The mammalian central nervous system (CNS) is comprised of two neural cell types – neurons and glia. The main types of glia are oligodendrocytes, which are the myelin-forming cells of the CNS, and astrocytes, which have a primary role in the extracellular K+ regulation during neuronal activity. A major feature of neural cells is their expression of inwardly rectifying K+ channels (Kir), which regulate excitability in neurons and maintain the strongly negative resting membrane potential of glia. A genome-wide microarray analysis of the mouse optic nerve identified prominent expression of the Kir7.1 subtype. Kir7.1 channels are expressed in epithelial tissues in the kidney, retina and gastrointestinal tract, where they are believed to be important for K+ recycling, but little is known about their expression or function in the CNS. Here, we have used immunohistochemistry to examine expression of Kir7.1 in the mouse brain. Mice aged postnatal day P0 to P40 (adult) were killed in accordance with the UK Animals Act (1986). Optic nerves were removed for tissue culture and brains immersion-fixed in 4% paraformaldehyde and sectioned using a vibratome (40-60µm). Immunolabelling was performed using antibodies to Kir7.1 and cell markers for neurons. Glial cells were identified by their expression of fluorescent reporters. Controls were treated with secondary antibody in the absence of primary antibody and exhibited no labeling. Immunolabelling was examined on an LSM710 confocal microscope (Zeiss) and analysed using Volocity software (PerkinElmer). In the adult mouse, there was prominent Kir7.1 immunolabelling in neuronal somata and primary dendrites, as well as on astrocytic and oligodendrocytic somata and processes, throughout the cerebral cortex, corpus callosum hippocampus and cerebellum. Comparison of mice at different ages revealed a developmental increase in Kir7.1 immunolabelling in astrocytes and oligodendrocytes between P7 and P15, whereas neurons appeared to express Kir7.1 at all stages of development. Analysis of cultured neurons and glia confirmed expression of Kir7.1 in these cells, and showed the same developmental increase in expression in astrocytes and oligodendrocytes observed in vivo. The results demonstrate prominent expression of Kir7.1 in neurons and glia and suggest this channel may play an important role in neuronal excitability, the astrocytic function of potassium regulation and the oligodendrocyte function of myelination. Supported by the MRC and IBBS