cell axons (parallel fibers). After this reorganization has been achieved, the explants can be transplanted with the missing elements to induce a second round of reorganization, with approximate restoration of the usual interneuronal relationships. Addition of both granule cells and glia resulted in a proliferation of clusters of Purkinje cell dendritic spines, which formed synapses with axon terminals of transplanted granule cells, and as synapse formation progressed, the spine clusters became reduced. Transplantation of Ara C-treated cultures with glia alone resulted in a proliferation of clusters of Purkinje cell dendritic spines, but in the absence of granule cells the spines remained unattached, and the clusters persisted throughout the period of observation. Purkinje cell dendritic spine proliferation was induced by exposure of Ara C-treated cultures to astrocyte-conditioned medium. When Ara C-treated cerebella cultures were transplanted with granule cells in the absence of functional glia, parallel fiber- Purkinje cell dendritic spine synapses formed, but no clusters of Purkinje cell dendritic spines were observed. These findings suggest that Purkinje cell dendritic spine proliferation is induced by an astrocyte-secreted factor, resulting in an expansion of postsynaptic sites available for synaptogenesis.

APA, Harvard, Vancouver, ISO, and other styles

15

Kessler, Markus, Bryant Kiliman, Carrie Humes, and Amy C. Arai. "Spontaneous activity in Purkinje cells: Multi-electrode recording from organotypic cerebellar slice cultures." Brain Research 1218 (July 2008): 54–69. http://dx.doi.org/10.1016/j.brainres.2008.04.063.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

17

Lossi, Laura, Graziana Gambino, Chiara Salio, and Adalberto Merighi. "Autophagy Regulates the Post-Translational Cleavage of BCL-2 and Promotes Neuronal Survival." Scientific World JOURNAL 10 (2010): 924–29. http://dx.doi.org/10.1100/tsw.2010.82.

Full text

Abstract:

B-cell lymphoma 2 protein (BCL-2) is one of the more widely investigated anti-apoptotic protein in mammals, and its levels are critical for protecting from programmed cell death. We report here that the cellular content of BCL-2 is regulated at post-translational level along the autophagy/lysosome pathways in organotypic cultures of post-natal mouse cerebellar cortex. Specifically this mechanism appears to be effective in the cerebellar granule cells (CGCs) that are known to undergo massive programmed cell death (apoptosis) during post-natal maturation. By the use of specific agonists/antagonist of calcium channels at the endoplasmic reticulum it was possible to understand the pivotal role of calcium release from intracellular stores in CGC neuroprotection. The more general significance of these findings is supported by a very recent study Niemann-Pick transgenic mice.

APA, Harvard, Vancouver, ISO, and other styles

18

Drake-Baumann, R., and F. J. Seil. "Influence of functional glia on the electrophysiology of Purkinje cells in organotypic cerebellar cultures." Neuroscience 88, no. 2 (January 1999): 507–19. http://dx.doi.org/10.1016/s0306-4522(98)00229-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Tanaka, Masahiko, Atsuhisa Tomita, Sachiko Yoshida, Masafumi Yano, and Hiroshi Shimizu. "Observation of the highly organized development of granule cells in rat cerebellar organotypic cultures." Brain Research 641, no. 2 (April 1994): 319–27. http://dx.doi.org/10.1016/0006-8993(94)90161-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Atterwill, Christopher K. "Brain Reaggregate Cultures in Neurotoxicological Investigations: Studies with Cholinergic Neurotoxins." Alternatives to Laboratory Animals 16, no. 3 (March 1989): 221–30. http://dx.doi.org/10.1177/026119298901600304.

Full text

Abstract:

The number of neurotoxicants which produce ‘lesions’ in organotypic brain reaggregate cultures in vitro, which correlate with known in vivo actions, is growing. With respect to cholinergic neurones, this includes kainic acid, organophosphorus compounds and, in our hands, ethylcholine mustard aziridinium (ECMA) and aluminium. We have demonstrated that in vitro exposure to low concentrations of ECMA (12.5μM) produces a two-stage lesion in rat whole-brain reaggregate cultures, corresponding to initial direct inhibition of choline acetyltransferase (ChAT), followed by a later loss of cholinergic neurones. Higher concentrations of ECMA (25–50μM) are more generally cytotoxic and also cause lesions in non-cholinergic cerebellar granule neurones in monolayer culture. Aluminium (0.1–0.01mM) similarly reduces ChAT activity in rat whole-brain reaggregate cultures. Both agents may be useful in providing brain cholinergic lesions in vitro analagous to those occurring in types of dementia in vivo. The use of brain reaggregates in a ‘stepwise’ procedure for testing potential neurotoxicants is also described.

