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Cited by 163Epilepsy research and treatmentNeuroinflammation and Neurodegeneration MechanismsTryptophan and brain disorders

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

Lehtimäki, K.A, Peltola, J, Koskikallio, E, Keränen, T, Honkaniemi, J·2003·Molecular Brain Research
DOI 10.1016/s0169-328x(02)00654-x
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Abstract

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.

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  • In animal models, seizures are associated with increased activation of microglia, especially the M1 subtype, and increased release of pro-inflammatory mediators.

    “Studies in animal models have reported that seizures are associated with increased activation of microglia, especially of the M1 subtype [189], and an increased release of pro-inflammatory mediators [190, 191].”

    From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [190]

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Authors
Lehtimäki, K. A., Peltola, J., Koskikallio, E., Keränen, T., & Honkaniemi, J.
Affiliations
Tampere University Hospital (FI)
Corresponding author
Honkaniemi, J
ORCID
Venue
Molecular Brain Research
Publisher
Elsevier BV
Published
2003-02
Volume
110
Issue
2
Pages
253-260
ISSN
0169-328X (ISSN-L)
DOI
10.1016/s0169-328x(02)00654-x
OpenAlex
W1995444099
Cited by
163
References
49
Citations by year
2026: 4 · 2025: 2 · 2024: 4 · 2023: 3 · 2022: 12 · 2021: 7 · 2020: 6 · 2019: 6 · 2018: 8 · 2017: 8 · 2016: 3 · 2015: 6 · 2014: 16 · 2013: 8 · 2012: 5
FWCI
4.28
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Molecular Brain Research (publishedVersion)
  • PubMed (publishedVersion)
  • Tampere University Institutional Repository (Tampere University) (submittedVersion)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
cytokines, cytokine receptors, kainic acid-induced seizures, status epilepticus, interleukin-6, leukemia inhibitory factor, IL-6 receptor, LIF receptor, gp130, IL-1β, TNF-α, hippocampus, meninges, cerebrospinal fluid, neuroinflammation, rat brain
MeSH terms
Animals, Brain, Epilepsy, Gene Expression Regulation, Growth Inhibitors, Interleukin-1, Lymphokines, Male, Neurons, RNA, Messenger, Tumor Necrosis Factor-alpha, Interleukin-6, Cytokines, Rats, Sprague-Dawley, Receptors, Cytokine, Neural Cell Adhesion Molecules, Receptors, Interleukin-6, Rats, Leukemia Inhibitory Factor, Receptors, OSM-LIF, Leukemia Inhibitory Factor Receptor alpha Subunit, Contactins

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