title: Inflammation and prevention of epileptogenesis.
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.
authors.affiliation: Department of Neuroscience, Mario Negri Institute for Pharmacological Research, Via G. La Masa 19, 20156 Milano, Italy. ravizza@marionegri.it
authors.forename: Teresa
authors.initials: T
authors.lastname: Ravizza
authors.forename: Silvia
authors.initials: S
authors.lastname: Balosso
authors.forename: Annamaria
authors.initials: A
authors.lastname: Vezzani
mesh_terms: D000818:Animals; D000927:Anticonvulsants / Q000008:administration & dosage*; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D004660:Encephalitis / Q000150:complications / Q000378:metabolism* / Q000517:prevention & control*; D004827:Epilepsy / Q000150:complications / Q000378:metabolism* / Q000517:prevention & control*; D006801:Humans
chemical_list: D000927:Anticonvulsants