Temporal patterns of the cerebral inflammatory response in the rat lithium–pilocarpine model of temporal lobe epilepsy

Abstract

To better understand the role of inflammatory responses in temporal lobe epilepsy, we characterized Interleukin1-β (IL1-β), Nuclear Factor-κB (NF-κB), and Cyclooxygenase-2 (COX-2) expression together with neurodegeneration in the rat lithium–pilocarpine model. The immunohistochemical expression of IL1-β, NF-κB, and COX-2 started by 12 h post-injection, persisted for 24 h (status epilepticus period), and returned to basal levels by 3 and 6 days (latent period). The regional distribution of IL1-β, NF-κB, and COX-2 occurred mainly in structures prone to develop neuronal damage. Using double-staining protocols, we detected IL1-β expression in glial cells, COX-2 expression in neurons, and NF-κB in both cell types. The presence of Fluoro-Jade-B-positive degenerating neurons was associated with IL1-β, NF-κB, and COX-2 proteins expression during status epilepticus but not during the latent period while neurons were still degenerating. These data suggest that seizure-related IL1-β, NF-κB, and COX-2 expression may contribute to the pathophysiology of epilepsy by inducing neuronal death and astrocytic activation.

Keywords

• Neurodegeneration
• Gliosis
• Fluoro-Jade B
• Immunohistochemistry
• Interleukin1-β
• Nuclear factor-κB