Aims: Intralaminar thalamocortical (TC) neurons exhibit pronounced bursting which is primarily based on the expression of a prominent low-threshold Ca²⁺ current (I_T). A-type K⁺ channels represent important functional antagonists of T-type Ca²⁺ channels by generating a 4-aminopyridine (4-AP)-sensitive transient outward current (I_A). To determine the influence of I_A on the unusual bursting behavior of intralaminar TC neurons, its voltage-dependent and pharmacological properties were analyzed in acutely isolated cells of the centrolateral nucleus. Methods: Whole-cell patch-clamp techniques, RT-PCR analysis, and immunohistochemical staining were combined in thalamic specimens of P14-21 rats. Results: When I_A was activated by stepping neurons to increasingly positive test potentials (-70 to +30 mV) from a conditioning potential of -120 mV, a threshold of around -50 mV and a half-maximal activation of -18 ± 2 mV (n = 8) was determined. When I_A was inactivated by holding neurons at increasingly positive conditioning potentials (-120 mV to -20 mV), and stepping to a constant analyzing potential of -20 mV, a half-maximal inactivation of -64 ± 2 mV (n = 7) was determined. Application of different concentrations of 4-AP revealed a doses-responses characteristic with an IC₅₀ value of 1.0 mM. During current-clamp recordings amplitude and duration of the low-threshold Ca²⁺ spike (LTS) was increased and prolonged in the presence of 4-AP, respectively. The use of specific primers and antibodies revealed the expression of K_V4.2 and K_V4.3 channels. Conclusion: These results point to a scenario where I_T activates at hyperpolarized membrane potentials of around -70 mV followed by the activation of I_A at more positive potentials of around -50 mV. Therefore I_A has only little influence on LTS initiation but shapes its amplitude and duration.