Microglia (brain macrophages) exist as resting/surveying cells with a highly ramified process network in the undisturbed brain. Homeostatic imbalance triggers their transition to the ''activated'' spectrum, which is morphologically equivalent to process retraction and somatic enlargement. Activated microglia orchestrate the inflammatory response in the brain, and chronic inflammation has been associated with excitotoxicity and neurodegeneration.

In this experimental work we sought to assess the impact of microglia activation on neuronal viability and excitability.

We investigated microglia in vitro, using organotypic hippocampal slice cultures that allow for long-term pharmacological manipulations. Microglia activation in vitro was achieved with long-term (72 hours) exposure to the Gram (-) bacterial endotoxin, lipopolysaccharide. The number and morphology of activated microglia were quantified using stereology and Sholl-analysis. Moreover, neuronal viability was assessed with the Fluoro-Jade®B fluorescent reporter. We determined neuronal excitability by measuring local field potentials in the CA1 hippocampal subregion and monitored the stimulus-evoked changes in extracellular potassium concentration ([K⁺]_o) using ion-sensitive microelectrodes.

The microglia activation pattern was morphologically equivalent with retraction of microglia processes and somatic enlargement. Nevertheless, no apoptotic/necrotic neurons were detected, and the short-term plasticity properties were not modified in cultures with proinflammatory profile versus controls. Furthermore, the rise and decay of [K⁺]_o after repetitive electrical stimulation had no significant differences between control and LPS-exposed cultures.

We conclude that lipopolysaccharide exposure is not associated either with neuronal death or with fundamental changes in neuronal function, despite inducing a sufficient proinflammatory reaction.