Intracerebroventricularly administered lipopolysaccharide enhances spike-wave discharges in freely moving WAG/Rij rats |
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Authors: | Kovács Zsolt Czurkó András Kékesi Katalin A Juhász Gábor |
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Institution: | a Department of Zoology, University of West Hungary, Savaria Campus, Szombathely, Károlyi Gáspár tér 4, 9700, Hungary b Laboratory of Proteomics, Eötvös Loránd University, Budapest, Pázmány Péter sétány 1C, 1117, Hungary c Institute of Medical Chemistry, University of Szeged, Szeged, Dóm tér 8, 6720, Hungary d Department of Physiology and Neurobiology, Eötvös Loránd University, Budapest, Pázmány Péter sétány 1C, 1117, Hungary |
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Abstract: | Peripheral lipopolysaccharide (LPS) injection enhances spike-wave discharges (SWDs) in the genetic rat model of absence epilepsy (Wistar Albino Glaxo/Rijswijk rats: WAG/Rij rats) parallel with the peripheral proinflammatory cytokine responses. The effect of centrally administered LPS on the absence-like epileptic activity is not known, however despite the important differences in inflammatory mechanisms. To examine the effect of centrally administered LPS on the pathological synchronization we intracerebroventricularly (i.c.v.) injected LPS into WAG/Rij rats and measured the number and duration of SWDs. I.c.v. injected LPS increased the number and duration of SWDs for 3 h, thereafter, a decrease in epileptic activity was observed. To further investigate the nature of this effect, a non-steroid anti-inflammatory drug (indomethacin; IND) or a competitive N-methyl-d-aspartate (NMDA) receptor antagonist (2-amino-5-phosphonopentanoic acid; AP5) was injected intraperitoneally (i.p.), preceding the i.c.v. LPS treatment. IND abolished the i.c.v. LPS induced changes in SWDs, while AP5 extended it for 5 h. As control treatments, both IND and AP5 application by themselves decreased the number of SWDs for 2 and 3 h, respectively. Our results show that centrally injected LPS, likewise the peripheral injection, can increase the number and duration of SWDs in the WAG/Rij rat, and the effect invoke inflammatory cytokines as well as excitatory neurotransmitters. |
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Keywords: | ACSF artificial cerebrospinal fluid AP5 2-amino-5-phosphonopentanoic acid COX-2 cyclooxygenase-2 i c v intracerebroventricular IL-1β interleukin-1β IL-1R interleukin-1 receptor IL-1ra endogenous antagonist of interleukin-1 receptor IL-6 interleukin-6 IL-10R interleukin-10 receptor IND indomethacin i p intraperitoneal LPS lipopolysaccharide NMDA receptor d-aspartate receptor" target="_blank">N-methyl-d-aspartate receptor NSAIDs non-steroid anti-inflammatory drugs PGE2 prostaglandin E2 PTC day post-treatment control day REM sleep rapid eye movement sleep SWD spike-wave discharge SWS slow-wave sleep TLR4 Toll-like receptor 4 TNF-α tumor necrosis factor-α WAG/Rij Wistar Albino Glaxo/Rijswijk |
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