A peculiarity of the PC dendrites is the enrichment in Ca channels (Llinás and Sugimori, 1980a,b), which include both HVA (Cav2.1) and multiple LVA (Cav3.1, Cav3.2, Cav3.3) subtypes (Ly et al., 2016). While Cav2.1 (the classical PC P-type channel) was known to regulate KCa1.1 (BK) channel activation and therefore the fast action potential AHP, the role of LVA channels remained uncertain. The present simulations show that LVA Ca channels (including at least cav3.1 and Cav3.3) are critical for BPR, since they are activated during the burst and then play a local but key role in activating the KCa2.2 (SK2) and KCa3.1 (SK4) channels, thereby regulating the pause. The relevant role of LVA calcium channels in EPSP generation by input bursts has recently been reported experimentally (Ly et al., 2016).