Journal articles: 'Cortical neuronal cultures'

1

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

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

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

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

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Synchronization of cortical neural cultures is studied as a function of the effective network connectivity in the phenomenon of synchronized firing(SF). The synchronized bursting frequency (during SF) of the network is found to be much slower than the characteristic time scale of a neuron and increases with the network connectivity. The synchronized bursting frequency f is characterized by a critical age (tc) as: [Formula: see text]. Furthermore, tc is found to scale with the cell plating density ρ as tc ~ ρ−β with β ≃ 0.44 ± 0.08. Although some aspects of the observed SF is similar to the array enhanced synchronization, detailed comparison of measured spike statistics from synchronized and non-synchronized cultures suggests that the nature of synchronization during SF is different from that of the array-enhanced synchronization. In particular, electrophysiological measurements using double patch technique revel that even though the bursting frequencies are synchronized, the intra-burst spikes are not.

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Nguyen, Lan, Sarah Wright, Mike Lee, Zhao Ren, John-Michael Sauer, Wherly Hoffman, Wagner Zago, Gene G. Kinney, and Michael P. Bova. "Quantifying Amyloid Beta (Aβ)–Mediated Changes in Neuronal Morphology in Primary Cultures." Journal of Biomolecular Screening 17, no. 6 (April 2, 2012): 835–42. http://dx.doi.org/10.1177/1087057112441972.

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Alzheimer’s disease (AD) is a devastating neurodegenerative disease affecting millions of people. The amyloid hypothesis suggests that the pathogenesis of AD is related to the accumulation of amyloid beta (Aβ) in the brain. Herein, the authors quantify Aβ-mediated changes in neuronal morphology in primary cultures using the Cellomics neuronal profiling version 3.5 (NPv3.5) BioApplication. We observed that Aβ caused a 33% decrease in neurite length in primary human cortical cultures after 24 h of treatment compared with control-treated cultures. We also determined that quantifying changes of neuronal morphology was a more sensitive indicator of nonlethal cell injury than traditional cytotoxicity assays. Aβ-mediated neuronal deficits observed in human cortical cultures were also observed in primary rat hippocampal cultures, where we demonstrated that the integrin-blocking antibody, 17E6, completely abrogated Aβ-mediated cytotoxicity. Finally, we showed that Aβ challenge to 21 days in vitro rat hippocampal cultures reduced synapsin staining to 14% of control-treated cultures. These results are consistent with the finding that loss of presynaptic integrity is one of the initial deficits observed in AD. The implementation of phenotypic screens to identify compounds that block Aβ-mediated cytotoxicity in primary neuronal cultures may lead to the development of novel strategies to prevent AD.

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Guaraldi, Mary, Sangmook Lee, and Thomas B. Shea. "Synaptic Signals from Glutamate-Treated Neurons Induce Aberrant Post-Synaptic Signals in Untreated Neuronal Networks." Open Neurology Journal 14, no. 1 (August 24, 2020): 59–62. http://dx.doi.org/10.2174/1874205x02014010059.

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Background and Objective: Glutamate neurotoxicity is associated with a wide range of disorders and can impair synaptic function. Failure to clear extracellular glutamate fosters additional cycles and spread of regional hyperexcitation. Methods and Results: Using cultured murine cortical neurons, herein it is demonstrated that synaptic signals generated by cultures undergoing glutamate-induced hyperactivity can invoke similar effects in other cultures not exposed to elevated glutamate. Conclusion: Since sequential synaptic connectivity can encompass extensive cortical regions, this study presents a potential additional contributor to the spread of damage resulting from glutamate excitotoxicity and should be considered in attempts to mitigate neurodegeneration.

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Kim, Sun H., Seok J. Won, Seonghyang Sohn, Hyuk J. Kwon, Jee Y. Lee, Jong H. Park, and Byoung J. Gwag. "Brain-derived neurotrophic factor can act as a pronecrotic factor through transcriptional and translational activation of NADPH oxidase." Journal of Cell Biology 159, no. 5 (December 2, 2002): 821–31. http://dx.doi.org/10.1083/jcb.200112131.

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Several lines of evidence suggest that neurotrophins (NTs) potentiate or cause neuronal injury under various pathological conditions. Since NTs enhance survival and differentiation of cultured neurons in serum or defined media containing antioxidants, we set out experiments to delineate the patterns and underlying mechanisms of brain-derived neurotrophic factor (BDNF)–induced neuronal injury in mixed cortical cell cultures containing glia and neurons in serum-free media without antioxidants, where the three major routes of neuronal cell death, oxidative stress, excitotoxicity, and apoptosis, have been extensively studied. Rat cortical cell cultures, after prolonged exposure to NTs, underwent widespread neuronal necrosis. BDNF-induced neuronal necrosis was accompanied by reactive oxygen species (ROS) production and was dependent on the macromolecular synthesis. cDNA microarray analysis revealed that BDNF increased the expression of cytochrome b558, the plasma membrane-spanning subunit of NADPH oxidase. The expression and activation of NADPH oxidase were increased after exposure to BDNF. The selective inhibitors of NADPH oxidase prevented BDNF-induced ROS production and neuronal death without blocking antiapoptosis action of BDNF. The present study suggests that BDNF-induced expression and activation of NADPH oxidase cause oxidative neuronal necrosis and that the neurotrophic effects of NTs can be maximized under blockade of the pronecrotic action.

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Zhang, Junhui, Geoffrey Thomas Gibney, Peng Zhao, and Ying Xia. "Neuroprotective role of δ-opioid receptors in cortical neurons." American Journal of Physiology-Cell Physiology 282, no. 6 (June 1, 2002): C1225—C1234. http://dx.doi.org/10.1152/ajpcell.00226.2001.

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We recently demonstrated that δ-opioid receptor (DOR) activation protects cortical neurons against glutamate-induced injury. Because glutamate is a mediator of hypoxic injury in neurons, we hypothesized that DOR is involved in neuroprotection during O2 deprivation and that its activation/inhibition may alter neuronal susceptibility to hypoxic stress. In this work, we tested the effect of opioid receptor activation and inhibition on cultured cortical neurons in hypoxia (1% O2). Cell injury was assessed by lactate dehydrogenase release, morphology-based quantification, and live/dead staining. Our results show that 1) immature neurons ( days 4 and 6) were not significantly injured by hypoxia until 72 h of exposure, whereas day 8 neurons were injured after only 24-h hypoxia; 2) DOR inhibition (naltrindole) caused neuronal injury in both day 4 and day 8 normoxic cultures and further augmented hypoxic injury in these neurons; 3) DOR activation ([d-Ala2,d-Leu5]enkephalin) reduced neuronal injury in day 8 cultures after 24 h of normoxic or hypoxic exposure and attenuated naltrindole-induced injury with prolonged exposure; and 4) μ- or κ-opioid receptor inhibition (β-funaltrexamine or nor-binaltorphimine) had little effect on neurons in either normoxic or hypoxic conditions. Collectively, these data suggest that DOR plays a crucial role in neuroprotection in normoxic and hypoxic environments.

