Inflammation and prevention of epileptogenesis

Research output: Contribution to journalArticle

127 Citations (Scopus)

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 languageEnglish
Pages (from-to)223-230
Number of pages8
JournalNeuroscience Letters
Volume497
Issue number3
DOIs
Publication statusPublished - Jun 27 2011

Fingerprint

Status Epilepticus
Pharmacology
Inflammation
Febrile Seizures
Neuronal Plasticity
GABA Receptors
Drug Design
Wounds and Injuries
Glutamate Receptors
Brain
Virus Diseases
Encephalitis
Anticonvulsants
Transcriptional Activation
Epilepsy
Seizures
Up-Regulation
Stroke
Genes

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 journalArticle

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