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 spiking (RS) layer II/III neurons into FRB cells, with this transformation being reversed by the putative persistent Na+ channel blocker, phenytoin (Traub et al. 2003). More specifically, it appears that a delicate balance between afterhyperpolarization (AHP)-generating currents and persistent Na+ channels is what determines the mode of firing in these cells because both experimental and modelling studies show that a transformation from RS to FRB behaviour can also be readily achieved by blocking large conductance Ca2+-activated (BK) K+ channels with iberiotoxin (Ibtx) (Traub et al. 2003).