APA, Harvard, Vancouver, ISO, and other styles

21

Sharma, Kapil, and Kumlesh K. Dev. "The Effects of Antipsychotics in Experimental Models of Krabbe Disease." Biomedicines 11, no. 5 (April 28, 2023): 1313. http://dx.doi.org/10.3390/biomedicines11051313.

Full text

Abstract:

The role of altered myelin in the onset and development of schizophrenia and changes in myelin due to antipsychotics remains unclear. Antipsychotics are D2 receptor antagonists, yet D2 receptor agonists increase oligodendrocyte progenitor numbers and limit oligodendrocyte injury. Conflicting studies suggest these drugs promote the differentiation of neural progenitors to oligodendrocyte lineage, while others report antipsychotics inhibit the proliferation and differentiation of oligodendrocyte precursors. Here, we utilised in-vitro (human astrocytes), ex-vivo (organotypic slice cultures) and in-vivo (twitcher mouse model) experimental study designs of psychosine-induced demyelination, a toxin that accumulates in Krabbe disease (KD), to investigate direct effects of antipsychotics on glial cell dysfunction and demyelination. Typical and atypical antipsychotics, and selective D2 and 5HT2A receptor antagonists, attenuated psychosine-induced cell viability, toxicity, and morphological aberrations in human astrocyte cultures. Haloperidol and clozapine reduced psychosine-induced demyelination in mouse organotypic cerebellar slices. These drugs also attenuated the effects of psychosine on astrocytes and microglia and restored non-phosphorylated neurofilament levels, indicating neuroprotective effects. In the demyelinating twitcher mouse model of KD, haloperidol improved mobility and significantly increased the survival of these animals. Overall, this study suggests that antipsychotics directly regulate glial cell dysfunction and exert a protective effect on myelin loss. This work also points toward the potential use of these pharmacological agents in KD.

APA, Harvard, Vancouver, ISO, and other styles

22

Yohay, Kaleb, Betty Tyler, Kyle D. Weaver, Andrea C. Pardo, Dan Gincel, Jaishri Blakeley, Henry Brem, and Jeffrey D. Rothstein. "Efficacy of local polymer-based and systemic delivery of the anti-glutamatergic agents riluzole and memantine in rat glioma models." Journal of Neurosurgery 120, no. 4 (April 2014): 854–63. http://dx.doi.org/10.3171/2013.12.jns13641.

Full text

Abstract:

Object The poor outcome of malignant gliomas is largely due to local invasiveness. Previous studies suggest that gliomas secrete excess glutamate and destroy surrounding normal peritumoral brain by means of excitotoxic mechanisms. In this study the authors assessed the effect on survival of 2 glutamate modulators (riluzole and memantine) in rodent glioma models. Methods In an in vitro growth inhibition assay, F98 and 9L cells were exposed to riluzole and memantine. Mouse cerebellar organotypic cultures were implanted with F98 glioma cells and treated with radiation, radiation + riluzole, or vehicle and assessed for tumor growth. Safety and tolerability of intracranially implanted riluzole and memantine CPP:SA polymers were tested in F344 rats. The efficacy of these drugs was tested against the 9L model and riluzole was further tested with and without radiation therapy (RT). Results In vitro assays showed effective growth inhibition of both drugs on F98 and 9L cell lines. F98 organotypic cultures showed reduced growth of tumors treated with radiation and riluzole in comparison with untreated cultures or cultures treated with radiation or riluzole alone. Three separate efficacy experiments all showed that localized delivery of riluzole or memantine is efficacious against the 9L gliosarcoma tumor in vivo. Systemic riluzole monotherapy was ineffective; however, riluzole given with RT resulted in improved survival. Conclusions Riluzole and memantine can be safely and effectively delivered intracranially via polymer in rat glioma models. Both drugs demonstrate efficacy against the 9L gliosarcoma and F98 glioma in vitro and in vivo. Although systemic riluzole proved ineffective in increasing survival, riluzole acted synergistically with radiation and increased survival compared with RT or riluzole alone.

