This paper presents the kinetic and pharmacological properties of voltage-gated K+ currents in anatomically identified glandular postganglionic sympathetic neurons isolated from the superior cervical ganglia in rats. The neurons were labelled by injecting the fluorescent tracer Fast Blue into the submandibular gland. The first group of neurons remained intact, i.e. innervated by the preganglionic axons until the day of current recordings (control neurons). The second group of neurons was denervated by severing the superior cervical trunk 4–6 weeks prior to current recordings (decentralized neurons). In every control and decentralized neuron three categories of voltage-dependent K+ currents were found. (i) The IAf K+ current, steady state, inactivated at hyperpolarized membrane potentials. This current was fast activated and fast time-dependently inactivated, insensitive to TEA and partially depressed by 4-AP. (ii) The IAs K+ current, which was steady-state inactivated at less hyperpolarized membrane potentials than IAf. The current activation and time-dependent inactivation kinetics were slower than those of IAf. IAs was blocked by TEA and partially inhibited by 4-AP. (iii) The IK K+ current did not undergo steady-state inactivation. In decentralized compared to control neurons the maximum IAf K+ current density (at +50 mV) increased from 116.9 ± 8.2 to 189.0 ± 11.5 pA/pF, the 10–90% current rise time decreased from 2.3 to 0.7 ms and the recovery from inactivation was faster. Similarly, in decentralized compared to control neurons the maximum IAs K+ current density (at +50 mV) increased from 49.9 ± 3.5 to 74.3 ± 5.0 pA/pF, the 10–90% current rise time shortened from 29 to 16 ms and the recovery from inactivation of the current was also faster. The maximum density (at +50 mV) of IK in decentralized compared to control neurons decreased from 76.6 ± 3.9 to 60.7 ± 6.3 pA/pF. We suggest that the upregulation of voltage-gated time-dependently-inactivated K+ currents and their faster recovery from inactivation serve to restrain the activity of glandular sympathetic neurons after decentralization.