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 omega‐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.