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C., L., C. R., C. H., M. T., Y. S., Pik-Yin Pik-Yin, and C. K. "Synchronized Bursting Induced by Network Connectivity in Cortical Neuronal Cultures." Journal of the Korean Physical Society 50, no. 91 (January 15, 2007): 207. http://dx.doi.org/10.3938/jkps.50.207.

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

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Kim, Eun Young, Jae Young Koh, Yang Hee Kim, Seonghyang Sohn, Eunhye Joe, and Byoung Joo Gwag. "Zn2+entry produces oxidative neuronal necrosis in cortical cell cultures." European Journal of Neuroscience 11, no. 1 (January 1999): 327–34. http://dx.doi.org/10.1046/j.1460-9568.1999.00437.x.

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12

Swaiman, Kenneth F., and Valynda L. Machen. "Effect of ferric nitrilotriacetate on predominantly cortical neuronal cell cultures." Neurochemical Research 14, no. 7 (July 1989): 683–88. http://dx.doi.org/10.1007/bf00964879.

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13

Monyer, Hannelore, Dean M. Hartley, and Dennis W. Choi. "21-Aminosteroids attenuate excitotoxic neuronal injury in cortical cell cultures." Neuron 5, no. 2 (August 1990): 121–26. http://dx.doi.org/10.1016/0896-6273(90)90302-v.

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14

Ramnath, R. R., K. Strange, and P. A. Rosenberg. "Neuronal injury evoked by depolarizing agents in rat cortical cultures." Neuroscience 51, no. 4 (December 1992): 931–39. http://dx.doi.org/10.1016/0306-4522(92)90530-f.

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15

Ueda, Hiroshi, Ryousuke Fujita, Akira Yoshida, Hayato Matsunaga, and Mutsumi Ueda. "Identification of prothymosin-α1, the necrosis–apoptosis switch molecule in cortical neuronal cultures." Journal of Cell Biology 176, no. 6 (March 12, 2007): 853–62. http://dx.doi.org/10.1083/jcb.200608022.

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We initially identified a nuclear protein, prothymosin-α1 (ProTα), as a key protein inhibiting necrosis by subjecting conditioned media from serum-free cultures of cortical neurons to a few chromatography steps. ProTα inhibited necrosis of cultured neurons by preventing rapid loss of cellular adenosine triphosphate levels by reversing the decreased membrane localization of glucose transporters but caused apoptosis through up-regulation of proapoptotic Bcl2-family proteins. The apoptosis caused by ProTα was further inhibited by growth factors, including brain-derived neurotrophic factor. The ProTα-induced cell death mode switch from necrosis to apoptosis was also reproduced in experimental ischemia-reperfusion culture experiments, although the apoptosis level was markedly reduced, possibly because of the presence of growth factors in the reperfused serum. Knock down of PKCβII expression prevented this cell death mode switch. Collectively, these results suggest that ProTα is an extracellular signal protein that acts as a cell death mode switch and could be a promising candidate for preventing brain strokes with the help of known apoptosis inhibitors.

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16

Gonzales, Jerry M., and Iris Mendez-Bobe. "Pentobarbital Enhances Cyclic Adenosine Monophosphate Production in the Brain by Effects on Neurons but Not Glia." Anesthesiology 84, no. 5 (May 1, 1996): 1148–55. http://dx.doi.org/10.1097/00000542-199605000-00017.

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Background Cyclic adenosine monophosphate (cAMP) is an important regulator of neuronal excitability. The effects of barbiturates on cAMP production in intact neurons are not known. This study used cultures of cortical neurons, cultures of glia, and slices of cerebral cortex from the rat to study the effects of barbiturates on cAMP regulation in the brain. Methods Primary cultures of cortical neurons or glia were prepared from 17-day gestational Sprague-Dawley rat fetuses and were used after 12-16 days in culture. Cross-cut slices (300 microns) were prepared from cerebral cortex of adult rats. Cyclic AMP accumulation was determined by measuring the conversion of [3H]adenosine triphosphate (ATP) to [3H]cAMP in cells preloaded with [3H]adenine. Results Pentobarbital enhanced isoproterenol- and forskolin-stimulated, but not basal, cAMP accumulation in cultures of cerebral neurons. Cyclic AMP production was enhanced by pentobarbital in a dose-dependent fashion up to a concentration of 250 microM; This concentration of pentobarbital increased cAMP production by 40-50% relative to that in controls without pentobarbital. At 500 microM pentobarbital, the magnitude of the enhancement was less. Pentobarbital had no effect on isoproterenol-stimulated cAMP production in cultures containing only glia. Pentobarbital also enhanced isoproterenol-stimulated, but not basal, cAMP production in slices of cerebral cortex by approximately 30% at concentrations of 62.5-250 microM and by almost 100% at 500 microM. Conclusions Pentobarbital enhances stimulated cAMP accumulation in cultured preparations from brain and fresh cortical slices. Neurons are required for this effect. Because cAMP modulates neuronal excitability, this effect of pentobarbital may be an important mechanism by which this anesthetic influences brain function.

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Tukker, Anke M., Fiona M. J. Wijnolts, Aart de Groot, and Remco H. S. Westerink. "Applicability of hiPSC-Derived Neuronal Cocultures and Rodent Primary Cortical Cultures for In Vitro Seizure Liability Assessment." Toxicological Sciences 178, no. 1 (August 31, 2020): 71–87. http://dx.doi.org/10.1093/toxsci/kfaa136.

