1. Whole-cell Na+-activated K+ (K-Na) channel currents and single K-Na
channels were studied with the patch-clamp method in small (20-25 mu
m) dorsal root ganglion (DRG) neurones in slices of rat dorsal root ga
nglia. 2. The whole-cell K-Na channel current was identified as an add
itional K+-selective leakage current which appeared after cell perfusi
on with internal solutions containing different [Na+]. The concentrati
on for half-maximal activation of K-Na channel current was 39 mM and t
he Hill coefficient was 3.5. At [Na+](i) above 12 mM, K-Na channel cur
rent dominated the unspecific leakage current. The ratio of maximum Ii
,, channel current to unspecific leakage current was 45. 3. K-Na chann
el current was not activated by internal Li+. It was suppressed by ext
ernal 20 mM Cs+ but not by 10 mM tetraethylammonium. 4. Single K-Na ch
annels with a conductance of 142 pS in 155 mM external K+ (K-o(+))-85
mM internal K+ (K-i(+)) solutions were observed at a high density of a
bout 2 channels mu m(-2) 5. In two-electrode experiments, a direct cor
relation was seen between development of whole-cell K-Na channel curre
nt and activation of single K-Na channels during perfusion of the neur
one with Na+-containing internal solution. 6. Under current-clamp cond
itions, K-Na channels did not contribute to the action potential. Howe
ver, internal perfusion of the neurone with Na+ shifted the resting po
tential towards the equilibrium potential for K+ (E-K). Varying extern
al [K+] indicated that in neurones perfused with Na+-containing intern
al solution the resting potential followed the E-K values predicted by
the Nernst equation over a broader voltage range than in neurones per
fused with Na+-free solution. 7. It is concluded that the function of
K-Na channels has no links to firing behaviour but that the channels c
ould be involved in setting or stabilizing the resting potential in sm
all DRG neurones.