The role of IL-1β and glutamate in the effects of lipopolysaccharide on the hippocampal electrical kindling of seizures

• LPS and IL-1β, injected into hippocampus, enhanced kindling in rapid kindling model.
• LPS increased IL-1β, but not TNF-α levels in stimulated hippocampus in kindled rats.
• In vivo acute LPS perfusion produced an increase in glutamate release in hippocampus.

In our study, we used rapid electrical hippocampal kindling and in vivo microdialysis methods to assess the involvement of inflammatory mediators: lipopolysaccharide (LPS) and proinflammatory interleukin-1β (IL-1β) in mechanisms of epileptogenesis. We observed, that both, LPS and IL-1β, administered into stimulated hippocampus, accelerated kindling process. LPS also increased the expression of IL-1β in stimulated hippocampus in kindled rats. In vivo acute LPS perfusion, via a microdialysis cannula implanted into the naïve rat's hippocampus, produced an increase in extracellular glutamate release. We suppose, that particularly IL-1β action and increased glutamate concentration may significantly contribute to LPS effects on kindling development.

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