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Axonal calcium entry during fast ‘sodium’ action potentials in rat cerebellar Purkinje neurones.
Author(s) -
Callewaert G,
Eilers J,
Konnerth A
Publication year - 1996
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1996.sp021622
Subject(s) - neuroscience , axon , biophysics , electrophysiology , chemistry , calcium , voltage dependent calcium channel , sodium channel , biology , sodium , organic chemistry
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.