Axonal calcium entry during fast 'sodium' action potentials in rat cerebellar Purkinje neurones

1. Using laser-scanning confocal microscopy, fast Ca²⁺ transients were recorded in individual not yet myelinated axons of Purkinje neurones in cerebellar slices from young rats. Axonal Ca²⁺ transients could be detected during a single action potential and had progressively larger amplitudes when the number of action potentials was increased. 2. Under voltage-clamp conditions, axonal Ca²⁺ transients were as large as those observed in dendrites and in the cell body. Axonal Ca²⁺ transients were completely blocked by 100 nM of the neurotoxin ω-agatoxin IVA, indicating that they were caused by Ca²⁺ entry through P-type voltage-gated Ca²⁺ channels. 3. In conclusion, our results demonstrate action potential-mediated Ca²⁺ entry through voltage-gated Ca²⁺ channels in axons of cerebellar Purkinje neurones. Experimental evidence indicates that the resulting transient Ca²⁺ accumulations regulate the frequency of action potentials travelling along the axon.