Abstract
We investigated the types and distribution of voltage-gated K+ channels in the soma and apical dendrite of layer 5 (L5) neocortical pyramidal neurones, of young rats (postnatal days 13-15), in acute brain slices. A slow inactivating outward K+ current and a fast inactivating outward K+ current were detected in nucleated patches. The slow K+ current was completely blocked by tetraethylammonium (TEA) with an IC50 of 5 +/- 1 mM (mean +/- s.e.m.) and was partially blocked by 4-aminopyridine (4-AP). The fast K+ current was blocked by 4-AP with an IC50 of 4.2 +/- 0.5 mM, but was not blocked by TEA. The activation kinetics of the slow K+ current were described by a second order Hodgkin-Huxley model. The slow K+ current displayed bi-exponential inactivation. A fourth order Hodgkin-Huxley model for activation and first order for inactivation described the kinetics of the fast K+ current. In somatic cell-attached recordings, three classes of single K+ channels could be differentiated based on their unitary conductance and inactivation kinetics, a fast inactivating channel having a conductance of 13 +/- 1 pS, a slow inactivating channel having a conductance of 9.5 +/- 0.5 pS, and a very slowly inactivating channel having a conductance of 16 +/- 1 pS. The inactivation time constants of the slow and of the very slow K+ channel corresponded to the two inactivation time constants of the slow K+ current observed in nucleated patches. This suggested that two distinct K+ channels mediated the slow K+ current in nucleated patches. The three subtypes of K+ channels that were observed in somatic recordings were present along the apical dendrite. The amplitude of ensemble K+ currents in cell-attached patches decreased along the apical dendrite as the distance from the soma increased, with a slope of -0.9 +/- 0.3 pA per 100 microm. The results suggest that the decrease of the voltage-gated K+ channel density from the soma along the apical dendrite of L5 pyramidal neurones helps to define a distal, low threshold region for the initiation of dendritic regenerative potentials.