1. The role of various Ca(2+)-activated K+ conductances were investigated using intracellular recording and single-electrode voltage clamp in neurones of superior cervical ganglia isolated in vitro from young adult rats. 2. Following replacement of Ca2+ with Co2+ (2 mM) or the addition of Cd2+ (100 microM), action potential amplitude and half-width either increased or decreased (in different cells), but both the after-hyperpolarization (AHP) and the outward tail current following a suprathreshold voltage step were markedly attenuated (by about 75%). 3. Addition of charybdotoxin (60 nM) or nifedipine (10 microM) increased action potential half-width (by about 25%) but had no significant effect on the AHP or tail current. 4. Addition of apamin (100 nM) or omega-conotoxin GVIA (100 nM) reduced the AHP and tail current (by about 60%) but did not significantly affect the action potential. A prolonged apamin-resistant component of the AHP present in 50% of neurones was blocked by ryanodine (20 microM). 5. Omega-Conotoxin MVIIC (150 nM) and omega agatoxin IVA (200 nM) had no significant effects on the action potential half-width or the AHP. 6. None of the Ca2+ channel blockers affected the prolonged ryanodine-sensitive component of the AHP and tail current. 7. We conclude that, in rat sympathetic neurones, Ca2+ entry via L-type channels selectively activates large conductance Ca(2+)-activated K+ channels (BK type) contributing to action potential repolarization, whereas Ca2+ entry via N-type channels selectively activates small conductance Ca(2+)-activated K+ channels (SK type) contributing to the AHP. Ca2+ entry via R-type Ca2+ channels prolongs the AHP by activating Ca2+ release from intracellular stores.