1. We investigated voltage-gated potassium channels in human peripheral mye
linated axons; apart from the I, S and F channels already described in amph
ibian and rat axons, we identified at least two other channel types.
2. The I channel activated between -70 and -40 mV, and inactivated very slo
wly (time constant 13.1 s at -40 mV). It had two gating modes: the dominant
('noisy') mode had a conductance of 30 pS (inward current, symmetrical 155
mM K+) and a deactivation time constant (tau) of 25 ms (-80 mV); it accoun
ted for most (similar to 50-75%) of the macroscopic K+ current in large pat
ches. The secondary ('flickery') gating mode had a conductance of 22 pS, an
d showed bi-exponential deactivation (tau = 16 and 102 ms; -80 mV); it cont
ributed part of the slow macroscopic Kf current. 3.
3. The I channel current was blocked by 1 mu M alpha-dendrotoxin (DTX); we
also observed two other DTX-sensitive K+ channel types (40 pS and 25 pS). T
he S and F channels were not blocked by 1 mu M DTX.
4. The conductance of the S channel was 7-10 pS, and it activated at slight
ly more negative potentials than the I channel; its deactivation was slow (
tau = 41.7 ms at -100 mV). It contributed a second component of the slow ma
croscopic K+ current.
5. The F channel had a conductance of 50 pS; it activated at potentials bet
ween -40 and +40 mV, deactivated very rapidly (tau = 1.4 ms at -100 mV), an
d inactivated rapidly (tau = 62 ms at +80 mV). It accounted for the fast-de
activating macroscopic K+ current and partly for fast K+ current inactivati
on.
6. We conclude that human and rat axonal K+ channels are closely similar, b
ut that the correspondence between K+ channel types and the macroscopic cur
rents usually attributed to them is only partial. At least five channel typ
es exist, and their characteristics overlap to a considerable extent.