APA, Harvard, Vancouver, ISO, and other styles

23

Llufriu-Dabén, Gemma, Delphine Meffre, Charbel Massaad, and Mehrnaz Jafarian-Tehrani. "A novel model of trauma-induced cerebellar injury and myelin loss in mouse organotypic cerebellar slice cultures using live imaging." Journal of Neuroscience Methods 311 (January 2019): 385–93. http://dx.doi.org/10.1016/j.jneumeth.2018.09.023.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Gähwiler, B. H., and I. Llano. "Sodium and potassium conductances in somatic membranes of rat Purkinje cells from organotypic cerebellar cultures." Journal of Physiology 417, no. 1 (October 1, 1989): 105–22. http://dx.doi.org/10.1113/jphysiol.1989.sp017793.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Mulholland, P. J., T. D. Stepanyan, R. L. Self, A. K. Hensley, B. R. Harris, A. Kowalski, J. M. Littleton, and M. A. Prendergast. "Corticosterone and dexamethasone potentiate cytotoxicity associated with oxygen-glucose deprivation in organotypic cerebellar slice cultures." Neuroscience 136, no. 1 (January 2005): 259–67. http://dx.doi.org/10.1016/j.neuroscience.2005.07.043.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Tanaka, Masahiko, Sachiko Yoshida, Masafumi Yano, and Fumio Hanaoka. "1236 Effects of N1-supplements, especially insulin, on the rat cerebellar development in organotypic cultures." Neuroscience Research Supplements 18 (January 1993): S130. http://dx.doi.org/10.1016/s0921-8696(05)81039-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Seil, Fredrick J., and Rosemarie Drake-Baumann. "Reduced cortical inhibitory synaptogenesis in organotypic cerebellar cultures developing in the absence of neuronal activity." Journal of Comparative Neurology 342, no. 3 (April 15, 1994): 366–77. http://dx.doi.org/10.1002/cne.903420305.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Lamoureux, Lise, Babu Sajesh, Jessy A. Slota, Sarah J. Medina, Matthew Mayor, Kathy L. Frost, Bryce Warner, et al. "Non-Productive Infection of Glial Cells with SARS-CoV-2 in Hamster Organotypic Cerebellar Slice Cultures." Viruses 14, no. 6 (June 3, 2022): 1218. http://dx.doi.org/10.3390/v14061218.

Full text

Abstract:

The numerous neurological syndromes associated with COVID-19 implicate an effect of viral pathogenesis on neuronal function, yet reports of direct SARS-CoV-2 infection in the brain are conflicting. We used a well-established organotypic brain slice culture to determine the permissivity of hamster brain tissues to SARS-CoV-2 infection. We found levels of live virus waned after inoculation and observed no evidence of cell-to-cell spread, indicating that SARS-CoV-2 infection was non-productive. Nonetheless, we identified a small number of infected cells with glial phenotypes; however, no evidence of viral infection or replication was observed in neurons. Our data corroborate several clinical studies that have assessed patients with COVID-19 and their association with neurological involvement.

APA, Harvard, Vancouver, ISO, and other styles

29

Stoyanova, Irina, Andrii Klymenko, Jeannette Willms, Thorsten Doeppner, Anton Tonchev, and David Lutz. "Ghrelin Regulates Expression of the Transcription Factor Pax6 in Hypoxic Brain Progenitor Cells and Neurons." Cells 11, no. 5 (February 23, 2022): 782. http://dx.doi.org/10.3390/cells11050782.

Full text

Abstract:

The nature of brain impairment after hypoxia is complex and recovery harnesses different mechanisms, including neuroprotection and neurogenesis. Experimental evidence suggests that hypoxia may trigger neurogenesis postnatally by influencing the expression of a variety of transcription factors. However, the existing data are controversial. As a proof-of-principle, we subjected cultured cerebral cortex neurons, cerebellar granule neurons and organotypic cerebral cortex slices from rat brains to hypoxia and treated these cultures with the hormone ghrelin, which is well-known for its neuroprotective functions. We found that hypoxia elevated the expression levels and stimulated nuclear translocation of ghrelin’s receptor GHSR1 in the cultured neurons and the acute organotypic slices, whereas ghrelin treatment reduced the receptor expression to normoxic levels. GHSR1 expression was also increased in cerebral cortex neurons of mice with induced experimental stroke. Additional quantitative analyses of immunostainings for neuronal proliferation and differentiation markers revealed that hypoxia stimulated the proliferation of neuronal progenitors, whereas ghrelin application during the phase of recovery from hypoxia counteracted these effects. At the mechanistic level, we provide a link between the described post-ischemic phenomena and the expression of the transcription factor Pax6, an important regulator of neural progenitor cell fate. In contrast to the neurogenic niches in the brain where hypoxia is known to increase Pax6 expression, the levels of the transcription factor in cultured hypoxic cerebral cortex cells were downregulated. Moreover, the application of ghrelin to hypoxic neurons normalised the expression levels of these factors. Our findings suggest that ghrelin stimulates neurogenic factors for the protection of neurons in a GHSR1-dependent manner in non-neurogenic brain areas such as the cerebral cortex after exposure to hypoxia.

APA, Harvard, Vancouver, ISO, and other styles

30

Lossi, Laura, Adalberto Merighi, Vittorino Novello, and Alessandra Ferrandino. "Protective Effects of Some Grapevine Polyphenols against Naturally Occurring Neuronal Death." Molecules 25, no. 12 (June 25, 2020): 2925. http://dx.doi.org/10.3390/molecules25122925.

