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

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Abstract
To investigate the ionic mechanisms controlling the dendrosomatic propagation of low-threshold Ca2+ 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 Ca2+ 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 Ca2+ channels increased the likelihood of recording Ca2+ 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 × 10−4m) charybdotoxin (CTX, 10−5m), rIberiotoxin (10−7m), and 4-aminopyridine (4-AP, 10−3m), but not by apamin (10−4m). 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 Ca2+ 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.