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Control of the propagation of dendritic low-threshold Ca2+ spikes in Purkinje cells from rat cerebellar slice cultures

To investigate the ionic mechanisms controlling the dendrosomatic propagation of low-threshold Ca 2+ spikes (LTS) in Purkinje cells (PCs), somatically evoked discharges of action potentials (APs) were recorded under current-clamp conditions. The whole-cell configuration of the patch-clamp method was...

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Bibliographic Details
Published in:The Journal of physiology 2002-04, Vol.540 (1), p.57-72
Main Authors: Cavelier, Pauline, Pouille, Frederic, Desplantez, Thomas, Beekenkamp, Huguette, Bossu, Jean‐Louis
Format: Article
Language:English
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Summary:To investigate the ionic mechanisms controlling the dendrosomatic propagation of low-threshold Ca 2+ spikes (LTS) in Purkinje cells (PCs), somatically evoked discharges of action potentials (APs) were recorded under current-clamp conditions. The whole-cell configuration of the patch-clamp method was used in PCs from rat cerebellar slice cultures. Full blockade of the P/Q-type Ca 2+ current revealed slow but transient depolarizations associated with bursts of fast Na + APs. These can occur as a single isolated event at the onset of current injection, or repetitively (i.e. a slow complex burst). The initial transient depolarization was identified as an LTS Blockade of P/Q-type Ca 2+ channels increased the likelihood of recording Ca 2+ spikes at the soma by promoting dendrosomatic propagation. Slow rhythmic depolarizations shared several properties with the LTS (kinetics, activation/inactivation, calcium dependency and dendritic origin), suggesting that they correspond to repetitively activated dendritic LTS, which reach the soma when P/Q channels are blocked. Somatic LTS and slow complex burst activity were also induced by K + channel blockers such as TEA (2.5 × 10 −4 m ) charybdotoxin (CTX, 10 −5 m ), rIberiotoxin (10 −7 m ), and 4-aminopyridine (4-AP, 10 −3 m ), but not by apamin (10 −4 m ). In the presence of 4-AP, slow complex burst activity occurred even at hyperpolarized potentials (−80 mV). In conclusion, we suggest that the propagation of dendritic LTS is controlled directly by 4-AP-sensitive K + channels, and indirectly modulated by activation of calcium-activated K + (BK) channels via P/Q-mediated Ca 2+ entry. The slow complex burst resembles strikingly the complex spike elicited by climbing fibre stimulation, and we therefore propose, as a hypothesis, that dendrosomatic propagation of the LTS could underlie the complex spike.
ISSN:0022-3751
1469-7793
DOI:10.1113/jphysiol.2001.013294