Full text

Abstract:

The interest in the biological properties of grapevine polyphenols (PPs) in neuroprotection is continuously growing in the hope of finding translational applications. However, there are several concerns about the specificity of action of these molecules that appear to act non-specifically on the permeability of cellular membranes. Naturally occurring neuronal death (NOND) during cerebellar maturation is a well characterized postnatal event that is very useful to investigate the death and rescue of neurons. We here aimed to establish a baseline comparative study of the potential to counteract NOND of certain grapevine PPs of interest for the oenology. To do so, we tested ex vivo the neuroprotective activity of peonidin- and malvidin-3-O-glucosides, resveratrol, polydatin, quercetin-3-O-glucoside, (+)-taxifolin, and (+)-catechin. The addition of these molecules (50 μM) to organotypic cultures of mouse cerebellum explanted at postnatal day 7, when NOND reaches a physiological peak, resulted in statistically significant (two-tailed Mann–Whitney test—p < 0.001) reductions of the density of dead cells (propidium iodide+ cells/mm2) except for malvidin-3-O-glucoside. The stilbenes were less effective in reducing cell death (to 51–60%) in comparison to flavanols, (+)-taxifolin and quercetin 3-O-glucoside (to 69–72%). Thus, molecules with a -OH group in ortho position (taxifolin, quercetin 3-O-glucoside, (+)-catechin, and peonidin 3-O-glucoside) have a higher capability to limit death of cerebellar neurons. As NOND is apoptotic, we speculate that PPs act by inhibiting executioner caspase 3.

APA, Harvard, Vancouver, ISO, and other styles

31

Seil, Fredrick J., Rosemarie Drake-Baumann, Arnold L. Leiman, Robert M. Herndon, and Kenneth L. Tiekotter. "Morphological correlates of altered neuronal activity in organotypic cerebellar cultures chronically exposed to anti-GABA agents." Developmental Brain Research 77, no. 1 (January 1994): 123–32. http://dx.doi.org/10.1016/0165-3806(94)90219-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Saha, A., L. Xu, R. Franczak, P. Noldner, N. Meadows, S. Buntz, R. Storms, A. Balber, and J. Kurtzberg. "Umbilical cord tissue derived mesenchymal stromal cells inhibit lysophosphatidylcholine mediated activation of microglia in organotypic cerebellar cultures." Cytotherapy 19, no. 5 (May 2017): S193. http://dx.doi.org/10.1016/j.jcyt.2017.02.279.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Amadio, Susanna, Chiara Parisi, Cinzia Montilli, Alberto Savio Carrubba, Savina Apolloni, and Cinzia Volonté. "P2Y12Receptor on the Verge of a Neuroinflammatory Breakdown." Mediators of Inflammation 2014 (2014): 1–15. http://dx.doi.org/10.1155/2014/975849.

Full text

Abstract:

In the CNS, neuroinflammation occurring during pathologies as amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) is the consequence of an intricate interplay orchestrated by various cell phenotypes. Among the molecular cues having a role in this process, extracellular nucleotides are responsible for intercellular communication and propagation of inflammatory stimuli. This occurs by binding to several receptor subtypes, defined P2X/P2Y, which are widespread in different tissues and simultaneously localized on multiple cells. For instance, the metabotropic P2Y12subtype is found in the CNS on microglia, affecting activation and chemotaxis, on oligodendrocytes, possessing a hypothesized role in myelination, and on astrocytes. By comparative analysis, we have established here that P2Y12receptor immunolabelled by antibodies against C-terminus or second intracellular loop, is, respectively, distributed and modulated under neuroinflammatory conditions on ramified microglia or myelinated fibers, in primary organotypic cerebellar cultures, tissue slices from rat striatum and cerebellum, spinal cord sections from symptomatic/end stage SOD1-G93A ALS mice, and finally autoptic cortical tissue from progressive MS donors. We suggest that modulation of P2Y12expression might play a dual role as analytic marker of branched/surveillant microglia and demyelinating lesions, thus potentially acquiring a predictive value under neuroinflammatory conditions as those found in ALS and MS.

APA, Harvard, Vancouver, ISO, and other styles

34

Jaudon, Fanny, Fabrice Raynaud, Rosine Wehrlé, Jean-Michel Bellanger, Mohamed Doulazmi, Guilan Vodjdani, Stéphane Gasman, et al. "The RhoGEF DOCK10 is essential for dendritic spine morphogenesis." Molecular Biology of the Cell 26, no. 11 (June 2015): 2112–27. http://dx.doi.org/10.1091/mbc.e14-08-1310.