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Abstract Seizures are life-threatening adverse drug reactions which are investigated late in drug development using rodent models. Consequently, if seizures are detected, a lot of time, money and animals have been used. Thus, there is a need for in vitro screening models using human cells to circumvent interspecies translation. We assessed the suitability of cocultures of human-induced pluripotent stem cell (hiPSC)-derived neurons and astrocytes compared with rodent primary cortical cultures for in vitro seizure liability assessment using microelectrode arrays. hiPSC-derived and rodent primary cortical neuronal cocultures were exposed to 9 known (non)seizurogenic compounds (pentylenetetrazole, amoxapine, enoxacin, amoxicillin, linopirdine, pilocarpine, chlorpromazine, phenytoin, and acetaminophen) to assess effects on neuronal network activity using microelectrode array recordings. All compounds affect activity in hiPSC-derived cocultures. In rodent primary cultures all compounds, except amoxicillin changed activity. Changes in activity patterns for both cell models differ for different classes of compounds. Both models had a comparable sensitivity for exposure to amoxapine (lowest observed effect concentration [LOEC] 0.03 µM), linopirdine (LOEC 1 µM), and pilocarpine (LOEC 0.3 µM). However, hiPSC-derived cultures were about 3 times more sensitive for exposure to pentylenetetrazole (LOEC 30 µM) than rodent primary cortical cultures (LOEC 100 µM). Sensitivity of hiPSC-derived cultures for chlorpromazine, phenytoin, and enoxacin was 10-30 times higher (LOECs 0.1, 0.3, and 0.1 µM, respectively) than in rodent cultures (LOECs 10, 3, and 3 µM, respectively). Our data indicate that hiPSC-derived neuronal cocultures may outperform rodent primary cortical cultures with respect to detecting seizures, thereby paving the way towards animal-free seizure assessment.

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Camp, J. Gray, Farhath Badsha, Marta Florio, Sabina Kanton, Tobias Gerber, Michaela Wilsch-Bräuninger, Eric Lewitus, et al. "Human cerebral organoids recapitulate gene expression programs of fetal neocortex development." Proceedings of the National Academy of Sciences 112, no. 51 (December 7, 2015): 15672–77. http://dx.doi.org/10.1073/pnas.1520760112.

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Cerebral organoids—3D cultures of human cerebral tissue derived from pluripotent stem cells—have emerged as models of human cortical development. However, the extent to which in vitro organoid systems recapitulate neural progenitor cell proliferation and neuronal differentiation programs observed in vivo remains unclear. Here we use single-cell RNA sequencing (scRNA-seq) to dissect and compare cell composition and progenitor-to-neuron lineage relationships in human cerebral organoids and fetal neocortex. Covariation network analysis using the fetal neocortex data reveals known and previously unidentified interactions among genes central to neural progenitor proliferation and neuronal differentiation. In the organoid, we detect diverse progenitors and differentiated cell types of neuronal and mesenchymal lineages and identify cells that derived from regions resembling the fetal neocortex. We find that these organoid cortical cells use gene expression programs remarkably similar to those of the fetal tissue to organize into cerebral cortex-like regions. Our comparison of in vivo and in vitro cortical single-cell transcriptomes illuminates the genetic features underlying human cortical development that can be studied in organoid cultures.

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Zhang, Wei, Min-Jeong Yi, Xiaoping Chen, Francesca Cole, Robert S. Krauss, and Jong-Sun Kang. "Cortical Thinning and Hydrocephalus in Mice Lacking the Immunoglobulin Superfamily Member CDO." Molecular and Cellular Biology 26, no. 10 (May 15, 2006): 3764–72. http://dx.doi.org/10.1128/mcb.26.10.3764-3772.2006.

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ABSTRACT CDO is a cell surface immunoglobulin superfamily member that positively regulates myogenic differentiation in vitro and in vivo and signals to posttranslationally activate myogenic basic helix-loop-helix (bHLH) transcription factors. The Cdo gene is also expressed in the dorsal aspect and midline structures of the developing central nervous system, and mice lacking CDO on the C57BL/6 background display holoprosencephaly with ∼80% penetrance, resulting in perinatal lethality. We report here that a fraction of Cdo −/− mice from this background have additional defects in brain development, including hydrocephalus and cortical thinning. Primary neural progenitor cultures from E14.5 Cdo −/− mutants display reduced proliferation, which may underlie the thinning. The cortical preplate and cortices of mutant animals also show reduced staining for β-tubulin III, indicating defective neuronal differentiation. CDO levels are strongly increased in cultured C17.2 neuronal precursor cells stimulated to differentiate; modulation of CDO levels in these cells by overexpression or interfering RNA approaches enhances or diminishes differentiation, respectively. Cotransfection of CDO enhances the activity of the neurogenic bHLH factor, neurogenin1, in reporter assays and enhances heterodimerization of neurogenin1 and E47. These results indicate that CDO promotes neuronal differentiation and support the hypothesis that CDO coordinates differentiation of multiple cell lineages by regulating the activity of tissue-specific bHLH factors.

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Schmuck, Gabriele, Elke Roehrdanz, Richard K. Haynes, and Regine Kahl. "Neurotoxic Mode of Action of Artemisinin." Antimicrobial Agents and Chemotherapy 46, no. 3 (March 2002): 821–27. http://dx.doi.org/10.1128/aac.46.3.821-827.2002.

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ABSTRACT We recently described a screening system designed to detect neurotoxicity of artemisinin derivatives based on primary neuronal brain stem cell cultures (G. Schmuck and R. K. Haynes, Neurotoxicity Res. 2:37-49, 2000). Here, we probe possible mechanisms of this brain stem-specific neurodegeneration, in which artemisinin-sensitive neuronal brain stem cell cultures are compared with nonsensitive cultures (cortical neurons, astrocytes). Effects on the cytoskeleton of brain stem cell cultures, but not that of cortical cell cultures, were visible after 7 days. However, after a recovery period of 7 days, this effect also became visible in cortical cells and more severe in brain stem cell cultures. Neurodegeneration appears to be induced by effects on intracellular targets such as the cytoskeleton, modulation of the energy status by mitochondrial or metabolic defects, oxidative stress or excitotoxic events. Artemisinin reduces intracellular ATP levels and the potential of the inner mitochondrial membrane below the cytotoxic concentration range in all three cell cultures, with these effects being most dominant in the brain stem cultures. Surprisingly, there were substantial effects on cortical neurons after 7 days and on astrocytes after 1 day. Artemisinin additionally induces oxidative stress, as observed as an increase of reactive oxygen species and of lipid peroxidation in both neuronal cell types. Interestingly, an induction of expression of AOE was only seen in astrocytes. Here, manganese superoxide dismutase (MnSOD) expression was increased more than 3-fold and catalase expression was increased more than 1.5-fold. In brain stem neurons, MnSOD expression was dose dependently decreased. Copper-zinc superoxide dismutase and glutathione peroxidase, two other antioxidant enzymes that were investigated, did not show any changes in their mRNA expression in all three cell types after exposure to artemisinin.

