Microglia are the resident immuno-competent cells of the CNS. They are involved in host defence and repair and the generation of neuro-inflammatory states. This latter aspect role has made them the target of potential therapies for diseases that generate CNS inflammation, e.g. Alzheimer’s disease. There has been a steady growth in research dedicated to the physiology of microglia, much of which has relied cultured rodent cells. Although a small number of physiological studies of human microglia exist such work is reliant on a supply of donor tissue. Here we present our initial data on a little studied human microglial cell-line C13-NJ. C13-NJ cells were cultured in DMEM supplemented with 10% FCS. Experiments were performed at room temperature on cells adhered to glass coverslips. Cell-attached and whole-cell patch clamp measurements were made with a range of bath and electrode solutions designed to characterise various channel types. Ratiometric Ca2+ imaging was performed on Fura-2 loaded cells using standard methods. In >95% of cell-attached recordings at a pipette potential of -70 mV, large outward-going channel openings were observed. The opening of these channels was greatly enhanced by the Ca2+ ionophore A-23187. These channel openings were absent from all patches recorded with paxilline (2 μM) in the pipette. This pharmacology, combined with gating and conductance measurements, indicates these are BK potassium channels. In current clamp recordings under approximately physiological ionic conditions C13-NJ cells had a resting potential of -49 ± 2 mV; more depolarized resting potentials were seen with Cs+-containing pipettes. The membrane time constant measured with a 20 pA current injection was 4.9 ± 1.0 ms. Mean membrane capacitance measured in voltage clamp was 20.8 ± 0.8 pF (n=184). Strong hyperpolarizing current injections from rest lead to an initial charging of the membrane which was followed, in a number of cells, by a slow hyperpolarizing drift, which appears to result from the slow closure of a depolarising conductance tonically open at rest. Voltage-clamp experiments indicate that this conductance is sensitive to flufenamic acid and can exhibit spontaneous time-dependent changes in activity. Step depolarization from negative voltage clamp potentials resulted in a small transient inward current followed by a larger outward current. Much of the latter was paxilline-sensitive and thus seems to arise from the BK channels invariably observed in cell-attached recordings. The former current has kinetics and pharmacology commensurate with activation of the cardiac Na+ channel isoform. In Ca2+ imaging ADP, ATP, histamine and LPS triggered acute [Ca2+]i elevations whereas β-amyloid42 and carbachol were ineffective.