Full text

Abstract:

By regulating actin cytoskeleton dynamics, Rho GTPases and their activators RhoGEFs are implicated in various aspects of neuronal differentiation, including dendritogenesis and synaptogenesis. Purkinje cells (PCs) of the cerebellum, by developing spectacular dendrites covered with spines, represent an attractive model system in which to decipher the molecular signaling underlying these processes. To identify novel regulators of dendritic spine morphogenesis among members of the poorly characterized DOCK family of RhoGEFs, we performed gene expression profiling of fluorescence-activated cell sorting (FACS)-purified murine PCs at various stages of their postnatal differentiation. We found a strong increase in the expression of the Cdc42-specific GEF DOCK10. Depleting DOCK10 in organotypic cerebellar cultures resulted in dramatic dendritic spine defects in PCs. Accordingly, in mouse hippocampal neurons, depletion of DOCK10 or expression of a DOCK10 GEF-dead mutant led to a strong decrease in spine density and size. Conversely, overexpression of DOCK10 led to increased spine formation. We show that DOCK10 function in spinogenesis is mediated mainly by Cdc42 and its downstream effectors N-WASP and PAK3, although DOCK10 is also able to activate Rac1. Our global approach thus identifies an unprecedented function for DOCK10 as a novel regulator of dendritic spine morphogenesis via a Cdc42-mediated pathway.

APA, Harvard, Vancouver, ISO, and other styles

35

Campeau, Jody L., Gengshu Wu, John R. Bell, Jay Rasmussen, and Valerie L. Sim. "Early Increase and Late Decrease of Purkinje Cell Dendritic Spine Density in Prion-Infected Organotypic Mouse Cerebellar Cultures." PLoS ONE 8, no. 12 (December 2, 2013): e81776. http://dx.doi.org/10.1371/journal.pone.0081776.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Frontzek, Karl, Marco Bardelli, Assunta Senatore, Anna Henzi, Regina R. Reimann, Seden Bedir, Marika Marino, et al. "A conformational switch controlling the toxicity of the prion protein." Nature Structural & Molecular Biology 29, no. 8 (August 2022): 831–40. http://dx.doi.org/10.1038/s41594-022-00814-7.

Full text

Abstract:

AbstractPrion infections cause conformational changes of the cellular prion protein (PrPC) and lead to progressive neurological impairment. Here we show that toxic, prion-mimetic ligands induce an intramolecular R208-H140 hydrogen bond (‘H-latch’), altering the flexibility of the α2–α3 and β2–α2 loops of PrPC. Expression of a PrP2Cys mutant mimicking the H-latch was constitutively toxic, whereas a PrPR207A mutant unable to form the H-latch conferred resistance to prion infection. High-affinity ligands that prevented H-latch induction repressed prion-related neurodegeneration in organotypic cerebellar cultures. We then selected phage-displayed ligands binding wild-type PrPC, but not PrP2Cys. These binders depopulated H-latched conformers and conferred protection against prion toxicity. Finally, brain-specific expression of an antibody rationally designed to prevent H-latch formation prolonged the life of prion-infected mice despite unhampered prion propagation, confirming that the H-latch is an important reporter of prion neurotoxicity.

APA, Harvard, Vancouver, ISO, and other styles

37

Meffre, Delphine, Ghjuvan’Ghjacumu Shackleford, Mehdi Hichor, Victor Gorgievski, Eleni T. Tzavara, Amalia Trousson, Abdel M. Ghoumari, et al. "Liver X receptors alpha and beta promote myelination and remyelination in the cerebellum." Proceedings of the National Academy of Sciences 112, no. 24 (May 28, 2015): 7587–92. http://dx.doi.org/10.1073/pnas.1424951112.

Full text

Abstract:

The identification of new pathways governing myelination provides innovative avenues for remyelination. Liver X receptors (LXRs) α and β are nuclear receptors activated by oxysterols that originated from the oxidation of cholesterol. They are crucial for cholesterol homeostasis, a major lipid constituent of myelin sheaths that are formed by oligodendrocytes. However, the role of LXRs in myelin generation and maintenance is poorly understood. Here, we show that LXRs are involved in myelination and remyelination processes. LXRs and their ligands are present in oligodendrocytes. We found that mice invalidated for LXRs exhibit altered motor coordination and spatial learning, thinner myelin sheaths, and reduced myelin gene expression. Conversely, activation of LXRs by either 25-hydroxycholesterol or synthetic TO901317 stimulates myelin gene expression at the promoter, mRNA, and protein levels, directly implicating LXRα/β in the transcriptional control of myelin gene expression. Interestingly, activation of LXRs also promotes oligodendroglial cell maturation and remyelination after lysolecithin-induced demyelination of organotypic cerebellar slice cultures. Together, our findings represent a conceptual advance in the transcriptional control of myelin gene expression and strongly support a new role of LXRs as positive modulators in central (re)myelination processes.

