Abstract
Limbic status epilepticus was induced in rats by unilateral 60-min electrical stimulation of the CA3 region of the ventral hippocampus. As assessed by RT-PCR followed by Southern blot analysis, transcripts of interleukin-1β, interleukin-6, interleukin-1 receptor antagonist and inducible nitric oxide synthase were significantly increased 2 h after status epilepticus in the stimulated hippocampus. Induction was maximal at 6 h for interleukin-1β (445%), interleukin-6 (405%) and tumour necrosis factor-α (264%) and at 24 h for interleukin-1 receptor antagonist (494%) and inducible nitric oxide synthase (432%). In rats with spontaneous seizures (60 days after status epilepticus), interleukin-1β mRNA was still higher than controls (241%). Immunocytochemical staining of interleukin-1β, interleukin-6 and tumour necrosis factor-α was enhanced in glia with a time-course similar to that of the respective transcripts. Sixty days after status epilepticus, interleukin-1β immunoreactivity was increased exclusively in neurons in one third of the animals. Multiple intracerebroventricular injections of interleukin-1 receptor antagonist (0.5 μg/3 μL) significantly decreased the severity of behavioural convulsions during electrical stimulation and selectively reduced tumour necrosis factor-α content in the hippocampus measured 18 h after status epilepticus. Thus, the induction of spontaneously recurring seizures in rats involves the activation of inflammatory cytokines and related pro- and anti-inflammatory genes in the hippocampus. These changes may play an active role in hyperexcitability of the epileptic tissue.
| Original language | English |
|---|---|
| Pages (from-to) | 2623-2633 |
| Number of pages | 11 |
| Journal | European Journal of Neuroscience |
| Volume | 12 |
| Issue number | 7 |
| DOIs | |
| Publication status | Published - 2000 |
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Keywords
- Interleukin-1
- Interleukin-1 receptor antagonist
- Interleukin-6
- Nitric oxide synthase
- Seizures
- Tumour necrosis factor-α
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Inflammatory cytokines and related genes are induced in the rat hippocampus by limbic status epilepticus. / De Simoni, Maria Grazia; Perego, Carlo; Ravizza, Teresa; Moneta, Daniela; Conti, Mirko; Marchesi, Francesco; De Luigi, Ada; Garattini, Silvio; Vezzani, Annamaria.
In: European Journal of Neuroscience, Vol. 12, No. 7, 2000, p. 2623-2633.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Inflammatory cytokines and related genes are induced in the rat hippocampus by limbic status epilepticus
AU - De Simoni, Maria Grazia
AU - Perego, Carlo
AU - Ravizza, Teresa
AU - Moneta, Daniela
AU - Conti, Mirko
AU - Marchesi, Francesco
AU - De Luigi, Ada
AU - Garattini, Silvio
AU - Vezzani, Annamaria
PY - 2000
Y1 - 2000
N2 - Limbic status epilepticus was induced in rats by unilateral 60-min electrical stimulation of the CA3 region of the ventral hippocampus. As assessed by RT-PCR followed by Southern blot analysis, transcripts of interleukin-1β, interleukin-6, interleukin-1 receptor antagonist and inducible nitric oxide synthase were significantly increased 2 h after status epilepticus in the stimulated hippocampus. Induction was maximal at 6 h for interleukin-1β (445%), interleukin-6 (405%) and tumour necrosis factor-α (264%) and at 24 h for interleukin-1 receptor antagonist (494%) and inducible nitric oxide synthase (432%). In rats with spontaneous seizures (60 days after status epilepticus), interleukin-1β mRNA was still higher than controls (241%). Immunocytochemical staining of interleukin-1β, interleukin-6 and tumour necrosis factor-α was enhanced in glia with a time-course similar to that of the respective transcripts. Sixty days after status epilepticus, interleukin-1β immunoreactivity was increased exclusively in neurons in one third of the animals. Multiple intracerebroventricular injections of interleukin-1 receptor antagonist (0.5 μg/3 μL) significantly decreased the severity of behavioural convulsions during electrical stimulation and selectively reduced tumour necrosis factor-α content in the hippocampus measured 18 h after status epilepticus. Thus, the induction of spontaneously recurring seizures in rats involves the activation of inflammatory cytokines and related pro- and anti-inflammatory genes in the hippocampus. These changes may play an active role in hyperexcitability of the epileptic tissue.
AB - Limbic status epilepticus was induced in rats by unilateral 60-min electrical stimulation of the CA3 region of the ventral hippocampus. As assessed by RT-PCR followed by Southern blot analysis, transcripts of interleukin-1β, interleukin-6, interleukin-1 receptor antagonist and inducible nitric oxide synthase were significantly increased 2 h after status epilepticus in the stimulated hippocampus. Induction was maximal at 6 h for interleukin-1β (445%), interleukin-6 (405%) and tumour necrosis factor-α (264%) and at 24 h for interleukin-1 receptor antagonist (494%) and inducible nitric oxide synthase (432%). In rats with spontaneous seizures (60 days after status epilepticus), interleukin-1β mRNA was still higher than controls (241%). Immunocytochemical staining of interleukin-1β, interleukin-6 and tumour necrosis factor-α was enhanced in glia with a time-course similar to that of the respective transcripts. Sixty days after status epilepticus, interleukin-1β immunoreactivity was increased exclusively in neurons in one third of the animals. Multiple intracerebroventricular injections of interleukin-1 receptor antagonist (0.5 μg/3 μL) significantly decreased the severity of behavioural convulsions during electrical stimulation and selectively reduced tumour necrosis factor-α content in the hippocampus measured 18 h after status epilepticus. Thus, the induction of spontaneously recurring seizures in rats involves the activation of inflammatory cytokines and related pro- and anti-inflammatory genes in the hippocampus. These changes may play an active role in hyperexcitability of the epileptic tissue.
KW - Interleukin-1
KW - Interleukin-1 receptor antagonist
KW - Interleukin-6
KW - Nitric oxide synthase
KW - Seizures
KW - Tumour necrosis factor-α
UR - http://www.scopus.com/inward/record.url?scp=0033943296&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0033943296&partnerID=8YFLogxK
U2 - 10.1046/j.1460-9568.2000.00140.x
DO - 10.1046/j.1460-9568.2000.00140.x
M3 - Article
VL - 12
SP - 2623
EP - 2633
JO - European Journal of Neuroscience
JF - European Journal of Neuroscience
SN - 0953-816X
IS - 7
ER -