Modulation by K + channels of action potential‐evoked intracellular Ca 2+ concentration rises in rat cerebellar basket cell axons

1 Action potential‐evoked [Ca 2+ ] i rises in basket cell axons of rat cerebellar slices were studied using two‐photon laser scanning microscopy and whole‐cell recording, to identify the K + channels controlling the shape of the axonal action potential. 2 Whole‐cell recordings of Purkinje cell IPSCs were used to screen K + channel subtypes which could contribute to axonal repolarization. α‐Dendrotoxin, 4‐aminopyridine, charybdotoxin and tetraethylammonium chloride increased IPSC rate and/or amplitude, whereas iberiotoxin and apamin failed to affect the IPSCs. 3 The effects of those K + channel blockers that enhanced transmitter release on the [Ca 2+ ] i rises elicited in basket cell axons by action potentials fell into three groups: 4‐aminopyridine strongly increased action potential‐evoked [Ca 2+ ] i ; tetraethylammonium and charybdotoxin were ineffective alone but augmented the effects of 4‐aminopyridine; α‐dendrotoxin had no effect. 4 We conclude that cerebellar basket cells contain at least three pharmacologically distinct K + channels, which regulate transmitter release through different mechanisms. 4‐Aminopyridine‐sensitive, α‐dendrotoxin‐insensitive K + channels are mainly responsible for repolarization in basket cell presynaptic terminals. K + channels blocked by charybdotoxin and tetraethylammonium have a minor role in repolarization. α‐Dendrotoxin‐sensitive channels are not involved in shaping the axonal action potential waveform. The two last types of channels must therefore exert control of synaptic activity through a pathway unrelated to axonal action potential broadening.