Abstract
CNS injuries such as trauma, stroke, viral infection, febrile seizures, status epilepticus occurring either in infancy or during a lifetime are considered common risk factors for developing epilepsy. Long term CNS inflammation develops rapidly after these events, suggesting that a pro-inflammatory state in the brain might play a role in the development of the epileptic process. This hypothesis is corroborated by two main lines of evidence: (1) the upregulation of pro-inflammatory signals during epileptogenesis in brain areas of seizure onset/generalization; (2) pharmacological targeting of specific pro-inflammatory pathways after status epilepticus or in kindling shows antiepileptogenic effects. The mechanisms by which pro-inflammatory molecules might favor the establishment of chronic neuronal network hyperexcitability involve both rapid, non-transcriptional effects on glutamate and GABA receptors, and transcriptional activation of genes involved in synaptic plasticity. This emerging evidence predicts that pharmacological interventions targeting brain inflammation might provide a key to new antiepileptic drug design.
| Original language | English |
|---|---|
| Pages (from-to) | 223-230 |
| Number of pages | 8 |
| Journal | Neuroscience Letters |
| Volume | 497 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Jun 27 2011 |
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Keywords
- Anti-inflammatory
- Brain development
- COX-2
- Cytokines
- Epilepsy
- Interleukin
- Lipopolysaccharide
- Toll-like receptor
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Inflammation and prevention of epileptogenesis. / Ravizza, Teresa; Balosso, Silvia; Vezzani, Annamaria.
In: Neuroscience Letters, Vol. 497, No. 3, 27.06.2011, p. 223-230.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Inflammation and prevention of epileptogenesis
AU - Ravizza, Teresa
AU - Balosso, Silvia
AU - Vezzani, Annamaria
PY - 2011/6/27
Y1 - 2011/6/27
N2 - CNS injuries such as trauma, stroke, viral infection, febrile seizures, status epilepticus occurring either in infancy or during a lifetime are considered common risk factors for developing epilepsy. Long term CNS inflammation develops rapidly after these events, suggesting that a pro-inflammatory state in the brain might play a role in the development of the epileptic process. This hypothesis is corroborated by two main lines of evidence: (1) the upregulation of pro-inflammatory signals during epileptogenesis in brain areas of seizure onset/generalization; (2) pharmacological targeting of specific pro-inflammatory pathways after status epilepticus or in kindling shows antiepileptogenic effects. The mechanisms by which pro-inflammatory molecules might favor the establishment of chronic neuronal network hyperexcitability involve both rapid, non-transcriptional effects on glutamate and GABA receptors, and transcriptional activation of genes involved in synaptic plasticity. This emerging evidence predicts that pharmacological interventions targeting brain inflammation might provide a key to new antiepileptic drug design.
AB - CNS injuries such as trauma, stroke, viral infection, febrile seizures, status epilepticus occurring either in infancy or during a lifetime are considered common risk factors for developing epilepsy. Long term CNS inflammation develops rapidly after these events, suggesting that a pro-inflammatory state in the brain might play a role in the development of the epileptic process. This hypothesis is corroborated by two main lines of evidence: (1) the upregulation of pro-inflammatory signals during epileptogenesis in brain areas of seizure onset/generalization; (2) pharmacological targeting of specific pro-inflammatory pathways after status epilepticus or in kindling shows antiepileptogenic effects. The mechanisms by which pro-inflammatory molecules might favor the establishment of chronic neuronal network hyperexcitability involve both rapid, non-transcriptional effects on glutamate and GABA receptors, and transcriptional activation of genes involved in synaptic plasticity. This emerging evidence predicts that pharmacological interventions targeting brain inflammation might provide a key to new antiepileptic drug design.
KW - Anti-inflammatory
KW - Brain development
KW - COX-2
KW - Cytokines
KW - Epilepsy
KW - Interleukin
KW - Lipopolysaccharide
KW - Toll-like receptor
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UR - http://www.scopus.com/inward/citedby.url?scp=79957807767&partnerID=8YFLogxK
U2 - 10.1016/j.neulet.2011.02.040
DO - 10.1016/j.neulet.2011.02.040
M3 - Article
VL - 497
SP - 223
EP - 230
JO - Neuroscience Letters
JF - Neuroscience Letters
SN - 0304-3940
IS - 3
ER -