Abstract

Chronic stimulation of the nervous system or acute administration of kainic acid results in a persistent increase in AP-1-like DNA-binding activity in the brain. However, the composition and function of these AP-1 complexes remain controversial. By comparing wild-type and fosB-null mice treated with kainic acid, we establish that the complexes comprise JunD in association with an ∼37 kDa Δ-FosB species. Δ-FosB was expressed persistently in neurons in many areas of the CNS, even though fosB mRNA only increased transiently. This implies that the 37 kDa protein is very stable. fosB−/− mice are predisposed to seizures. Therefore, the chronic expression of Δ-FosB elicited by kainic acid seizures may be indicative of a compensatory/protective role in the pathophysiology of epilepsy.