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Brain Res Bull. 2014 May;104:7-18. doi: 10.1016/j.brainresbull.2014.03.003. Epub 2014 Apr 1.

Lipopolysaccharide induced increase in seizure activity in two animal models of absence epilepsy WAG/Rij and GAERS rats and Long Evans rats.

Author information

1
Department of Zoology, University of West Hungary Savaria Campus, Károlyi Gáspár tér 4, 9700 Szombathely, Hungary. Electronic address: zskovacs@ttk.nyme.hu.
2
Laboratory of Molecular and Systems Neurobiology, Institute of Biology, Hungarian Academy of Sciences and Eötvös Loránd University, Pázmány Péter sétány 1C, 1117 Budapest, Hungary; Laboratory of Neuromorphology, Department of Anatomy, Histology and Embryology, Semmelweis University, Tűzoltó u. 58, 1094 Budapest, Hungary. Electronic address: dobolyi@med.semmelweis-univ.hu.
3
Laboratory of Proteomics, Eötvös Loránd University, Pázmány Péter sétány 1C, 1117 Budapest, Hungary. Electronic address: gjuhasz@dec001.geobio.elte.hu.
4
Laboratory of Proteomics, Eötvös Loránd University, Pázmány Péter sétány 1C, 1117 Budapest, Hungary; Department of Physiology and Neurobiology, Eötvös Loránd University, Pázmány Péter sétány 1C, 1117 Budapest, Hungary. Electronic address: kakekesi@dec001.geobio.elte.hu.

Abstract

We showed previously that the number and time of spike-wave discharges (SWDs) were increased after intraperitoneal (i.p.) injection of lipopolysaccharide (LPS), an effect, which was completely abolished by cyclooxygenase-2 (COX-2) inhibitor indomethacin (IND) pretreatment in Wistar Albino Glaxo/Rijswijk (WAG/Rij) rats. These and other results suggest that injection of LPS to genetically absence epileptic animals, such as WAG/Rij rats, may allow us to investigate relationships between absence epilepsy and LPS evoked neuroinflammation processes. However, LPS may evoke different effects on absence epileptic activity in various animal strains. Thus, to extend our previous results, we injected two doses of LPS (50 μg/kg and 350 μg/kg i.p.) alone and in combination with IND (10mg/kg IND i.p. +50 μg/kg LPS) into rats of two model animal strains (WAG/Rij rats; GAERS rats: Genetic Absence Epileptic Rats from Strasbourg) and into Long Evans rats. The effects of treatments on SWD number and SWD duration were examined. Both doses of LPS increased the SWD number and the total time of SWDs dose-dependently during the whole 4-h recording period, which was abolished by IND pretreatment in all three investigated strains. These results extend our previous results suggesting that our methods using LPS injection into freely moving absence epileptic rats is applicable not only in well-established animal models of absence epilepsy such as WAG/Rij rats and GAERS rats but also in Long Evans rats to investigate links between inflammation and absence epilepsy.

KEYWORDS:

Absence epileptic rats; Indomethacin; Lipopolysaccharide; Spike–wave discharges

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