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Fujimoto, Shinji, Hiroshi Katsuki, Masatoshi Ohnishi, Mikako Takagi, Toshiaki Kume, and Akinori Akaike. "Plasminogen Potentiates Thrombin Cytotoxicity and Contributes to Pathology of Intracerebral Hemorrhage in Rats." Journal of Cerebral Blood Flow & Metabolism 28, no. 3 (October 17, 2007): 506–15. http://dx.doi.org/10.1038/sj.jcbfm.9600547.

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Thrombin and plasmin are serine proteases involved in blood coagulation and fibrinolysis, whose precursors are circulating in blood stream. These blood-derived proteases might play important roles in the pathogenesis of intracerebral hemorrhage by acting on brain parenchymal cells. We previously reported that thrombin induced delayed neuronal injury through extracellular signal-regulated kinase (ERK)-dependent pathways. Here, we investigated potential cytotoxic actions of plasminogen, a precursor protein of plasmin, using slice cultures prepared from neonatal rat brain and intracortical microinjection model in adult rats. Although plasminogen alone did not evoke prominent neuronal injury, plasminogen caused significant neuronal injury when combined with a moderate concentration of thrombin (30 U/mL) in the cerebral cortex of slice cultures. The cortical injury was prevented by tranexamic acid and aprotinin. The combined neurotoxicity of thrombin and plasminogen was also prevented by PD98059, an inhibitor of ERK pathway, as well as by other agents that have been shown to prevent cortical injury induced by a higher concentration (100 U/mL) of thrombin alone. Extracellular signal-regulated kinase phosphorylation after plasminogen exposure was localized in cortical astrocytes. Moreover, microinjection of plasminogen in vivo potentiated thrombin-induced cortical injury, and inhibition of plasmin ameliorated hemorrhage-induced neuronal loss in the cerebral cortex. These results suggest that plasminogen/plasmin system augmenting thrombin neurotoxicity participates in hemorrhagic cortical injury.

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Saavedra, Lorena, Kathleen Wallace, Theresa F. Freudenrich, Moritz Mall, William R. Mundy, Jorge Davila, Timothy J. Shafer, Marius Wernig, and Daniel Haag. "Comparison of Acute Effects of Neurotoxic Compounds on Network Activity in Human and Rodent Neural Cultures." Toxicological Sciences 180, no. 2 (February 4, 2021): 295–312. http://dx.doi.org/10.1093/toxsci/kfab008.

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Abstract Assessment of neuroactive effects of chemicals in cell-based assays remains challenging as complex functional tissue is required for biologically relevant readouts. Recent in vitro models using rodent primary neural cultures grown on multielectrode arrays allow quantitative measurements of neural network activity suitable for neurotoxicity screening. However, robust systems for testing effects on network function in human neural models are still lacking. The increasing number of differentiation protocols for generating neurons from human-induced pluripotent stem cells (hiPSCs) holds great potential to overcome the unavailability of human primary tissue and expedite cell-based assays. Yet, the variability in neuronal activity, prolonged ontogeny and rather immature stage of most neuronal cells derived by standard differentiation techniques greatly limit their utility for screening neurotoxic effects on human neural networks. Here, we used excitatory and inhibitory neurons, separately generated by direct reprogramming from hiPSCs, together with primary human astrocytes to establish highly functional cultures with defined cell ratios. Such neuron/glia cocultures exhibited pronounced neuronal activity and robust formation of synchronized network activity on multielectrode arrays, albeit with noticeable delay compared with primary rat cortical cultures. We further investigated acute changes of network activity in human neuron/glia cocultures and rat primary cortical cultures in response to compounds with known adverse neuroactive effects, including gamma amino butyric acid receptor antagonists and multiple pesticides. Importantly, we observed largely corresponding concentration-dependent effects on multiple neural network activity metrics using both neural culture types. These results demonstrate the utility of directly converted neuronal cells from hiPSCs for functional neurotoxicity screening of environmental chemicals.

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Rose, K., C. W. Christine, and D. W. Choi. "Magnesium removal induces paroxysmal neuronal firing and NMDA receptor-mediated neuronal degeneration in cortical cultures." Neuroscience Letters 115, no. 2-3 (July 1990): 313–17. http://dx.doi.org/10.1016/0304-3940(90)90474-n.

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Santo, Stefano Di, Stefanie Seiler, Raphael Guzman, and Hans Rudolf Widmer. "Endothelial Progenitor Cell-Derived Factors Exert Neuroprotection in Cultured Cortical Neuronal Progenitor Cells." Cell Transplantation 29 (January 1, 2020): 096368972091268. http://dx.doi.org/10.1177/0963689720912689.

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There is substantial evidence that stem and progenitor cells secrete trophic factors that have potential for repairing injured tissues. We have previously reported that the conditioned medium (CM) obtained from endothelial progenitor cells (EPC) cultures protects striatal neurons against 3-nitropropionic acid-induced toxicity. In the present study we tested the hypothesis that EPC-CM may support cortical neuronal cell function and/or survival. EPC were isolated from the peripheral blood of healthy human donors and cultured in hypoxic conditions (1.5% O2) to stimulate the secretion of growth factors. The supernatant or conditioned medium (EPC-CM) was then collected and used for the various experiments. Primary cultures of cerebral cortex from fetal rat embryonic day 14 were treated with EPC-CM and challenged by glucose and serum deprivation. We observed that EPC-CM treatment significantly increased total cell number and cell viability in the cultures. Similarly, the number of lba1-expressing cells was significantly upregulated by EPC-CM, while western blot analyses for the astroglial marker glial fibrillary acidic protein did not show a marked difference. Importantly, the number of beta-lll-tubulin-positive neurons in the cultures was significantly augmented after EPC-CM treatment. Similarly, western blot analyses for beta-III-tubulin showed significant higher signal intensities. Furthermore, EPC-CM administration protected neurons against glucose- and serum deprivation-induced cell loss. In sum, our findings identified EPC-CM as a means to promote viability and/or differentiation of cortical neurons and suggest that EPC-CM might be useful for neurorestorative approaches.

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Wilson, Melinda E., Ying Liu, and Phyllis M. Wise. "Estradiol enhances Akt activation in cortical explant cultures following neuronal injury." Molecular Brain Research 102, no. 1-2 (June 2002): 48–54. http://dx.doi.org/10.1016/s0169-328x(02)00181-x.

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Gáspár, Tamás, Ferenc Domoki, Laura Lenti, Ádám Institoris, James A. Snipes, Ferenc Bari, and David W. Busija. "Neuroprotective effect of adenoviral catalase gene transfer in cortical neuronal cultures." Brain Research 1270 (May 2009): 1–9. http://dx.doi.org/10.1016/j.brainres.2009.03.006.

