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. 1996 Sep 15;495(Pt 3):641–647. doi: 10.1113/jphysiol.1996.sp021622

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

G Callewaert 1, J Eilers 1, A Konnerth 1
PMCID: PMC1160771  PMID: 8887772

Abstract

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.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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