Abstract
Originalsprog | Engelsk |
---|---|
Tidsskrift | European Journal of Neuroscience |
Vol/bind | 32 |
Udgave nummer | 8 |
Sider (fra-til) | 1364-79 |
Antal sider | 15 |
ISSN | 0953-816X |
DOI | |
Status | Udgivet - 2010 |
Bibliografisk note
© 2010 The Authors. European Journal of Neuroscience © 2010 Federation of European Neuroscience Societies and Blackwell Publishing Ltd.Adgang til dokumentet
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Gene expression analysis of the emergence of epileptiform activity after focal injection of kainic acid into mouse hippocampus. / Motti, Dario; Le Duigou, Caroline; Eugène, Emmanuel; Chemaly, Nicole; Wittner, Lucia; Lazarevic, Dejan; Krmac, Helena; Marstrand, Troels; Valen, Eivind; Sanges, Remo; Stupka, Elia; Sandelin, Albin; Cherubini, Enrico; Gustincich, Stefano; Miles, Richard.
I: European Journal of Neuroscience, Bind 32, Nr. 8, 2010, s. 1364-79.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Gene expression analysis of the emergence of epileptiform activity after focal injection of kainic acid into mouse hippocampus
AU - Motti, Dario
AU - Le Duigou, Caroline
AU - Eugène, Emmanuel
AU - Chemaly, Nicole
AU - Wittner, Lucia
AU - Lazarevic, Dejan
AU - Krmac, Helena
AU - Marstrand, Troels
AU - Valen, Eivind
AU - Sanges, Remo
AU - Stupka, Elia
AU - Sandelin, Albin
AU - Cherubini, Enrico
AU - Gustincich, Stefano
AU - Miles, Richard
N1 - © 2010 The Authors. European Journal of Neuroscience © 2010 Federation of European Neuroscience Societies and Blackwell Publishing Ltd.
PY - 2010
Y1 - 2010
N2 - We report gene profiling data on genomic processes underlying the progression towards recurrent seizures after injection of kainic acid (KA) into the mouse hippocampus. Focal injection enabled us to separate the effects of proepileptic stimuli initiated by KA injection. Both the injected and contralateral hippocampus participated in the status epilepticus. However, neuronal death induced by KA treatment was restricted to the injected hippocampus, although there was some contralateral axonal degeneration. We profiled gene expression changes in dorsal and ventral regions of both the injected and contralateral hippocampus. Changes were detected in the expression of 1526 transcripts in samples from three time-points: (i) during the KA-induced status epilepticus, (ii) at 2 weeks, before recurrent seizures emerged, and (iii) at 6 months after seizures emerged. Grouping genes with similar spatio-temporal changes revealed an early transcriptional response, strong immune, cell death and growth responses at 2 weeks and an activation of immune and extracellular matrix genes persisting at 6 months. Immunostaining for proteins coded by genes identified from array studies provided evidence for gliogenesis and suggested that the proteoglycan biglycan is synthesized by astrocytes and contributes to a glial scar. Gene changes at 6 months after KA injection were largely restricted to tissue from the injection site. This suggests that either recurrent seizures might depend on maintained processes including immune responses and changes in extracellular matrix proteins near the injection site or alternatively might result from processes, such as growth, distant from the injection site and terminated while seizures are maintained.
AB - We report gene profiling data on genomic processes underlying the progression towards recurrent seizures after injection of kainic acid (KA) into the mouse hippocampus. Focal injection enabled us to separate the effects of proepileptic stimuli initiated by KA injection. Both the injected and contralateral hippocampus participated in the status epilepticus. However, neuronal death induced by KA treatment was restricted to the injected hippocampus, although there was some contralateral axonal degeneration. We profiled gene expression changes in dorsal and ventral regions of both the injected and contralateral hippocampus. Changes were detected in the expression of 1526 transcripts in samples from three time-points: (i) during the KA-induced status epilepticus, (ii) at 2 weeks, before recurrent seizures emerged, and (iii) at 6 months after seizures emerged. Grouping genes with similar spatio-temporal changes revealed an early transcriptional response, strong immune, cell death and growth responses at 2 weeks and an activation of immune and extracellular matrix genes persisting at 6 months. Immunostaining for proteins coded by genes identified from array studies provided evidence for gliogenesis and suggested that the proteoglycan biglycan is synthesized by astrocytes and contributes to a glial scar. Gene changes at 6 months after KA injection were largely restricted to tissue from the injection site. This suggests that either recurrent seizures might depend on maintained processes including immune responses and changes in extracellular matrix proteins near the injection site or alternatively might result from processes, such as growth, distant from the injection site and terminated while seizures are maintained.
U2 - 10.1111/j.1460-9568.2010.07403.x
DO - 10.1111/j.1460-9568.2010.07403.x
M3 - Journal article
C2 - 20950280
VL - 32
SP - 1364
EP - 1379
JO - European Journal of Neuroscience
JF - European Journal of Neuroscience
SN - 0953-816X
IS - 8
ER -