A. Scholz et al., Properties and functions of calcium-activated K+ channels in small neurones of rat dorsal root ganglion studied in a thin slice preparation, J PHYSL LON, 513(1), 1998, pp. 55-69
1. Properties, kinetics and functions of large conductance calcium-activate
d K+ channels (BKCa) were investigated by the patch-clamp technique in smal
l neurones (A delta- and C-type) of a dorsal root ganglion (DRG) thin slice
preparation without enzymatic treatment.
2. Unitary conductance of BK,, channels measured in symmetrical high Kf sol
utions (155 mM) was 200 pS for inward currents, and chord conductance in co
ntrol solution was 72 pS. Potentials of half-maximum activation (V-1/2) of
the channels were Linearly shifted by 43 mV per log,, [Ca2+](i) unit (pCa)
in the range of -28 mV (pCa 4) to +100 mV (pCa 7). Open probabilities incre
ased e-times per 15-32 mV depolarization of potential.
3. In mean open probability, fast changes with time were mainly observed at
pCa > 6 and at potentials > +20 mV, without obvious changes in the experim
ental conditions.
4. BK,, channels were half-maximally blocked by 0.4 mM TEA, measured by app
arent amplitude reductions. They were completely blocked by 100 nM charybdo
toxin and 50 nM iberiotoxin by reduction of open probability.
5. Two subtypes of small DRG neurones could be distinguished by the presenc
e (type I) or absence (type II) of BKCa channels. In addition, less than 10
% of small neurones showed fast (similar to 135 V s(-1)) and short (similar
to 0.8 ms) action potentials (AP).
6. The main functions of BK,, channels were found to be shortening of AP du
ration, increasing of the speed of repolarization and contribution to the f
ast after-hyperpolarization. As a consequence, BKCa channels may reduce the
amount of calcium entering a neurone during an AP.
7. BKCa channel currents suppressed a subsequent AP and prolonged the refra
ctory period, which might lead to a reduced repetitive activity. We suggest
that the BKCa current is a possible mechanism of the reported conduction f
ailure during repetitive stimulation in DRG neurones.