APA, Harvard, Vancouver, ISO, and other styles

38

Schousboe, Inger, Niels Tønder, Jens Zimmer, and Arne Schousboe. "A developmental study of lactate dehydrogenase isozyme and aspartate aminotransferase activity in organotypic rat hippocampal slice cultures and primary cultures of mouse neocortical and cerebellar neurons." International Journal of Developmental Neuroscience 11, no. 6 (December 1993): 765–72. http://dx.doi.org/10.1016/0736-5748(93)90065-l.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Peña‐Contreras, Z., D. Davila‐Vera, and R. V. Mendoza‐Briceño. "[P1.50]: Atrazine delays Purkinje cell development in vitro as evidenced by Golgi method in primary organotypic cultures of mouse cerebellar cortex." International Journal of Developmental Neuroscience 26, no. 8 (November 25, 2008): 858. http://dx.doi.org/10.1016/j.ijdevneu.2008.09.100.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Gehmeyr, Julian, Abdelouahid Maghnouj, Jonas Tjaden, Matthias Vorgerd, Stephan Hahn, Veronika Matschke, Verena Theis, and Carsten Theiss. "Disabling VEGF-Response of Purkinje Cells by Downregulation of KDR via miRNA-204-5p." International Journal of Molecular Sciences 22, no. 4 (February 22, 2021): 2173. http://dx.doi.org/10.3390/ijms22042173.

Full text

Abstract:

The vascular endothelial growth factor (VEGF) is well known for its wide-ranging functions, not only in the vascular system, but also in the central (CNS) and peripheral nervous system (PNS). To study the role of VEGF in neuronal protection, growth and maturation processes have recently attracted much interest. These effects are mainly mediated by VEGF receptor 2 (VEGFR-2). Current studies have shown the age-dependent expression of VEGFR-2 in Purkinje cells (PC), promoting dendritogenesis in neonatal, but not in mature stages. We hypothesize that microRNAs (miRNA/miR) might be involved in the regulation of VEGFR-2 expression during the development of PC. In preliminary studies, we performed a miRNA profiling and identified miR204-5p as a potential regulator of VEGFR-2 expression. In the recent study, organotypic slice cultures of rat cerebella (postnatal day (p) 1 and 9) were cultivated and VEGFR-2 expression in PC was verified via immunohistochemistry. Additionally, PC at age p9 and p30 were isolated from cryosections by laser microdissection (LMD) to analyse VEGFR-2 expression by quantitative RT-PCR. To investigate the influence of miR204-5p on VEGFR-2 levels in PC, synthetic constructs including short hairpin (sh)-miR204-5p cassettes (miRNA-mimics), were microinjected into PC. The effects were analysed by confocal laser scanning microscopy (CLSM) and morphometric analysis. For the first time, we could show that miR204-5p has a negative effect on VEGF sensitivity in juvenile PC, resulting in a significant decrease of dendritic growth compared to untreated juvenile PC. In mature PC, the overexpression of miR204-5p leads to a shrinkage of dendrites despite VEGF treatment. The results of this study illustrate, for the first time, which miR204-5p expression has the potential to play a key role in cerebellar development by inhibiting VEGFR-2 expression in PC.

APA, Harvard, Vancouver, ISO, and other styles

41

Lonchamp, Etienne, Jean-Luc Dupont, Huguette Beekenkamp, Bernard Poulain, and Jean-Louis Bossu. "The Mouse Cerebellar Cortex in Organotypic Slice Cultures: An In Vitro Model to Analyze the Consequences of Mutations and Pathologies on Neuronal Survival, Development, and Function." Critical Reviews™ in Neurobiology 18, no. 1-2 (2006): 179–86. http://dx.doi.org/10.1615/critrevneurobiol.v18.i1-2.180.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Kunhiraman, Haritha, and Anna Kenney. "BIOL-08. IGFBP2 PROMOTES TUMOR METASTASIS IN SHH MEDULLOBLASTOMA." Neuro-Oncology 23, Supplement_1 (June 1, 2021): i4. http://dx.doi.org/10.1093/neuonc/noab090.015.

