Prominent spike ADPs similar to those observed during mAChR-induced HT bursting are also a common feature of rhythmic bursting in several other types of neurons. For example, such events play a central role in repetitive bursting at 40–80 Hz in pyramidal cells of the electrosensory lateral line lobe of the weakly electric fish, an activity which, interestingly, is blocked by selectively applying TTX to the proximal apical dendritic region (Lemon and Turner 2000). Similarly, spike ADPs are an important determinant of the so-called chattering or fast rhythmic bursting (FRB) activity which occurs at 20–80 Hz, is present in a subset of layer II/III neocortical pyramidal neurons (Gray and McCormick 1996; Brumberg et al. 2000) and which, again, is highly sensitive to an inhibition of Na+ channels (Brumberg et al. 2000). With regard to FRB, it appears that persistent rather than transient Na+ channels are the key component in generating ADPs because potentiating these channels by applying either the Na+ channel toxin, ATX II (Brumberg et al. 2000), or the NO donor, S-nitroso-N-acetylpenicillamine (SNAP) (Traub et al. 2003), can transform regular
