Control of the propagation of dendritic low‐threshold Ca 2+ 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 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.