TY  - JOUR
AU  - Györffy, Balázs
AU  - Kovács, Zsolt
AU  - Gulyássy, Péter
AU  - Attila, Simor
AU  - Völgyi, Katalin
AU  - Orbán, Gergely
AU  - Péter, Baracskay
AU  - Szabó, Zoltán
AU  - Janáky, Tamás
AU  - Dobolyi, Árpád
AU  - Juhász, Gábor Dénes
AU  - Czurkó, András
AU  - Kékesi, Adrienna Katalin
TI  - Brain protein expression changes in WAG/Rij rats, a genetic rat model of absence epilepsy after peripheral lipopolysaccharide treatment
JF  - BRAIN BEHAVIOR AND IMMUNITY
J2  - BRAIN BEHAV IMMUN
VL  - 35
PY  - 2014
SP  - 86
EP  - 95
PG  - 10
SN  - 0889-1591
DO  - 10.1016/j.bbi.2013.09.001
UR  - https://m2.mtmt.hu/api/publication/2390640
ID  - 2390640
N1  - Laboratory of Proteomics, Institute of Biology, Eötvös Loránd University, Pázmány P. stny. 1/c, Budapest H-1117, Hungary            
            Department of Zoology, The University of West Hungary, Savaria Campus, Karolyi Gaspar ter 4, Szombathely H-9700, Hungary            
            Institute of Medical Chemistry, University of Szeged, Dóm tér 8, Szeged H-6720, Hungary            
            Semmelweis University and the Hungarian Academy of Sciences, Department of Anatomy, Histology and Embryology, Neuromorphological and Neuroendocrine Research Laboratory, Tuzoltó utca 58, Budapest H-1094, Hungary            
            Department of Physiology and Neurobiology, Eötvös Loránd University, Pázmány P. stny. 1/c, Budapest H-1117, Hungary            
            Cited By :20            
            Export Date: 16 November 2023            
            CODEN: BBIME            
            Correspondence Address: Kékesi, K.A.; Laboratory of Proteomics, Pázmány P. stny. 1/c, Budapest H-1117, Hungary; email: kakekesi@dec001.geobio.elte.hu
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Kovács, Zsolt
AU  - Kékesi, Adrienna Katalin
AU  - Szilágyi, Nóra
AU  - Ábrahám, István
AU  - Székács, D
AU  - Király, N
AU  - Papp, E
AU  - Császár, I
AU  - Szegő, Éva Mónika
AU  - Barabás, Klaudia
AU  - Péterfy, H
AU  - Erdei, Anna
AU  - Bártfai, T
AU  - Juhász, Gábor Dénes
TI  - Facilitation of spike-wave discharge activity by lipopolysaccharides in Wistar Albino Glaxo/Rijswijk rats
JF  - NEUROSCIENCE
J2  - NEUROSCIENCE
VL  - 140
PY  - 2006
IS  - 2
SP  - 731
EP  - 742
PG  - 12
SN  - 0306-4522
DO  - 10.1016/j.neuroscience.2006.02.023
UR  - https://m2.mtmt.hu/api/publication/1223704
ID  - 1223704
N1  - Export Date: 27 January 2024; CODEN: NRSCD
AB  - In normal rats the proinflammatory cytokines like interleukin-1?, interleukin-6, which are induced by bacterial lipopolysaccharides, are able to control thalamo-cortical excitability by exerting strong effects on physiological synchronization such as sleep and on pathological synchronization like that in epileptic discharges. To investigate whether proinflammatory cytokines or lipopolysaccharides could modulate absence seizures resulting from a very different generator mechanism than the already investigated bicuculline-, kindling- and kainate-induced seizures, we used a genetically epileptic Wistar Albino Glaxo/Rijswijk rat strain, which is spontaneously generating high voltage spike-wave discharges. Wistar Albino Glaxo/Rijswijk rats responded with an increase of the number of spike-wave discharges to lipopolysaccharide injection (from 10 ?g/kg to 350 ?g/kg). Repetitive administration of 350 ?g/kg lipopolysaccharides daily for 5 days increased the number of spike-wave discharges on the first, second and third days but the number of spike-wave discharges returned to the control value on day 5, at the 5th injection of lipopolysaccharides, showing a tolerance to lipopolysaccharides. The lipopolysaccharide-induced increase in spike-wave discharges was not directly correlated with the elevation of the core body temperature, as it is in febrile seizures, although lipopolysaccharide induced prostaglandin and is clearly pyrogenic at the doses used. Indomethacin, the prostaglandin synthesis inhibitor, efficiently blocked lipopolysaccharide-induced enhancement of spike-wave discharge genesis suggesting that the spike-wave discharge facilitating effect of lipopolysaccharides involves induction of cyclooxygenase 2 and subsequent synthesis and actions of prostaglandin E2. Low dose (40 mg/kg, i.p.) of competitive N-methyl-d-aspartate receptor antagonist 2-amino-5-phosphonopentanoic acid, and low dose of lipopolysaccharide (20 ?g/kg) showed a synergistic interaction to increase the number of spike-wave discharges, whereas at supramaximal doses of lipopolysaccharide and the N-methyl-d-aspartate antagonist no synergy was present. The data reveal a functional connection between absence epileptic activity and lipopolysaccharide induction of prostaglandin synthesis and prostaglandin action and suggest some common cellular targets in epilepsy and lipopolysaccharide-induced inflammation. Š 2006 IBRO.
LA  - English
DB  - MTMT
ER  -