K_v7 (KCNQ) channel subunits are widely expressed in peripheral and central neurons, where they give rise to a muscarinic-sensitive, subthreshold and noninactivating K⁺ current (M-current). Until recently it was thought that M-current contributes to spike frequency adaptation during sustained depolarisations, but is too slow to influence the repolarisation of solitary spikes. This concept, however, was based mainly on experiments with muscarinic agonists, whose multiple effects on membrane conductances may overshadow the distinctive effects of M-current block. Using more selective blockers of K_v7 channels (linopirdine and XE991) we have recently shown that M-current plays a crucial role in spike termination in principal cortical neurons, such as CA1 and CA3 pyramidal cells. A solitary spike in these neurons is followed by a distinct, albeit subthreshold, spike afterdepolarisation (ADP). Blocking M-current generated by perisomatic K_v7 channels greatly facilitates the spike ADP beyond spike threshold, thereby converting solitary ('simple') spikes to high-frequency bursts of 3-7 spikes ('complex' spikes). This dramatic effect is not seen when other K⁺ currents are selectively blocked. Thus, perisomatic K_v7 channels normally down-regulate the spike ADP and limit its duration, thereby precluding its escalation to a spike burst. Intriguingly this action is strongly modulated by intracellular Ca²⁺, which can facilitate the spike ADP and induce bursting by inhibiting K_v7 channel activity.