A possible explanation for the distinction between mGluR- and mAchR-induced HT bursting relates to the differential distribution of these receptors on the somatodendritic axis of TC neurons (Fig. 3). mAchRs are located at relatively proximal sites (Erisir et al. 1997a,b) and their domain of influence may therefore not extend to the more distal regions where Ca2+ spike generation occurs (Jahnsen and Llinás 1984). On the other hand, they are ideally situated to modulate proximal Na+ channel-dependent events (Williams and Stuart 2000) explaining the appearance of a large spike ADP following Cch application. In contrast to mAchRs, and as mentioned above, mGluRs are a located more distally in a position that is presumably close to the dendritic Ca2+ spike generating machinery. However, because the domain of influence of mGluRs extends to the soma (von Krosigk et al. 1999; Turner and Salt 2000; Hughes et al. 2002), activation of these receptors can also affect proximal Na+ channel-dependent events, albeit to a lesser extent than mAchR activation. One interesting aspect of the difference between mGluR- and mAchR-induced HT bursting is that the former
