Modulation by K+ channels of action potential-evoked intracellular Ca2+ concentration rises in rat cerebellar basket cell axons

1. Action potential-evoked [Ca2+](i) rises in basket cell axons of rat cere bellar slices were studied using two-photon laser scanning microscopy and w hole-cell recording, to identify the K+ channels controlling the shape of t he axonal action potential. 2. Whole-cell recordings of Purkinje cell IPSCs were used to screen K+ chan nel subtypes which could contribute to axonal repolarization. alpha-Dendrot oxin, 4-aminopyridine, charybdotoxin and tetraethylammonium chloride increa sed IPSC rate and/or amplitude, whereas iberiotoxin and apamin failed to af fect the IPSCs. 3. The effects of those K+ channel blockers that enhanced transmitter relea se on the [Ca2+](i) rises elicited in basket cell axons by action potential s fell into three groups: 4-aminopyridine strongly increased action potenti al-evoked [Ca2+](i); tetraethylammonium and charybdotoxin were ineffective alone but augmented the effects of 4-aminopyridine; alpha-dendrotoxin had n o effect. 4. We conclude that cerebellar basket cells contain at least three pharmaco logically distinct K+ channels, which regulate transmitter release through different mechanisms. 4-Aminopyridine-sensitive alpha-dendrotoxin-insensiti ve K+ channels are mainly responsible for repolarization in basket cell pre synaptic terminals. K+ channels blocked by charybdotoxin and tetraethylammo nium have a minor role in repolarization. alpha-Dendrotoxin-sensitive chann els are not involved in shaping the axonal action potential waveform. The t wo last types of channels must therefore exert control of synaptic activity through a pathway unrelated to axonal action potential broadening.