The ionic nature of the mechanism was confirmed by specific manipulations of the Ca/KCa ionic mechanisms. When either dendritic KCa conductances or Ca conductances were set to zero, the BPR was altered with a marginal reduction of burst duration (from 0% to −16.7%) but a much more dramatic reduction of the pause (from −20% to −80%) (Figure 3B). It should be noted that all Ca channels proved critical for BPR, especially Cav2.1 and Cav3.1 (Cav3.2 switch-off blocked pacemaking; Masoli et al., 2015) as well as all KCa channels, including KCa1.1, KCa2.2, KCa3.1.