Cortical and limbic excitability in rats with absence epilepsy

被引:29
作者
Tolmacheva, EA
van Luijtelaar, G
Chepurnov, SA
Kaminskij, Y
Mares, P
机构
[1] Radboud Univ Nijmegen, Dept Biol Psychol, Nijmegen Inst Cognit & Informat, NL-6500 HE Nijmegen, Netherlands
[2] Moscow MV Lomonosov State Univ, Fac Biol, Moscow, Russia
[3] Acad Sci Czech Republ, Inst Physiol, Prague, Czech Republic
关键词
excitability; cortex; sensory-motor cortex; rats WAG/Rij; absence epilepsy; afterdischarges;
D O I
10.1016/j.eplepsyres.2004.09.001
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The classical cortico-reticular theory on absence epilepsy suggests that a hyperexcitable cortex is a precondition for the occurrence of absence seizures. In the present experiment seizure thresholds and characteristics of cortical and limbic epileptic afterdischarges (AD) were determined in a comparative cortical stimulation study in young and old adult genetically epileptic WAG/Rij, congenic ACI and Wistar rats. Fifteen-second series of 8 Hz stimulation of the sensory-motor cortex were applied in 80- and 180-day-old rats with implanted electrodes. Strain differences were found for the threshold for movements directly induced by stimulation, low frequency spike-and-wave AD, maximal clonic intensity of seizures accompanying direct stimulation, and frequency characteristics of low frequency AD. None of these results agreed with a higher cortical excitability exclusively in WAG/Rij rats. However, WAG/Rij rats had the longest duration of the low frequency AD, and the lowest threshold for the transition to the limbic type of AD. The decrease of this threshold correlated with the increase of the incidence and total duration of spontaneous SWDs in WAG/Rij rats. It is concluded that the elevated excitability of the limbic system or pathways mediating the spread of the epileptic activity into this system can be attributed to the development of genetic epileptic phenotype in WAG/Rij rats. (C) 2004 Elsevier B.V. All rights reserved.
引用
收藏
页码:189 / 198
页数:10
相关论文
共 38 条
[1]  
Avanzini G, 1992, J Neural Transm Suppl, V35, P85
[2]   A RETICULORETICULAR COMMISSURAL PATHWAY IN THE RAT THALAMUS [J].
BATTAGLIA, G ;
LIZIER, C ;
COLACITTI, C ;
PRINCIVALLE, A ;
SPREAFICO, R .
JOURNAL OF COMPARATIVE NEUROLOGY, 1994, 347 (01) :127-138
[3]   CONNECTIONS OF THE THALAMIC RETICULAR NUCLEUS WITH THE CONTRALATERAL THALAMUS IN THE RAT [J].
CHEN, S ;
RAOS, V ;
BENTIVOGLIO, M .
NEUROSCIENCE LETTERS, 1992, 147 (01) :85-88
[4]   Genetic animal models for absence epilepsy: A review of the WAG/Rij strain of rats [J].
Coenen, AML ;
van Luijtelaar, ELJM .
BEHAVIOR GENETICS, 2003, 33 (06) :635-655
[5]   GENETIC MODELS OF ABSENCE EPILEPSY, WITH EMPHASIS ON THE WAG RIJ STRAIN OF RATS [J].
COENEN, AML ;
DRINKENBURG, WHIM ;
INOUE, M ;
VANLUIJTELAAR, ELJM .
EPILEPSY RESEARCH, 1992, 12 (02) :75-86
[6]   Childhood absence epilepsy: Genes, channels, neurons and networks [J].
Crunelli, V ;
Leresche, N .
NATURE REVIEWS NEUROSCIENCE, 2002, 3 (05) :371-382
[7]   Auditory information processing in rat genotypes with different dopaminergic properties [J].
de Bruin, NMWJ ;
van Luijtelaar, ELJM ;
Cools, AR ;
Ellenbroek, BA .
PSYCHOPHARMACOLOGY, 2001, 156 (2-3) :352-359
[8]  
Dyer R S, 1979, Neurobehav Toxicol, V1, P5
[9]   Lower density of A1 adenosine receptors in nucleus reticularis thalami in rats with genetic absence epilepsy [J].
Ekonomou, A ;
Angelatou, F ;
Vergnes, M ;
Kostopoulos, G .
NEUROREPORT, 1998, 9 (09) :2135-2140
[10]   Resistance to propagation of amygdaloid kindling seizures in rats with genetic absence epilepsy [J].
Eskazan, E ;
Onat, FY ;
Aker, R ;
Öner, G .
EPILEPSIA, 2002, 43 (10) :1115-1119