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  A genetic switch for epilepsy in adult mice

Krestel, H. E., Shimshek, D. R., Jensen, V., Nevian, T., Kim, J.-H., Geng, Y., et al. (2004). A genetic switch for epilepsy in adult mice. The Journal of Neuroscience, 24(46), 10568-10578. doi:10.1523/JNEUROSCI.4579-03.2004.

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Datensatz-Permalink: https://hdl.handle.net/11858/00-001M-0000-002A-2C1F-A Versions-Permalink: https://hdl.handle.net/11858/00-001M-0000-002A-2C20-4
Genre: Zeitschriftenartikel
Alternativer Titel : A genetic switch for epilepsy in adult mice

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 Urheber:
Krestel, Heinz Eric1, Autor           
Shimshek, Derya R.1, Autor           
Jensen, Vidar, Autor
Nevian, Thomas2, Autor           
Kim, Jin-Hyun, Autor
Geng, Yu, Autor
Bast, Thomas, Autor
Depaulis, Antoine, Autor
Schonig, Kai, Autor
Schwenk, Frieder, Autor
Bujard, Hermann, Autor
Hvalby, Øivind, Autor
Sprengel, Rolf1, Autor           
Seeburg, Peter H.1, Autor           
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              
2Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497701              

Inhalt

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Schlagwörter: Hippocampus, temporal Cre regulation, altered AMPA receptors, RNA editing, spinous calcium transients
 Zusammenfassung: Premature death from seizures afflicts gene-targeted mice expressing the Q/R site-unedited glutamate receptor subunit GluR-B(Q) of AMPA receptors in central neurons. Early seizure-related death has now been circumvented by a genetic switch that restricts GluR-B(Q) expression to forebrain principal neurons from postnatal stages onward, prominently in hippocampus and striatum and less so in cortex and amygdala. When switched on, functional receptor incorporation of GluR-B(Q) could be demonstrated by imaging evoked AMPA channel-mediated spinous Ca2+ transients in CA1 pyramidal cells. Sustained GluR-B(Q) expression in adult mice led to smaller excitatory postsynaptic responses in the CA1 region with unchanged presynaptic fiber excitability. Notably, despite the smaller excitatory response, the CA1 cells exhibited a reduced population spike threshold, which might underlie the spontaneous manifestations of epilepsy, including myocloni and generalized seizures with limbic components, observed by synchronous video monitoring and electroencephalographic recordings. No neuropathological symptoms developed when GluR-B(Q) expression was restricted to only hippocampal neurons. Our results show that seizure susceptibility is triggered by GluR-B(Q) expression also in the adult brain and that circuit hyperexcitability is not an immediate consequence of GluR-B(Q) but requires yet unknown downstream events, likely to be induced by non-Hebbian plasticity from Ca2+-permeable AMPA channels in principal neurons.

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Sprache(n): eng - English
 Datum: 2004-08-272003-06-112004-09-302004-11-17
 Publikationsstatus: Erschienen
 Seiten: 10
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: eDoc: 665868
DOI: 10.1523/JNEUROSCI.4579-03.2004
URI: http://www.ncbi.nlm.nih.gov/pubmed/15548671
URI: http://www.jneurosci.org/content/24/46/10568
URI: http://www.jneurosci.org/content/24/46/10568.full
Anderer: 6005
 Art des Abschluß: -

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Titel: The Journal of Neuroscience
  Andere : J. Neurosci.
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: Baltimore, MD : The Society
Seiten: - Band / Heft: 24 (46) Artikelnummer: - Start- / Endseite: 10568 - 10578 Identifikator: ISSN: 0270-6474
CoNE: https://pure.mpg.de/cone/journals/resource/954925502187