Full text

Abstract:

Abstract Medulloblastoma (MB) is the most common pediatric brain malignancy. MB comprises 5 major subgroups known as WNT, SHH p53wt, SHH p53mut, Group 3 and Group 4. Among the four MB subgroups SHH group is the most dominant molecular subgroup in infants and adults. These tumors are proposed to arise from cerebellar granule neuron precursors (CGNPs), whose developmental expansion requires SHH signaling from the neighboring Purkinje neurons. Previous reports suggest that SHH group features a unique tumor microenvironment compared with other MB groups. Recently, we performed cytokine array analysis of culture media from different MB cell lines. Interestingly, our data showed increased levels of IGFBP2 produced by SHH MB cell lines compared to others. We confirmed these results using ELISA and Western blotting from 3 human SHH MB cell lines, and Smo/A1 mouse tumor cells. IGFBP2 is a member of IGFBP super family of proteins; it plays important roles in tumor cell proliferation, metastasis and drug resistance. We analyzed the role of IGFBP2 in SHH group medulloblastoma tumor growth and metastasis. IGFBP2 knock-down stable cell lines showed phenotypic changes including reduced cell proliferation, cell migration and colony size. Our preliminary in vitro data suggest IGFBP2 exerts it metastasis-promoting role in SHH MB by regulating the expression of EMT marker proteins such as N cadherin, slug etc. and matrix remodeling proteins like MMPs and TIMPs. We are currently performing functional studies in organotypic tumor slice cultures to validate these findings and establish IGFBP2 as a novel regulator of aggressive tumor growth and spread in SHH MB.

APA, Harvard, Vancouver, ISO, and other styles

43

Min, Hyunjung, Li Xu, Roberta Parrott, Joanne Kurtzberg, and Anthony Filiano. "Abstract 4 Umbilical Cord-Derived Mesenchymal Stromal Cells Suppress Neuroinflammation and Promote Remyelination in the Spinal Cord." Stem Cells Translational Medicine 11, Supplement_1 (September 1, 2022): S6. http://dx.doi.org/10.1093/stcltm/szac057.004.

Full text

Abstract:

Abstract Introduction Mesenchymal stromal cells (MSCs) are one of the most widely tested cell therapies due to their ability to suppress inflammation. Demyelinating diseases of the central nervous system (CNS) are commonly accompanied by neuroinflammation, including infiltrating proinflammatory leukocytes and activation of resident macrophages (microglia and border-associated macrophages in the meninges). The precise mechanism of how MSCs suppress neuroinflammation is unclear; however, we recently described a novel pathway where MSCs physically interact with macrophages to reprogram the immune response through the transfer of a cytoplasmic organelle called a processing body (p-body). Objective We set out to study how human umbilical cord tissue-derived MSCs interact with CNS microglia and border macrophages to protect in a mouse model of spinal cord demyelination. Methods We manufactured several MSC lines under GMP conditions and tested their ability to interact with CNS macrophages and promote remyelination in multiple preclinical assays. To determine if p-bodies are critical for these steps, we depleted p-bodies using CRISPR/Cas9 targeting to DDX6. To test for effects on acute demyelination, we injected lysophosphatidylcholine (LPC) into the spinal cord or added LPC to organotypic cerebellar slice cultures. To test direct effects on microglia activation, we treated primary microglia or a microglia cell line with lipopolysaccharide. Results We determined that MSC promoted remyelination in the spinal cord and that this was dependent on p-bodies. MSC directly contacted CNS macrophages and inhibited their activation. Using primary microglia and a microglia cell line, we determined that MSCs suppress the release of proinflammation cytokines, IL-6, and TNF. Discussion We determined that MSCs suppress microglial cell activation and enhance remyelination of the spinal cord. Our study offers insight into a novel mechanism about how MSCs can alter the immune response via transferring p-bodies and enhance remyelination in CNS. Furthermore, our results may lead to a quick and simple potency assay to establish the efficacy of MSCs for suppressing neuroinflammation.

APA, Harvard, Vancouver, ISO, and other styles

44

Malhotra, Sunny, Carme Costa, Herena Eixarch, Christian W. Keller, Lukas Amman, Helios Martínez-Banaclocha, Luciana Midaglia, et al. "NLRP3 inflammasome as prognostic factor and therapeutic target in primary progressive multiple sclerosis patients." Brain 143, no. 5 (April 13, 2020): 1414–30. http://dx.doi.org/10.1093/brain/awaa084.

