Microglia is considered as the resident macrophages of the central nervous system. It is generally accepted that microglia shifts between different activated phenotypes: depending on the stimulus, microglia can execute pro-inflammatory or anti-inflammatory actions in terms of e.g. nitric oxide or cytokine production. Moreover, a continuum of activation stages exists between these two extremes. Controlling the activation stage of microglia is believed to be a good therapeutic strategy in the treatment of diseases with a neuro-inflammatory context. In this study the microglial activation phenotypes were investigated using an electrophysiological approach. Differential expression of ion channels (voltage-gated and inward rectifier potassium channels), transporters and receptors is known to occur during strong activation of immune cells. Yet, a correlation of the expression profile of these proteins with the various activation stages is lacking. The electrophysiological phenotyping of microglia is performed on ex vivo brain slices of adult CX3CR1+/eGFP mice subjected to autoimmune encephalomyelitits (EAE). In these mice the microglia/macrophages are eGFP-labeled and EAE lesion in the brain slices are recognized by an increased density of these cells. In addition, the different activation stages are hypothesized to play a role in the balance between pro- and anti-inflammatory events during the disease progression of EAE and therefore microglial phenotypes are studied at different time points of the disease: before the onset, during the onset, at the peak an in the chronic phase of the disease. Microglia present in the active EAE lesions of brain slices of EAE animals in the peak and chronic stage show increased functional expression of delayed rectifier potassium channels. Preliminary results show no differential expression of ligand-gated ion channels (glycine, glutamate, serotonin acetylcholine).