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McDonald, John W., Mark P. Goldberg, Byoung J. Gwag, Shu-Ing Chi, and Dennis W. Choi. "Cyclosporine induces neuronal apoptosis and selective oligodendrocyte death in cortical cultures." Annals of Neurology 40, no. 5 (November 1996): 750–58. http://dx.doi.org/10.1002/ana.410400511.

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Rojo-Bustamante, Estefania, Ignacio Íñigo-Marco, Miguel Angel Abellanas, Rodrigo Vinueza-Gavilanes, Ana Baltanás, Esther Luquin, Montserrat Arrasate, and Maria S. Aymerich. "CB2 Receptors and Neuron–Glia Interactions Modulate Neurotoxicity Generated by MAGL Inhibition." Biomolecules 10, no. 8 (August 18, 2020): 1198. http://dx.doi.org/10.3390/biom10081198.

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Monoacylglycerol lipase inhibition (MAGL) has emerged as an interesting therapeutic target for neurodegenerative disease treatment due to its ability to modulate the endocannabinoid system and to prevent the production of proinflammatory mediators. To obtain a beneficial response, it is necessary to understand how this inhibition affects the neuron–glia crosstalk and neuron viability. In this study, the effect of MAGL inhibition by KML29 was evaluated in two types of rat cortical primary cultures; mixed cultures, including neuron and glial cells, and neuron-enriched cultures. The risk of neuronal death was estimated by longitudinal survival analysis. The spontaneous neuronal risk of death in culture was higher in the absence of glial cells, a process that was enhanced by KML29 addition. In contrast, neuronal survival was not compromised by MAGL inhibition in the presence of glial cells. Blockade of cannabinoid type 2 (CB2) receptors expressed mainly by microglial cells did not affect the spontaneous neuronal death risk but decreased neuronal survival when KML29 was added. Modulation of cannabinoid type 1 (CB1) receptors did not affect neuronal survival. Our results show that neuron–glia interactions are essential for neuronal survival. CB2 receptors play a key role in these protective interactions when neurons are exposed to toxic conditions.

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Degos, Vincent, Tifenn Le charpentier, Vibol Chhor, Olivier Brissaud, Sophie Lebon, Leslie Schwendimann, Nathalie Bednareck, Sandrine Passemard, Jean Mantz, and Pierre Gressens. "Neuroprotective Effects of Dexmedetomidine against Glutamate Agonist-induced Neuronal Cell Death Are Related to Increased Astrocyte Brain-derived Neurotrophic Factor Expression." Anesthesiology 118, no. 5 (May 1, 2013): 1123–32. http://dx.doi.org/10.1097/aln.0b013e318286cf36.

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Abstract Background: Brain-derived neurotrophic factor (BDNF) plays a prominent role in neuroprotection against perinatal brain injury. Dexmedetomidine, a selective agonist of α2-adrenergic receptors, also provides neuroprotection against glutamate-induced damage. Because adrenergic receptor agonists can modulate BDNF expression, our goal was to examine whether dexmedetomidine’s neuroprotective effects are mediated by BDNF modulation in mouse perinatal brain injury. Methods: The protective effects against glutamate-induced injury of BDNF and dexmedetomidine alone or in combination with either a neutralizing BDNF antibody or an inhibitor of the extracellular signal-regulated kinase pathway (PD098059) were compared in perinatal ibotenate-induced cortical lesions (n = 10–20 pups/groups) and in mouse neuronal cultures (300 μm of ibotenate for 6 h). The effect of dexmedetomidine on BDNF expression was examined in vivo and in vitro with cortical neuronal and astrocyte isolated cultures. Results: Both BDNF and dexmedetomidine produced a significant neuroprotective effect in vivo and in vitro. Dexmedetomidine enhanced Bdnf4 and Bdnf5 transcription and BDNF protein cortical expression in vivo. Dexmedetomidine also enhanced Bdnf4 and Bdnf5 transcription and increased BDNF media concentration in isolated astrocyte cultures but not in neuronal cultures. Dexmedetomidine’s protective effect was inhibited with BDNF antibody (mean lesion size ± SD: 577 ± 148 μm vs. 1028 ± 213 μm, n = 14–20, P < 0.001) and PD098059 in vivo but not in isolated neuron cultures. Finally, PD098059 inhibited the increased release of BDNF induced by dexmedetomidine in astrocyte cultures. Conclusion: These results suggest that dexmedetomidine increased astrocyte expression of BDNF through an extracellular signal-regulated kinase-dependent pathway, inducing subsequent neuroprotective effects.

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Domoki, Ferenc, Béla Kis, Tamás Gáspár, James A. Snipes, John S. Parks, Ferenc Bari, and David W. Busija. "Rosuvastatin induces delayed preconditioning against oxygen-glucose deprivation in cultured cortical neurons." American Journal of Physiology-Cell Physiology 296, no. 1 (January 2009): C97—C105. http://dx.doi.org/10.1152/ajpcell.00366.2008.

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We tested whether rosuvastatin (RST) protected against oxygen-glucose deprivation (OGD)-induced cell death in primary rat cortical neuronal cultures. OGD reduced neuronal viability (%naive controls, mean ± SE, n = 24–96, P < 0.05) to 44 ± 1%, but 3-day pretreatment with RST (5 μM) increased survival to 82 ± 2% ( P < 0.05). One-day RST treatment was not protective. RST-induced neuroprotection was abolished by mevalonate or geranylgeranyl pyrophosphate (GGPP), but not by cholesterol coapplication. Furthermore, RST-induced decreases in neuronal cholesterol levels were abolished by mevalonate but not by GGPP. Reactive oxygen species (ROS) levels were reduced in RST-preconditioned neurons after OGD, and this effect was also reversed by both mevalonate and GGPP. These data suggested that GGPP, but not cholesterol depletion, were responsible for the induction of neuroprotection. Therefore, we tested whether 3-day treatments with perillic acid, a nonspecific inhibitor of both geranylgeranyl transferase (GGT) GGT 1 and Rab GGT, and the GGT 1-specific inhibitor GGTI-286 would reproduce the effects of RST. Perillic acid, but not GGTI-286, elicited robust neuronal preconditioning against OGD. RST, GGTI-286, and perillic acid all decreased mitochondrial membrane potential and lactate dehydrogenase activity in the cultured neurons, but only RST and perillic acid reduced neuronal ATP and membrane Rab3a protein levels. In conclusion, RST preconditions cultured neurons against OGD via depletion of GGPP, leading to decreased geranylgeranylation of proteins that are probably not isoprenylated by GGT 1. Reduced neuronal ATP levels and ROS production after OGD may be directly involved in the mechanism of neuroprotection.

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Estévez-Priego, Estefanía, Sara Teller, Clara Granell, Alex Arenas, and Jordi Soriano. "Functional strengthening through synaptic scaling upon connectivity disruption in neuronal cultures." Network Neuroscience 4, no. 4 (January 2020): 1160–80. http://dx.doi.org/10.1162/netn_a_00156.

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An elusive phenomenon in network neuroscience is the extent of neuronal activity remodeling upon damage. Here, we investigate the action of gradual synaptic blockade on the effective connectivity in cortical networks in vitro. We use two neuronal cultures configurations—one formed by about 130 neuronal aggregates and another one formed by about 600 individual neurons—and monitor their spontaneous activity upon progressive weakening of excitatory connectivity. We report that the effective connectivity in all cultures exhibits a first phase of transient strengthening followed by a second phase of steady deterioration. We quantify these phases by measuring GEFF, the global efficiency in processing network information. We term hyperefficiency the sudden strengthening of GEFF upon network deterioration, which increases by 20–50% depending on culture type. Relying on numerical simulations we reveal the role of synaptic scaling, an activity–dependent mechanism for synaptic plasticity, in counteracting the perturbative action, neatly reproducing the observed hyperefficiency. Our results demonstrate the importance of synaptic scaling as resilience mechanism.

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Sattler, Rita, Milton P. Charlton, Mathias Hafner, and Michael Tymianski. "Determination of the Time Course and Extent of Neurotoxicity at Defined Temperatures in Cultured Neurons Using a Modified Multiwell Plate Fluorescence Scanner." Journal of Cerebral Blood Flow & Metabolism 17, no. 4 (April 1997): 455–63. http://dx.doi.org/10.1097/00004647-199704000-00011.

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The cellular and molecular mechanisms of hypoxic/ischemic neurodegeneration are sensitive to numerous factors that modulate the time course and degree of neuronal death. Among such factors is hypothermia, which can dramatically protect neurons from injury. To examine and control for temperature-dependent effects, we developed a technique that provides for a high-throughput, accurate, and reproducible determination of the time course and degree of neurotoxicity in cultured cortical neurons at precisely defined temperatures. We used a fluorescence multiwell plate scanner, modified by us to permit the control of temperature, to perform serial quantitative measurements of propidium iodide (PI) fluorescence in cortical neuronal cultures exposed to excitotoxic insults. In validating this approach, we show that these time course measurements correlate highly with manual counts of PI-stained cells in the same cultures ( r = 0.958, p < 0.0001) and with lactate dehydrogenase release ( r = 0.964, p < 0.0001). This method represents an efficient approach to mechanistic and quantitative studies of cell death as well as a high-throughput technique for screening new neuroprotective therapies in vitro.

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Malaplate, Catherine, Aurelia Poerio, Marion Huguet, Claire Soligot, Elodie Passeri, Cyril J. F. Kahn, Michel Linder, Elmira Arab-Tehrany, and Frances T. Yen. "Neurotrophic Effect of Fish-Lecithin Based Nanoliposomes on Cortical Neurons." Marine Drugs 17, no. 7 (July 9, 2019): 406. http://dx.doi.org/10.3390/md17070406.

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Lipids play multiple roles in preserving neuronal function and synaptic plasticity, and polyunsaturated fatty acids (PUFAs) have been of particular interest in optimizing synaptic membrane organization and function. We developed a green-based methodology to prepare nanoliposomes (NL) from lecithin that was extracted from fish head by-products. These NL range between 100–120 nm in diameter, with an n-3/n-6 fatty acid ratio of 8.88. The high content of n-3 PUFA (46.3% of total fatty acid content) and docosahexanoic acid (26%) in these NL represented a means for enrichment of neuronal membranes that are potentially beneficial for neuronal growth and synaptogenesis. To test this, the primary cultures of rat embryo cortical neurons were incubated with NL on day 3 post-culture for 24 h, followed by immunoblots or immunofluorescence to evaluate the NL effects on synaptogenesis, axonal growth, and dendrite formation. The results revealed that NL-treated cells displayed a level of neurite outgrowth and arborization on day 4 that was similar to those of untreated cells on day 5 and 6, suggesting accelerated synapse formation and neuronal development in the presence of NL. We propose that fish-derived NL, by virtue of their n-3 PUFA profile and neurotrophic effects, represent a new innovative bioactive vector for developing preventive or curative treatments for neurodegenerative diseases.

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Coronas, Valérie, Patricia Arnault, and Michel Roger. "Cortical diffusible factors increase MAP-2 immunoreactive neuronal population in thalamic cultures." Neuroscience Research 43, no. 1 (May 2002): 57–67. http://dx.doi.org/10.1016/s0168-0102(02)00020-2.

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Nogueira, T. B., S. da Costa Araújo, F. Carvalho, F. C. Pereira, E. Fernandes, M. L. Bastos, V. M. Costa, and J. P. Capela. "Modeling chronic brain exposure to amphetamines using primary rat neuronal cortical cultures." Neuroscience 277 (September 2014): 417–34. http://dx.doi.org/10.1016/j.neuroscience.2014.07.009.

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Kang, Sang Hwan, Young Ae Lee, Seok Joon Won, Ki-Hyeong Rhee, and Byoung Joo Gwag. "Caffeine-induced neuronal death in neonatal rat brain and cortical cell cultures." NeuroReport 13, no. 15 (October 2002): 1945–50. http://dx.doi.org/10.1097/00001756-200210280-00023.

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Munns, Shane E., Bruno P. Meloni, Neville W. Knuckey, and Peter G. Arthur. "Primary cortical neuronal cultures reduce cellular energy utilization during anoxic energy deprivation." Journal of Neurochemistry 87, no. 3 (September 26, 2003): 764–72. http://dx.doi.org/10.1046/j.1471-4159.2003.02049.x.

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Strasser, Uta, Doug Lobner, M. Margarita Behrens, Lorella M. T. Canzoniero, and Dennis W. Choi. "Antagonists for group I mGluRs attenuate excitotoxic neuronal death in cortical cultures." European Journal of Neuroscience 10, no. 9 (September 1998): 2848–55. http://dx.doi.org/10.1111/j.1460-9568.1998.00291.x.

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Clifford, Meredith A., Jessleen K. Kanwal, Rhonda Dzakpasu, and Maria J. Donoghue. "EphA4 expression promotes network activity and spine maturation in cortical neuronal cultures." Neural Development 6, no. 1 (2011): 21. http://dx.doi.org/10.1186/1749-8104-6-21.

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Kamioka, Hirqyuki, Yasuhiko Jimbo, and Akio Kawana. "1131 Developmental changes of neuronal activity in long-term cortical slice cultures." Neuroscience Research 25 (January 1996): S121. http://dx.doi.org/10.1016/0168-0102(96)88894-8.

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Nakajima, Shingo, and Hiroshi Kunugi. "Lauric acid promotes neuronal maturation mediated by astrocytes in primary cortical cultures." Heliyon 6, no. 5 (May 2020): e03892. http://dx.doi.org/10.1016/j.heliyon.2020.e03892.

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Eglen, Richard M., and Terry Reisine. "Human iPS Cell-Derived Patient Tissues and 3D Cell Culture Part 2: Spheroids, Organoids, and Disease Modeling." SLAS TECHNOLOGY: Translating Life Sciences Innovation 24, no. 1 (January 22, 2019): 18–27. http://dx.doi.org/10.1177/2472630318803275.

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Human induced pluripotent stem cells (HiPSCs) provide several advantages for drug discovery, but principally they provide a source of clinically relevant tissue. Furthermore, the use of HiPSCs cultured in three-dimensional (3D) systems, as opposed to traditional two-dimensional (2D) culture approaches, better represents the complex tissue architecture in vivo. The use of HiPSCs in 3D spheroid and organoid culture is now growing, but particularly when using myocardial, intestinal enteric nervous system, and retinal cell lines. However, organoid cell culture is perhaps making the most notable impact in research and drug discovery, in which 3D neuronal cell cultures allow direct modeling of cortical cell layering and neuronal circuit activity. Given the specific degeneration seen in discrete neuronal circuitry in Alzheimer’s disease (AD) and Parkinson’s disease (PD), HiPSC culture systems are proving to be a major advance. In the present review, the second part of a two-part review, we discuss novel methods in which 3D cell culture systems (principally organoids) are now being used to provide insights into disease mechanisms. (The use of HiPSCs in target identification was reviewed in detail in Part 1.)

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Blanco-Suárez, Elena, Maria Fiuza, Xun Liu, Elavazhagan Chakkarapani, and Jonathan G. Hanley. "Differential Tiam1/Rac1 Activation in Hippocampal and Cortical Neurons Mediates Differential Spine Shrinkage in Response to Oxygen/Glucose Deprivation." Journal of Cerebral Blood Flow & Metabolism 34, no. 12 (September 24, 2014): 1898–906. http://dx.doi.org/10.1038/jcbfm.2014.158.

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Distinct neuronal populations show differential sensitivity to global ischemia, with hippocampal CA1 neurons showing greater vulnerability compared to cortical neurons. The mechanisms that underlie differential vulnerability are unclear, and we hypothesize that intrinsic differences in neuronal cell biology are involved. Dendritic spine morphology changes in response to ischemic insults in vivo, but cell type-specific differences and the molecular mechanisms leading to such morphologic changes are unexplored. To directly compare changes in spine size in response to oxygen/glucose deprivation (OGD) in cortical and hippocampal neurons, we used separate and equivalent cultures of each cell type. We show that cortical neurons exhibit significantly greater spine shrinkage compared to hippocampal neurons. Rac1 is a Rho-family GTPase that regulates the actin cytoskeleton and is involved in spine dynamics. We show that Rac1 and the Rac guanine nucleotide exchange factor (GEF) Tiam1 are differentially activated by OGD in hippocampal and cortical neurons. Hippocampal neurons express more Tiam1 than cortical neurons, and reducing Tiam1 expression in hippocampal neurons by shRNA enhances OGD-induced spine shrinkage. Tiam1 knockdown also reduces hippocampal neuronal vulnerability to OGD. This work defines fundamental differences in signalling pathways that regulate spine morphology in distinct neuronal populations that may have a role in the differential vulnerability to ischemia.

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Opitz, Thoralf, Ana D. De Lima, and Thomas Voigt. "Spontaneous Development of Synchronous Oscillatory Activity During Maturation of Cortical Networks In Vitro." Journal of Neurophysiology 88, no. 5 (November 1, 2002): 2196–206. http://dx.doi.org/10.1152/jn.00316.2002.

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Recent studies have focused attention on mechanisms of spontaneous large-scale wavelike activity during early development of the neocortex. In this study, we describe and characterize synchronous neuronal activity that occurs in cultured cortical networks naturally without pharmacological intervention. The synchronous activity that can be detected by means of Fluo-3 fluorescence imaging starts to develop at the beginning of the second week in culture and eventually includes the entire neuronal population about 1 wk later. A synchronous increase of [Ca2+]i in the neuronal population is associated with a burst of action potentials riding on a long-lasting depolarization recorded in a single cell. It is suggested that this depolarization results directly from synaptic current, which was comprised of at least three different components mediated by AMPA, N-methyl-d-aspartate (NMDA), and GABAA receptors. We never observed a gradually depolarizing pacemaker potential and found no evidence for a change of excitability during inter-burst periods. However, we found evidence for a period of synaptic depression after bursts. Network excitability recovers gradually over seconds from this depression that can explain the episodic nature of spontaneous network activity. Using pharmacological manipulation to investigate the propagation of activity in the network, we show that synchronous network activity depends on both glutamatergic and GABAAergic neurotransmission during a brief period. Reversal potential of GABAA receptor-mediated current was found to be significantly more positive than resting membrane potential both at 1 and 2 wk in culture, suggesting depolarizing action of GABA. However, in cultures older than 2 wk, inhibition of GABAAreceptors does not result in block of synchronous network activity but in modulation of burst width and frequency.

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John, Joseph G. Rudolph, J. Lemasters, and Fulton T. Crews. "Effects of Chronic Ethanol Exposure on Oxidation and NMDA-Stimulated Neuronal Death in Primary Cortical Neuronal Cultures." Alcoholism: Clinical and Experimental Research 22, no. 9 (December 1998): 2080–85. http://dx.doi.org/10.1111/j.1530-0277.1998.tb05919.x.

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Van’t Spijker, Heleen M., Dáire Rowlands, Jean Rossier, Barbara Haenzi, James W. Fawcett, and Jessica C. F. Kwok. "Neuronal Pentraxin 2 Binds PNNs and Enhances PNN Formation." Neural Plasticity 2019 (October 20, 2019): 1–13. http://dx.doi.org/10.1155/2019/6804575.

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The perineuronal net (PNN) is a mesh-like proteoglycan structure on the neuronal surface which is involved in regulating plasticity. The PNN regulates plasticity via multiple pathways, one of which is direct regulation of synapses through the control of AMPA receptor mobility. Since neuronal pentraxin 2 (Nptx2) is a known regulator of AMPA receptor mobility and Nptx2 can be removed from the neuronal surface by PNN removal, we investigated whether Nptx2 has a function in the PNN. We found that Nptx2 binds to the glycosaminoglycans hyaluronan and chondroitin sulphate E in the PNN. Furthermore, in primary cortical neuron cultures, the addition of NPTX2 to the culture medium enhances PNN formation during PNN development. These findings suggest Nptx2 as a novel PNN binding protein with a role in the mechanism of PNN formation.

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Petermann, Thomas, Tara C. Thiagarajan, Mikhail A. Lebedev, Miguel A. L. Nicolelis, Dante R. Chialvo, and Dietmar Plenz. "Spontaneous cortical activity in awake monkeys composed of neuronal avalanches." Proceedings of the National Academy of Sciences 106, no. 37 (August 26, 2009): 15921–26. http://dx.doi.org/10.1073/pnas.0904089106.

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Spontaneous neuronal activity is an important property of the cerebral cortex but its spatiotemporal organization and dynamical framework remain poorly understood. Studies in reduced systems—tissue cultures, acute slices, and anesthetized rats—show that spontaneous activity forms characteristic clusters in space and time, called neuronal avalanches. Modeling studies suggest that networks with this property are poised at a critical state that optimizes input processing, information storage, and transfer, but the relevance of avalanches for fully functional cerebral systems has been controversial. Here we show that ongoing cortical synchronization in awake rhesus monkeys carries the signature of neuronal avalanches. Negative LFP deflections (nLFPs) correlate with neuronal spiking and increase in amplitude with increases in local population spike rate and synchrony. These nLFPs form neuronal avalanches that are scale-invariant in space and time and with respect to the threshold of nLFP detection. This dimension, threshold invariance, describes a fractal organization: smaller nLFPs are embedded in clusters of larger ones without destroying the spatial and temporal scale-invariance of the dynamics. These findings suggest an organization of ongoing cortical synchronization that is scale-invariant in its three fundamental dimensions—time, space, and local neuronal group size. Such scale-invariance has ontogenetic and phylogenetic implications because it allows large increases in network capacity without a fundamental reorganization of the system.

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Davis, D. R., J. P. Brion, A. M. Couck, J. M. Gallo, D. P. Hanger, K. Ladhani, C. Lewis, et al. "The phosphorylation state of the microtubule-associated protein tau as affected by glutamate, colchicine and β-amyloid in primary rat cortical neuronal cultures." Biochemical Journal 309, no. 3 (August 1, 1995): 941–49. http://dx.doi.org/10.1042/bj3090941.

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The effects of the excitatory amino acid glutamate, the microtubule destabilizing agent colchicine, and beta 25-35-amyloid peptide on the phosphorylation state of tau were studied in rat cortical neurons in primary culture. Using immunocytochemistry and Western-blot analysis, we demonstrated that a proportion of tau in these cultures is normally highly phosphorylated, but most of this tau fraction is dephosphorylated after treatment of the cultures with glutamate or colchicine, but not with beta-amyloid; the glutamate- and colchicine-induced changes in tau phosphorylation commenced before cell death, as assessed by release of lactate dehydrogenase. Dephosphorylation of tau was readily revealed by using the monoclonal antibodies Tau.1 and AT8, which have phosphate-sensitive epitopes that both centre around serine-199 and -202 (numbering of the largest tau isoform). On Western blots and by immunocytochemistry, AT8 labelling strongly decreased after glutamate and colchicine treatments, whereas Tau.1 staining was more intense. Neurofilament monoclonal antibodies, including RT97, 8D8, SMI31 and SMI310, all additionally known to recognize tau in a phosphorylation-dependent manner, also demonstrated that glutamate and colchicine treatments of the cultures induced a dephosphorylation of tau. We also showed immunocytochemically that there is an increase in tau immunoreactivity in neuronal perikarya in response to glutamate and colchicine treatment, and this occurs concomitantly with the dephosphorylation of tau. Treatment of the primary rat cortical neuronal cultures with beta 25-35-amyloid peptide, under conditions which induce neuronal degeneration, did not induce a change in tau phosphorylation, and failed to act synergistically with glutamate to produce an increase in dephosphorylation of tau over that produced by glutamate treatment alone. These findings demonstrate that glutamate and colchicine induce tau dephosphorylation, as opposed to increased tau phosphorylation, which would be more indicative of Alzheimer-type neurodegeneration.

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Rogove, A. D., C. Siao, B. Keyt, S. Strickland, and S. E. Tsirka. "Activation of microglia reveals a non-proteolytic cytokine function for tissue plasminogen activator in the central nervous system." Journal of Cell Science 112, no. 22 (November 15, 1999): 4007–16. http://dx.doi.org/10.1242/jcs.112.22.4007.

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Tissue plasminogen activator mediates excitotoxin-induced neurodegeneration and microglial activation in the mouse hippocampus. Here we show that tissue plasminogen activator (tPA) acts in a protease-independent manner to modulate the activation of microglia, the cells of the central nervous system with macrophage properties. Cultured microglia from tPA-deficient mice can phagocytose as efficiently as wild-type microglia. However, tPA-deficient microglia in mixed cortical cultures exhibit attenuated activation in response to lipopolysaccharide, as judged by morphological changes, increased expression of the activation marker F4/80 and the release of the pro-inflammatory cytokine tumor necrosis factor-(α). When tPA is added to tPA deficient cortical cultures prior to endotoxin stimulation, microglial activation is restored to levels comparable to that observed in wild-type cells. Proteolytically-inactive tPA can also restore activation of tPA-deficient microglia in culture and in vivo. However, this inactive enzyme does not restore susceptibility of tPA-deficient hippocampal neurons to excitotoxin-mediated cell death. These results dissociate two different functions of tPA: inactive enzyme can mediate microglial activation, whereas proteolytically-competent protein also promotes neuronal degeneration. Thus tPA is identified as a new cytokine in the central nervous system.

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Chay, Kee-Oh, Kyoung Young Nam Koong, Shinae Hwang, Jong-Keun Kim, and Choon Sang Bae. "NADPH Oxidase Mediates β-Amyloid Peptide-Induced Neuronal Death in Mouse Cortical Cultures." Chonnam Medical Journal 53, no. 3 (2017): 196. http://dx.doi.org/10.4068/cmj.2017.53.3.196.

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Journal articles on the topic 'Cortical neuronal cultures'

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