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Epilepsy-Induced Motility of Differentiated Neurons

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Epilepsy-Induced Motility of Differentiated Neurons. / Chai, Xuejun; Münzner, Gert; Zhao, Shanting; Tinnes, Stefanie; Kowalski, Janina; Häussler, Ute; Young, Christina; Haas, Carola A; Frotscher, Michael.

in: CEREB CORTEX, Jahrgang 24, Nr. 8, 2014, S. 2130-2140.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Chai, X, Münzner, G, Zhao, S, Tinnes, S, Kowalski, J, Häussler, U, Young, C, Haas, CA & Frotscher, M 2014, 'Epilepsy-Induced Motility of Differentiated Neurons', CEREB CORTEX, Jg. 24, Nr. 8, S. 2130-2140. https://doi.org/10.1093/cercor/bht067

APA

Chai, X., Münzner, G., Zhao, S., Tinnes, S., Kowalski, J., Häussler, U., Young, C., Haas, C. A., & Frotscher, M. (2014). Epilepsy-Induced Motility of Differentiated Neurons. CEREB CORTEX, 24(8), 2130-2140. https://doi.org/10.1093/cercor/bht067

Vancouver

Chai X, Münzner G, Zhao S, Tinnes S, Kowalski J, Häussler U et al. Epilepsy-Induced Motility of Differentiated Neurons. CEREB CORTEX. 2014;24(8):2130-2140. https://doi.org/10.1093/cercor/bht067

Bibtex

@article{5feb0261fe4443a78a5dd72e7790e59c,
title = "Epilepsy-Induced Motility of Differentiated Neurons",
abstract = "Neuronal ectopia, such as granule cell dispersion (GCD) in temporal lobe epilepsy (TLE), has been assumed to result from a migration defect during development. Indeed, recent studies reported that aberrant migration of neonatal-generated dentate granule cells (GCs) increased the risk to develop epilepsy later in life. On the contrary, in the present study, we show that fully differentiated GCs become motile following the induction of epileptiform activity, resulting in GCD. Hippocampal slice cultures from transgenic mice expressing green fluorescent protein in differentiated, but not in newly generated GCs, were incubated with the glutamate receptor agonist kainate (KA), which induced GC burst activity and GCD. Using real-time microscopy, we observed that KA-exposed, differentiated GCs translocated their cell bodies and changed their dendritic organization. As found in human TLE, KA application was associated with decreased expression of the extracellular matrix protein Reelin, particularly in hilar interneurons. Together these findings suggest that KA-induced motility of differentiated GCs contributes to the development of GCD and establish slice cultures as a model to study neuronal changes induced by epileptiform activity.",
author = "Xuejun Chai and Gert M{\"u}nzner and Shanting Zhao and Stefanie Tinnes and Janina Kowalski and Ute H{\"a}ussler and Christina Young and Haas, {Carola A} and Michael Frotscher",
year = "2014",
doi = "10.1093/cercor/bht067",
language = "English",
volume = "24",
pages = "2130--2140",
journal = "CEREB CORTEX",
issn = "1047-3211",
publisher = "Oxford University Press",
number = "8",

}

RIS

TY - JOUR

T1 - Epilepsy-Induced Motility of Differentiated Neurons

AU - Chai, Xuejun

AU - Münzner, Gert

AU - Zhao, Shanting

AU - Tinnes, Stefanie

AU - Kowalski, Janina

AU - Häussler, Ute

AU - Young, Christina

AU - Haas, Carola A

AU - Frotscher, Michael

PY - 2014

Y1 - 2014

N2 - Neuronal ectopia, such as granule cell dispersion (GCD) in temporal lobe epilepsy (TLE), has been assumed to result from a migration defect during development. Indeed, recent studies reported that aberrant migration of neonatal-generated dentate granule cells (GCs) increased the risk to develop epilepsy later in life. On the contrary, in the present study, we show that fully differentiated GCs become motile following the induction of epileptiform activity, resulting in GCD. Hippocampal slice cultures from transgenic mice expressing green fluorescent protein in differentiated, but not in newly generated GCs, were incubated with the glutamate receptor agonist kainate (KA), which induced GC burst activity and GCD. Using real-time microscopy, we observed that KA-exposed, differentiated GCs translocated their cell bodies and changed their dendritic organization. As found in human TLE, KA application was associated with decreased expression of the extracellular matrix protein Reelin, particularly in hilar interneurons. Together these findings suggest that KA-induced motility of differentiated GCs contributes to the development of GCD and establish slice cultures as a model to study neuronal changes induced by epileptiform activity.

AB - Neuronal ectopia, such as granule cell dispersion (GCD) in temporal lobe epilepsy (TLE), has been assumed to result from a migration defect during development. Indeed, recent studies reported that aberrant migration of neonatal-generated dentate granule cells (GCs) increased the risk to develop epilepsy later in life. On the contrary, in the present study, we show that fully differentiated GCs become motile following the induction of epileptiform activity, resulting in GCD. Hippocampal slice cultures from transgenic mice expressing green fluorescent protein in differentiated, but not in newly generated GCs, were incubated with the glutamate receptor agonist kainate (KA), which induced GC burst activity and GCD. Using real-time microscopy, we observed that KA-exposed, differentiated GCs translocated their cell bodies and changed their dendritic organization. As found in human TLE, KA application was associated with decreased expression of the extracellular matrix protein Reelin, particularly in hilar interneurons. Together these findings suggest that KA-induced motility of differentiated GCs contributes to the development of GCD and establish slice cultures as a model to study neuronal changes induced by epileptiform activity.

U2 - 10.1093/cercor/bht067

DO - 10.1093/cercor/bht067

M3 - SCORING: Journal article

C2 - 23505288

VL - 24

SP - 2130

EP - 2140

JO - CEREB CORTEX

JF - CEREB CORTEX

SN - 1047-3211

IS - 8

ER -