Expression of cytokines and cytokine receptors in the rat brain after kainic acid-induced seizures

被引:127
|
作者
Lehtimäki, KA
Peltola, J
Koskikallio, E
Keränen, T
Honkaniemi, J
机构
[1] Univ Tampere, Dept Neurol & Rehabil, FIN-33101 Tampere, Finland
[2] Tampere Univ Hosp, FIN-33101 Tampere, Finland
来源
MOLECULAR BRAIN RESEARCH | 2003年 / 110卷 / 02期
关键词
seizure; interleukin-6; leukemia inhibitory factor; cytokine receptor;
D O I
10.1016/S0169-328X(02)00654-X
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We have previously shown that IL-6 protein levels are increased in cerebrospinal fluid in humans after recent tonic-clonic seizures with unchanged levels of IL-1beta and TNFalpha. Here we studied the expression of cytokines IL-6, LIF, IL-1beta and TNFalpha and cytokine receptors IL-6R, LIFR and Gp130 in the rat brain after kainic acid-induced status epilepticus using Northern blot analysis and in situ hybridization histochemistry. After seizures, IL-6 mRNA was induced in the hippocampus, cortex, amygdala and meninges, and IL-6R was up-regulated in the hippocampus. LIF was up-regulated in the hippocampus, cortex and meninges after seizures, and LIFR mRNA was induced in the hippocampus and cortex. Gp130 was constitutively expressed in the brain. After seizures, Gp130 transcription was rapidly induced in the meninges. In thalamus, cortex, amygdala and hippocampus Gp130 mRNA was induced in a delayed fashion. IL-1beta transcription was induced in the temporal lobe cortex and thalamus, and TNFalpha in the hippocampus. In general, the cytokine and their receptor mRNA levels were low in intact rat brain, but were induced by seizures. Since IL-6 and LIF transcripts were induced in the meninges after seizures, the protein products of these transcripts may be more readily released in cerebrospinal fluid after seizures. In addition, the activity of IL-6 and LIF signaling pathways may be influenced by increased expression of their receptors after seizures. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:253 / 260
页数:8
相关论文
共 50 条
  • [31] Temporal specific patterns of semaphorin gene expression in rat brain after kainic acid-induced status epilepticus
    Barnes, G
    Puranam, RS
    Luo, YL
    McNamara, JO
    HIPPOCAMPUS, 2003, 13 (01) : 1 - 20
  • [32] DIFFERENTIAL INCREASES IN BRAIN LEVELS OF NEUROPEPTIDE-Y AND VASOACTIVE INTESTINAL POLYPEPTIDE AFTER KAINIC ACID-INDUCED SEIZURES IN THE RAT
    MARKSTEINER, J
    SPERK, G
    MAAS, D
    NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY, 1989, 339 (1-2) : 173 - 177
  • [33] Cynarin protects against seizures and neuronal death in a rat model of kainic acid-induced seizures
    Lu, Cheng-Wei
    Lin, Tzu-Yu
    Pan, Wun-Jing
    Chiu, Kuan-Ming
    Lee, Ming-Yi
    Wang, Su-Jane
    FOOD & FUNCTION, 2025,
  • [34] BENEFICIAL EFFECTS OF SOMATOSTATIN ANALOGUES AGAINST KAINIC ACID-INDUCED SEIZURES IN THE RAT
    Kokkinou, E.
    Vasilaki, A.
    Asprodini, E.
    EPILEPSIA, 2010, 51 : 85 - 86
  • [35] BLOOD-BRAIN-BARRIER CHANGES WITH KAINIC ACID-INDUCED LIMBIC SEIZURES
    ZUCKER, DK
    WOOTEN, GF
    LOTHMAN, EW
    EXPERIMENTAL NEUROLOGY, 1983, 79 (02) : 422 - 433
  • [36] Microglial activation during kainic acid-induced hippocampal seizures in the rat.
    Taniwaki, Y
    Araki, T
    Kobayashi, T
    Kato, M
    EPILEPSIA, 1996, 37 : 64 - 65
  • [37] Altered expression of GABAB receptors in the hippocampus after kainic-acid-induced seizures in rats
    Furtinger, S
    Bettler, B
    Sperk, G
    MOLECULAR BRAIN RESEARCH, 2003, 113 (1-2): : 107 - 115
  • [38] The expression of Fos following kainic acid-induced seizures is age-dependent
    Silveira, DC
    Sogawa, Y
    Holmes, GL
    EUROPEAN JOURNAL OF NEUROSCIENCE, 2002, 15 (02) : 329 - 344
  • [39] Changes in the expression of GABAA receptor subunit mRNAs in parahippocampal areas after kainic acid-induced seizures
    Drexel, Meinrad
    Kirchmair, Elke
    Sperk, Guenther
    FRONTIERS IN NEURAL CIRCUITS, 2013, 7
  • [40] KAINIC ACID-INDUCED LIMBIC SEIZURES - ELECTROPHYSIOLOGIC STUDIES
    LOTHMAN, EW
    COLLINS, RC
    FERRENDELLI, JA
    NEUROLOGY, 1981, 31 (07) : 806 - 812