1. In rat sympathetic ganglion cells, axotomy induces the appearance of a depolarizing after-potential (ADP) produced by a calcium-activated chloride current. Here we report that this current is also present in normal sympathetic neurones from the mouse. 2. In an in vitro preparation of the superior cervical ganglion, an ADP was observed after spike firing in 50% of the cells studied with single-electrode current- and voltage-clamp techniques. 3. When the cells were voltage clamped at -50 mV in the presence of tetrodotoxin (TTX) and tetraethylammonium chloride (TEA), depolarizing jumps evoked inward calcium currents which were contaminated by outward chloride currents, followed by slowly decaying inward chloride tail currents. 4. The ADP and the inward tail currents disappeared when calcium was removed from the extracellular solution or when cadmium was added. 5. The reversal potential for the inward tail current was approximately -24 mV and was displaced in agreement with the Nernst equation for chloride when the extracellular NaCl was replaced by sucrose or sodium isethionate. The chloride channel blocker anthracene-9-carboxylic acid (9AC) inhibited both the ADP and the tail current. 6. Using intracellular injection of neurobiotin, we found that cells with shorter dendrites had larger ADPs. In axotomized ganglia practically all cells showed very pronounced ADPs. 7. We conclude that normal mouse sympathetic ganglion cells have a calcium-activated chloride current that generates an ADP. The channels responsible for this current are probably located in the dendrites.