Full text

Abstract:

Abstract Primary progressive multiple sclerosis is a poorly understood disease entity with no specific prognostic biomarkers and scarce therapeutic options. We aimed to identify disease activity biomarkers in multiple sclerosis by performing an RNA sequencing approach in peripheral blood mononuclear cells from a discovery cohort of 44 untreated patients with multiple sclerosis belonging to different clinical forms and activity phases of the disease, and 12 healthy control subjects. A validation cohort of 58 patients with multiple sclerosis and 26 healthy control subjects was included in the study to replicate the RNA sequencing findings. The RNA sequencing revealed an interleukin 1 beta (IL1B) signature in patients with primary progressive multiple sclerosis. Subsequent immunophenotyping pointed to blood monocytes as responsible for the IL1B signature observed in this group of patients. Functional experiments at baseline measuring apoptosis-associated speck-like protein containing a CARD (ASC) speck formation showed that the NOD-leucine rich repeat and pyrin containing protein 3 (NLRP3) inflammasome was overactive in monocytes from patients with primary progressive multiple sclerosis, and canonical NLRP3 inflammasome activation with a combination of ATP plus lipopolysaccharide was associated with increased IL1B production in this group of patients. Primary progressive multiple sclerosis patients with high IL1B gene expression levels in peripheral blood mononuclear cells progressed significantly faster compared to patients with low IL1B levels based on the time to reach an EDSS of 6.0 and the Multiple Sclerosis Severity Score. In agreement with peripheral blood findings, both NLRP3 and IL1B expression in brain tissue from patients with primary progressive multiple sclerosis was mainly restricted to cells of myeloid lineage. Treatment of mice with a specific NLRP3 inflammasome inhibitor attenuated established experimental autoimmune encephalomyelitis disease severity and improved CNS histopathology. NLRP3 inflammasome-specific inhibition was also effective in reducing axonal damage in a model of lipopolysaccharide-neuroinflammation using organotypic cerebellar cultures. Altogether, these results point to a role of IL1B and the NLRP3 inflammasome as prognostic biomarker and potential therapeutic target, respectively, in patients with primary progressive multiple sclerosis.

APA, Harvard, Vancouver, ISO, and other styles

45

Kurimoto, Yui, Tadashi Ogo, Kazuto Kobayashi, Naohiro Hozumi, Chitoshi Takayama, Atsuo Fukuda, and Sachiko Yoshida. "Developmental change of VGAT-Venus expression in organotypic cultured cerebellar cortex and cultured glial cells." Neuroscience Research 68 (January 2010): e127. http://dx.doi.org/10.1016/j.neures.2010.07.2132.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Selmaj, K., K. Renkawek, R. Alam, E. Kida, M. Maszewska, and J. Rozniecki. "Studies on lymphokine-mediated demyelination in organotypic rat cerebellum in culture." Acta Neurologica Scandinavica 74, no. 3 (September 1986): 186–89. http://dx.doi.org/10.1111/j.1600-0404.1986.tb07853.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Rimvall, Karin, Flavio Keller, and Peter G. Waser. "Development of cholinergic projections in organotypic cultures of rat septum, hippocampus and cerebellum." Developmental Brain Research 19, no. 2 (April 1985): 267–78. http://dx.doi.org/10.1016/0165-3806(85)90198-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Zhu, Caihong, Uli S. Herrmann, Jeppe Falsig, Irina Abakumova, Mario Nuvolone, Petra Schwarz, Katrin Frauenknecht, Elisabeth J. Rushing, and Adriano Aguzzi. "A neuroprotective role for microglia in prion diseases." Journal of Experimental Medicine 213, no. 6 (May 16, 2016): 1047–59. http://dx.doi.org/10.1084/jem.20151000.

Full text

Abstract:

Microglial activation is a hallmark of most neurodegenerative disorders, and is particularly conspicuous in prion diseases. However, the role of microglia, which function as both primary immune effector cells and professional phagocytes in the central nervous system, remains contentious in the context of neurodegeneration. Here, we evaluated the effect of microglial depletion/deficiency on prion pathogenesis. We found that ganciclovir-mediated microglial ablation on tga20/CD11b-thymidine kinase of Herpes simplex virus (HSVTK) cerebellar organotypic cultured slices markedly aggravated prion-induced neurotoxicity. A similar deterioration of disease was recapitulated in in vivo microglial depletion in prion-infected tga20/CD11b-HSVTK mice. Additionally, deficiency of microglia in interleukin 34 knockout (IL34−/−) mice again resulted in significantly augmented proteinase K–resistant prion protein deposition and accelerated prion disease progression. These results provide unambiguous evidence for a general protective role of microglia in prion pathogenesis.

APA, Harvard, Vancouver, ISO, and other styles

49

Sullivan, A. M., and A. J. Morton. "Endothelins Induce Fos Expression in Neurons and Glia in Organotypic Cultures of Rat Cerebellum." Journal of Neurochemistry 67, no. 4 (November 23, 2002): 1409–18. http://dx.doi.org/10.1046/j.1471-4159.1996.67041409.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Obata, Kunihiko. "Excitatory and Trophic Action of GABA and Related Substances in Newborn Mice and Organotypic Cerebellar Culture." Developmental Neuroscience 19, no. 1 (1997): 117–19. http://dx.doi.org/10.1159/000111195.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Organotypic cerebellar cultures'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles