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Journal articles on the topic 'Organotypic spinal cultures'

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Author: Grafiati

Published: 11 March 2023

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1

Li, Bin, Xiao-Yun Liu, Zhe Li, Hui Bu, Meng-Meng Sun, Yan-Su Guo, and Chun-Yan Li. "Effect of ALS IgG on Motor Neurons in Organotypic Spinal Cord Cultures." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 35, no. 2 (May 2008): 220–25. http://dx.doi.org/10.1017/s0317167100008672.

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Objective:Reports about the role of autoimmunity in amyotrophic lateral sclerosis (ALS) are inconsistent. The aim of this work was to investigate the effect of IgG from patients with ALS on motor neurons in a physiological-like surrounding.Methods:Using affinity chromatography, IgG from six ALS patients, four disease controls and five healthy subjects was purified. Organotypic spinal cord cultures, which conserve the structure of the spinal cord in a horizontal plane and are suitable for studies with long-term treatment, were used and IgG with different concentrations ranging from 0.05 mg/mL to 0.5 mg/mL was added to the culture medium. Ventral motor neuron survival was evaluated by morphology and SMI-32 immunohistochemistry staining. Lactate dehydrogenase (LDH) level in the culture medium was measured by colorimetry.Results:After cultures were treated with ALS IgG for three weeks, the number and morphology of motor neurons showed little change. In addition, there was no significant difference in lactate dehydrogenase release between cultures treated with medium alone, normal control IgG, disease control IgG or ALS IgG.Conclusions:The results indicate that IgG from these ALS patients was insufficient per se to induce motor neuron death in Organotypic slice cultures. However, this does not preclude the possibility that other changes may have occurred in the motor neurons. This work offered a new model to evaluate the role of IgG in the pathogenesis of ALS. Organotypic cultures contribute to study of the impact of IgG on motor neurons by mimicking physiological conditions.

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2

Weidenheim, K. M., Y. Kress, W. K. Rashbaum, and W. D. Lyman. "ANTIBODY-ASSOCIATED MYELINOPATHY IN HUMAN FETAL SPINAL CORD ORGANOTYPIC CULTURES." Journal of Neuropathology and Experimental Neurology 54, no. 3 (May 1995): 465. http://dx.doi.org/10.1097/00005072-199505000-00233.

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3

Czarnecki, Antonny, Vincent Magloire, and Jürg Streit. "Local oscillations of spiking activity in organotypic spinal cord slice cultures." European Journal of Neuroscience 27, no. 8 (April 2008): 2076–88. http://dx.doi.org/10.1111/j.1460-9568.2008.06171.x.

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4

MASUROVSKY, E., E. PETERSON, S. CRAIN, and S. HORWITZ. "Taxol effects on GLIA in organotypic mouse spinal cord-DRG cultures." Cell Biology International Reports 9, no. 6 (June 1985): 539–46. http://dx.doi.org/10.1016/0309-1651(85)90018-9.

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5

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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6

Lee, Yu-Shang, Janie Baratta, Jen Yu, Vernon W. Lin, and Richard T. Robertson. "aFGF Promotes Axonal Growth in Rat Spinal Cord Organotypic Slice Co-Cultures." Journal of Neurotrauma 19, no. 3 (March 2002): 357–67. http://dx.doi.org/10.1089/089771502753594927.

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7

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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8

Shahar, A., S. Lustig, Y. Akov, Y. David, P. Schneider, A. Friedmann, and R. Levin. "West nile virions aligned along myelin lamellae in organotypic spinal cord cultures." Journal of Neuroscience Research 26, no. 4 (August 1990): 495–500. http://dx.doi.org/10.1002/jnr.490260413.

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9

Mazzone, Graciela L., and Andrea Nistri. "S100β as an early biomarker of excitotoxic damage in spinal cord organotypic cultures." Journal of Neurochemistry 130, no. 4 (May 19, 2014): 598–604. http://dx.doi.org/10.1111/jnc.12748.

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10

KUSAKA, HIROFUMI, ASAO HlRANO, Murray B. Bornstein, and Cedric S. Raine. "Basal Lamina Formation by Astrocytes in Organotypic Cultures of Mouse Spinal Cord Tissue." Journal of Neuropathology and Experimental Neurology 44, no. 3 (May 1985): 295–303. http://dx.doi.org/10.1097/00005072-198505000-00007.

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11

Hirano, A., H. Kusaka, M. B. Bornstein, and C. S. Raine. "REGIONAL DIFFERENCES IN ASTROCYTE ORGANIZATION IN ORGANOTYPIC CULTURES OF MOUSE SPINAL CORD TISSUE." Journal of Neuropathology and Experimental Neurology 44, no. 3 (May 1985): 343. http://dx.doi.org/10.1097/00005072-198505000-00118.

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12

Vos, C. "Cytotoxicity by Matrix Metalloprotease-1 in Organotypic Spinal Cord and Dissociated Neuronal Cultures." Experimental Neurology 163, no. 2 (June 2000): 324–30. http://dx.doi.org/10.1006/exnr.2000.7388.

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13

Avossa, D., M. D. Rosato-Siri, F. Mazzarol, and L. Ballerini. "Spinal circuits formation: a study of developmentally regulated markers in organotypic cultures of embryonic mouse spinal cord." Neuroscience 122, no. 2 (January 2003): 391–405. http://dx.doi.org/10.1016/j.neuroscience.2003.07.006.

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14

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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15

Magloire, Vincent, and Jürg Streit. "Intrinsic activity and positive feedback in motor circuits in organotypic spinal cord slice cultures." European Journal of Neuroscience 30, no. 8 (October 2009): 1487–97. http://dx.doi.org/10.1111/j.1460-9568.2009.06978.x.

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16

Krassioukov, Andrei V., Alun Ackery, Gwen Schwartz, Yana Adamchik, Yang Liu, and Michael G. Fehlings. "An in vitro model of neurotrauma in organotypic spinal cord cultures from adult mice." Brain Research Protocols 10, no. 2 (October 2002): 60–68. http://dx.doi.org/10.1016/s1385-299x(02)00180-0.

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17

Calderó, J., N. Brunet, O. Tarabal, L. Piedrafita, M. Hereu, V. Ayala, and J. E. Esquerda. "Lithium prevents excitotoxic cell death of motoneurons in organotypic slice cultures of spinal cord." Neuroscience 165, no. 4 (February 2010): 1353–69. http://dx.doi.org/10.1016/j.neuroscience.2009.11.034.

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18

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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19

Eckle, Veit-Simon, Monika Balk, Horst Thiermann, Bernd Antkowiak, and Christian Grasshoff. "Botulinum toxin B increases intrinsic muscle activity in organotypic spinal cord–skeletal muscle co-cultures." Toxicology Letters 244 (February 2016): 167–71. http://dx.doi.org/10.1016/j.toxlet.2015.08.003.

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20

Levy, A., M. Garcia Segura, Z. Nevo, Y. David, A. Shahar, and F. Naftolin. "Action of steroid hormones on growth and differentiation of CNS and spinal cord organotypic cultures." Cellular and Molecular Neurobiology 16, no. 3 (June 1996): 445–50. http://dx.doi.org/10.1007/bf02088111.

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21

Pinkernelle, Josephine, Hisham Fansa, Uwe Ebmeyer, and Gerburg Keilhoff. "Prolonged Minocycline Treatment Impairs Motor Neuronal Survival and Glial Function in Organotypic Rat Spinal Cord Cultures." PLoS ONE 8, no. 8 (August 13, 2013): e73422. http://dx.doi.org/10.1371/journal.pone.0073422.

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22

Mazzone, G. L., and A. Nistri. "Delayed neuroprotection by riluzole against excitotoxic damage evoked by kainate on rat organotypic spinal cord cultures." Neuroscience 190 (September 2011): 318–27. http://dx.doi.org/10.1016/j.neuroscience.2011.06.013.

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23

Crain, S. M., and A. Chalazonitis. "Development of opioid networks in organotypic cultures of fetal mouse spinal corddorsal root ganglion (drg) explants." International Journal of Developmental Neuroscience 3, no. 4 (1985): 416. http://dx.doi.org/10.1016/0736-5748(85)90081-4.

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24

Gerardo-Nava, Jose, Dorothee Hodde, Istvan Katona, Ahmet Bozkurt, Torsten Grehl, Harry W. M. Steinbusch, Joachim Weis, and Gary A. Brook. "Spinal cord organotypic slice cultures for the study of regenerating motor axon interactions with 3D scaffolds." Biomaterials 35, no. 14 (May 2014): 4288–96. http://dx.doi.org/10.1016/j.biomaterials.2014.02.007.

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25

Romeo-Guitart, David, Tatiana Leiva-Rodriguez, Joaquim Forés, and Caty Casas. "Improved Motor Nerve Regeneration by SIRT1/Hif1a-Mediated Autophagy." Cells 8, no. 11 (October 30, 2019): 1354. http://dx.doi.org/10.3390/cells8111354.

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Complete restoring of functional connectivity between neurons or target tissue after traumatic lesions is still an unmet medical need. Using models of nerve axotomy and compression, we investigated the effect of autophagy induction by genetic and pharmacological manipulation on motor nerve regeneration. ATG5 or NAD+-dependent deacetylase sirtuin-1 (SIRT1) overexpression on spinal motoneurons stimulates mTOR-independent autophagy and facilitates a growth-competent state improving motor axonal regeneration with better electromyographic records after nerve transection and suture. In agreement with this, using organotypic spinal cord cultures and the human cell line SH-SY5Y, we observed that the activation of SIRT1 and autophagy by NeuroHeal increased neurite outgrowth and length extension and that this was mediated by downstream HIF1a. To conclude, SIRT1/Hifα-dependent autophagy confers a more pro-regenerative phenotype to motoneurons after peripheral nerve injury. Altogether, we provide evidence showing that autophagy induction by SIRT1/Hifα activation or NeuroHeal treatment is a novel therapeutic option for improving motor nerve regeneration and functional recovery after injury.

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26

Drexler, Berthold, Julia Grenz, Christian Grasshoff, and Bernd Antkowiak. "Allopregnanolone Enhances GABAergic Inhibition in Spinal Motor Networks." International Journal of Molecular Sciences 21, no. 19 (October 7, 2020): 7399. http://dx.doi.org/10.3390/ijms21197399.

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The neurosteroid allopregnanolone (ALLO) causes unconsciousness by allosteric modulation of γ-aminobutyric acid type A (GABAA) receptors, but its actions on the spinal motor networks are unknown. We are therefore testing the hypothesis that ALLO attenuates the action potential firing of spinal interneurons and motoneurons predominantly via enhancing tonic, but not synaptic GABAergic inhibition. We used video microscopy to assess motoneuron-evoked muscle activity in organotypic slice cultures prepared from the spinal cord and muscle tissue. Furthermore, we monitored GABAA receptor-mediated currents by performing whole-cell voltage-clamp recordings. We found that ALLO (100 nM) reduced the action potential firing of spinal interneurons by 27% and that of α-motoneurons by 33%. The inhibitory effects of the combination of propofol (1 µM) and ALLO on motoneuron-induced muscle contractions were additive. Moreover, ALLO evoked a tonic, GABAA receptor-mediated current (amplitude: 41 pA), without increasing phasic GABAergic transmission. Since we previously showed that at a clinically relevant concentration of 1 µM propofol enhanced phasic, but not tonic GABAergic inhibition, we conclude that ALLO and propofol target distinct subpopulations of GABAA receptors. These findings provide first evidence that the combined application of ALLO and propofol may help to reduce intraoperative movements and undesired side effects that are frequently observed under total intravenous anesthesia.

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27

Delfs, John, Judith Friend, Shinji Ishimoto, and Daniel Saroff. "Ventral and dorsal horn acetylcholinesterase neurons are maintained in organotypic cultures of postnatal rat spinal cord explants." Brain Research 488, no. 1-2 (May 1989): 31–42. http://dx.doi.org/10.1016/0006-8993(89)90690-2.

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28

Grasshoff, Christian, and Bernd Antkowiak. "Organotypic Cultures of Spinal Cord Ventral Horn Are Valuable Tools for Investigating Immobility-Related Mechanisms In Vitro." Anesthesia & Analgesia 110, no. 2 (February 2010): 638. http://dx.doi.org/10.1213/ane.0b013e3181c531c8.

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29

Antognini, Joseph F., and Steven L. Jinks. "Organotypic Cultures of Spinal Cord Ventral Horn Are Valuable Tools for Investigating Immobility-Related Mechanisms In Vitro." Anesthesia & Analgesia 110, no. 2 (February 2010): 638. http://dx.doi.org/10.1213/ane.0b013e3181c531e3.

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30

Streit, J. "Regular oscillations of synaptic activity in spinal networks in vitro." Journal of Neurophysiology 70, no. 3 (September 1, 1993): 871–78. http://dx.doi.org/10.1152/jn.1993.70.3.871.

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1. Spontaneous synaptic potentials were recorded in motoneurons grown in organotypic slice cultures of embryonic rat spinal cord. In 71 of 85 cells these potentials appeared without obvious temporal structure (random patterns); in the remaining 14 cells they appeared in bursts (rhythmic patterns). 2. Random activity patterns could be converted into rhythmic patterns by treating the cultures with strychnine, bicuculline, or both. The excitatory amino acid N-methyl-D-aspartate (NMDA) transiently increased the rate of spontaneous synaptic activity without inducing rhythmic patterns. The NMDA antagonist 7-chloro-kynurenate reduced the burst rate while leaving the burst length unchanged in rhythmic patterns. In random patterns it reduced the rate of spontaneous synaptic activity by 68%. 3. Histograms of interevent times of the random patterns were best fitted by the sum of two expontentials, suggesting that the random type of activity could not be described simply as a Poisson process but involved at least one additional mechanism. 4. Rhythmic patterns consisted of bursts of activity with a mean burst length of 2.2 s that were separated by interburst intervals with a mean length of 6.6 s. Within the bursts autocorrelograms revealed regular oscillations with a mean period of 226 ms in 6 of 11 experiments with rhythmic patterns. The period showed little variation between individual experiments (202-288 ms). In random patterns no oscillations were detected. 5. Within the spontaneous bursts the excitatory postsynaptic potentials (EPSPs) progressively declined in amplitude. A corresponding depression of EPSPs was observed when trains of electrical stimuli were applied at 5 Hz to the dorsal horns of the spinal cord slices.(ABSTRACT TRUNCATED AT 250 WORDS)

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31

Herrando-Grabulosa, Mireia, Caty Casas, and José Aguilera. "The C-terminal domain of tetanus toxin protects motoneurons against acute excitotoxic damage on spinal cord organotypic cultures." Journal of Neurochemistry 124, no. 1 (November 15, 2012): 36–44. http://dx.doi.org/10.1111/jnc.12062.

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32

Perrier, Jean-François, Jens Noraberg, Magda Simon, and Jørn Hounsgaard. "Dedifferentiation of intrinsic response properties of motoneurons in organotypic cultures of the spinal cord of the adult turtle." European Journal of Neuroscience 12, no. 7 (July 2000): 2397–404. http://dx.doi.org/10.1046/j.1460-9568.2000.00134.x.

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33

Ballerini, Laura, and Micaela Galante. "Network bursting by organotypic spinal slice cultures in the presence of bicuculline and/or strychnine is developmentally regulated." European Journal of Neuroscience 10, no. 9 (September 1998): 2871–79. http://dx.doi.org/10.1111/j.1460-9568.1998.00296.x.

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34

Maragakis, Nicholas J., Mandy Jackson, Raquelli Ganel, and Jeffrey D. Rothstein. "Topiramate protects against motor neuron degeneration in organotypic spinal cord cultures but not in G93A SOD1 transgenic mice." Neuroscience Letters 338, no. 2 (February 2003): 107–10. http://dx.doi.org/10.1016/s0304-3940(02)01386-1.

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35

Bajrektarevic, Dzejla, and Andrea Nistri. "Delayed application of the anesthetic propofol contrasts the neurotoxic effects of kainate on rat organotypic spinal slice cultures." NeuroToxicology 54 (May 2016): 1–10. http://dx.doi.org/10.1016/j.neuro.2016.03.001.

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36

Kusaka, H., A. Hirano, M. B. Bornstein, G. R. W. Moore, and C. S. Raine. "Transformation of cells of astrocyte lineage into macrophage-like cells in organotypic cultures of mouse spinal cord tissue." Journal of the Neurological Sciences 72, no. 1 (January 1986): 77–89. http://dx.doi.org/10.1016/0022-510x(86)90037-7.

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37

Delfs, J. R., D. M. Saroff, Y. Nishida, J. Friend, and C. Geula. "Effects of NMDA and its antagonists on ventral horn cholinergic neurons in organotypic roller tube spinal cord cultures." Journal of Neural Transmission 104, no. 1 (January 1997): 31–51. http://dx.doi.org/10.1007/bf01271292.

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38

Elkhenany, Hoda, Pablo Bonilla, Esther Giraldo, Ana Alastrue Agudo, Michael J. Edel, María Jesus Vicent, Fernando Gisbert Roca, et al. "A Hyaluronic Acid Demilune Scaffold and Polypyrrole-Coated Fibers Carrying Embedded Human Neural Precursor Cells and Curcumin for Surface Capping of Spinal Cord Injuries." Biomedicines 9, no. 12 (December 16, 2021): 1928. http://dx.doi.org/10.3390/biomedicines9121928.

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Tissue engineering, including cell transplantation and the application of biomaterials and bioactive molecules, represents a promising approach for regeneration following spinal cord injury (SCI). We designed a combinatorial tissue-engineered approach for the minimally invasive treatment of SCI—a hyaluronic acid (HA)-based scaffold containing polypyrrole-coated fibers (PPY) combined with the RAD16-I self-assembling peptide hydrogel (Corning® PuraMatrix™ peptide hydrogel (PM)), human induced neural progenitor cells (iNPCs), and a nanoconjugated form of curcumin (CURC). In vitro cultures demonstrated that PM preserves iNPC viability and the addition of CURC reduces apoptosis and enhances the outgrowth of Nestin-positive neurites from iNPCs, compared to non-embedded iNPCs. The treatment of spinal cord organotypic cultures also demonstrated that CURC enhances cell migration and prompts a neuron-like morphology of embedded iNPCs implanted over the tissue slices. Following sub-acute SCI by traumatic contusion in rats, the implantation of PM-embedded iNPCs and CURC with PPY fibers supported a significant increase in neuro-preservation (as measured by greater βIII-tubulin staining of neuronal fibers) and decrease in the injured area (as measured by the lack of GFAP staining). This combination therapy also restricted platelet-derived growth factor expression, indicating a reduction in fibrotic pericyte invasion. Overall, these findings support PM-embedded iNPCs with CURC placed within an HA demilune scaffold containing PPY fibers as a minimally invasive combination-based alternative to cell transplantation alone.

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39

Gaja-Capdevila, Núria, Neus Hernández, Sandra Yeste, Raquel F. Reinoso, Javier Burgueño, Ana Montero, Manuel Merlos, José M. Vela, Mireia Herrando-Grabulosa, and Xavier Navarro. "EST79232 and EST79376, Two Novel Sigma-1 Receptor Ligands, Exert Neuroprotection on Models of Motoneuron Degeneration." International Journal of Molecular Sciences 23, no. 12 (June 16, 2022): 6737. http://dx.doi.org/10.3390/ijms23126737.

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Motor neuron diseases (MNDs) include sporadic and hereditary neurological disorders characterized by progressive degeneration of motor neurons (MNs). Sigma-1 receptor (Sig-1R) is a protein enriched in MNs, and mutations on its gene lead to various types of MND. Previous studies have suggested that Sig-1R is a target to prevent MN degeneration. In this study, two novel synthesized Sig-1R ligands, coded EST79232 and EST79376, from the same chemical series, with the same scaffold and similar physicochemical properties but opposite functionality on Sig-1R, were evaluated as neuroprotective compounds to prevent MN degeneration. We used an in vitro model of spinal cord organotypic cultures under chronic excitotoxicity and two in vivo models, the spinal nerve injury and the superoxide dismutase 1 (SOD1)G93A mice, to characterize the effects of these Sig-1R ligands on MN survival and modulation of glial reactivity. The antagonist EST79376 preserved MNs in vitro and after spinal nerve injury but was not able to improve MN death in SOD1G93A mice. In contrast, the agonist EST79232 significantly increased MN survival in the three models of MN degeneration evaluated and had a mild beneficial effect on motor function in SOD1G93A mice. In vivo, Sig-1R ligand EST79232 had a more potent effect on preventing MN degeneration than EST79376. These data further support the interest in Sig-1R as a therapeutic target for neurodegeneration.

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40

Mazzone, G. L., M. Mladinic, and A. Nistri. "Excitotoxic cell death induces delayed proliferation of endogenous neuroprogenitor cells in organotypic slice cultures of the rat spinal cord." Cell Death & Disease 4, no. 10 (October 2013): e902-e902. http://dx.doi.org/10.1038/cddis.2013.431.

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41

Chalazonitis, A., and S. M. Crain. "Maturation of opioid sensitivity of fetal mouse dorsal root ganglion neuron perikarya in organotypic cultures: Regulation by spinal cord." Neuroscience 17, no. 4 (April 1986): 1181–98. http://dx.doi.org/10.1016/0306-4522(86)90086-2.

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42

Brunet, Núria, Olga Tarabal, Josep E. Esquerda, and Jordi Calderó. "Excitotoxic motoneuron degeneration induced by glutamate receptor agonists and mitochondrial toxins in organotypic cultures of chick embryo spinal cord." Journal of Comparative Neurology 516, no. 4 (October 1, 2009): 277–90. http://dx.doi.org/10.1002/cne.22118.

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43

Senn, W., Th Wannier, J. Kleinle, H. R. Lüscher, L. Müller, J. Streit, and K. Wyler. "Pattern Generation by Two Coupled Time-Discrete Neural Networks with Synaptic Depression." Neural Computation 10, no. 5 (July 1, 1998): 1251–75. http://dx.doi.org/10.1162/089976698300017449.

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Numerous animal behaviors, such as locomotion in vertebrates, are produced by rhythmic contractions that alternate between two muscle groups. The neuronal networks generating such alternate rhythmic activity are generally thought to rely on pacemaker cells or well-designed circuits consisting of inhibitory and excitatory neurons. However, experiments in organotypic cultures of embryonic rat spinal cord have shown that neuronal networks with purely excitatory and random connections may oscillate due to their synaptic depression, even without pacemaker cells. In this theoretical study, we investigate what happens if two such networks are symmetrically coupled by a small number of excitatory connections. We discuss a time-discrete mean-field model describing the average activity and the average synaptic depression of the two networks. Depending on the parameter values of the depression, the oscillations will be in phase, antiphase, quasiperiodic, or phase trapped. We put forward the hypothesis that pattern generators may rely on activity-dependent tuning of synaptic depression.

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Bajrektarevic, Dzejla, and Andrea Nistri. "Ceftriaxone-mediated upregulation of the glutamate transporter GLT-1 contrasts neurotoxicity evoked by kainate in rat organotypic spinal cord cultures." NeuroToxicology 60 (May 2017): 34–41. http://dx.doi.org/10.1016/j.neuro.2017.02.013.

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Raffa, Paolo, Maria Easler, Francesca Cecchinato, Beatrice Auletta, Valentina Scattolini, Silvia Perin, Mattia Francesco Maria Gerli, et al. "Decellularized Skeletal Muscles Support the Generation of In Vitro Neuromuscular Tissue Models." Applied Sciences 11, no. 20 (October 13, 2021): 9485. http://dx.doi.org/10.3390/app11209485.

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Decellularized skeletal muscle (dSkM) constructs have received much attention in recent years due to the versatility of their applications in vitro. In search of adequate in vitro models of the skeletal muscle tissue, the dSkM offers great advantages in terms of the preservation of native-tissue complexity, including three-dimensional organization, the presence of residual signaling molecules within the construct, and their myogenic and neurotrophic abilities. Here, we attempted to develop a 3D model of neuromuscular tissue. To do so, we repopulated rat dSkM with human primary myogenic cells along with murine fibroblasts and we coupled them with organotypic rat spinal cord samples. Such culture conditions not only maintained multiple cell type viability in a long-term experimental setup, but also resulted in functionally active construct capable of contraction. In addition, we have developed a customized culture system which enabled easy access, imaging, and analysis of in vitro engineered co-cultures. This work demonstrates the ability of dSkM to support the development of a contractile 3D in vitro model of neuromuscular tissue fit for long-term experimental evaluations.

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Ulrich, D., and H. R. Luscher. "Miniature excitatory synaptic currents corrected for dendritic cable properties reveal quantal size and variance." Journal of Neurophysiology 69, no. 5 (May 1, 1993): 1769–73. http://dx.doi.org/10.1152/jn.1993.69.5.1769.

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1. Non-NMDA (N-Methyl-D-aspartate) receptor mediated miniature excitatory synaptic currents (mEPSCs) were recorded from motoneurons in organotypic cultures of embryonic rat spinal cord. 2. Amplitude histograms of mEPSCs were unimodal and skewed toward larger events. The mean of the modes of the amplitude histograms was -18 pA with a maximal amplitude range of -4 to -160 pA for individual mEPSCs. 3. Current transients to a short voltage pulse were used to estimate the passive cable parameters of the motoneurons. The mean membrane time constant (tau) and the mean electrotonic length (L) were 20 and 0.96 ms, respectively. 4. The amplitudes of the mEPSCs were corrected for imperfect space and voltage clamp. The resulting amplitude histograms could be fitted by the sum of two Gaussian curves, revealing a mean quantal size of -48 pA with a coefficient of variation (cv) of 0.28. 5. Our data suggest that quantal size and its variance are masked by the cable properties of the neurons and that simultaneous release of elementary quanta occurs occasionally.

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Tashiro, Jun, Seiji Kikuchi, Kazuyoshi Shinpo, Riichiro Kishimoto, Sachiko Tsuji, and Hidenao Sasaki. "Role of p53 in neurotoxicity induced by the endoplasmic reticulum stress agent tunicamycin in organotypic slice cultures of rat spinal cord." Journal of Neuroscience Research 85, no. 2 (February 1, 2007): 395–401. http://dx.doi.org/10.1002/jnr.21120.

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Sobkowicz, Hanna M., Andrew J. Waclawik, and Benjamin K. August. "The astroglial cell that guides nerve fibers from growth cone to synapse in organotypic cultures of the fetal mouse spinal cord." Synapse 59, no. 4 (2005): 183–200. http://dx.doi.org/10.1002/syn.20222.

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Oishi, Yosuke, Janie Baratta, Richard T. Robertson, and Oswald Steward. "Assessment of Factors Regulating Axon Growth between the Cortex and Spinal Cord in Organotypic Co-Cultures: Effects of Age and Neurotrophic Factors." Journal of Neurotrauma 21, no. 3 (March 2004): 339–56. http://dx.doi.org/10.1089/089771504322972121.

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Galante, Micaela, Daniela Avossa, Marcelo Rosato-Siri, and Laura Ballerini. "Homeostatic plasticity induced by chronic block of AMPA/kainate receptors modulates the generation of rhythmic bursting in rat spinal cord organotypic cultures." European Journal of Neuroscience 14, no. 6 (September 2001): 903–17. http://dx.doi.org/10.1046/j.0953-816x.2001.01710.x.

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