Chunk #13 — Activation of metabotropic glutamate receptors (mGluRs) or muscarinic Ach receptors (mAchRs) induces rhythmic bursting at α/θ frequencies in TC neurons
Following application of the Na+ channel blocker tetrodotoxin (TTX) to block action potentials, mGluR-induced HT bursting is replaced by a residual oscillation comprising rhythmic dendritic Ca2+ spikes (Fig. 1C) (Jahnsen and Llinás 1984; Williams and Stuart 2000; Hughes et al. 2004), indicating that these events are the primary driving force behind burst activity (Hughes et al. 2004). Indeed, dendritic Ca2+ spikes can be regularly observed in HT bursting cells even before TTX treatment (Fig. 1C) whilst a blockade of Ca2+ channels with Ni2+ converts HT bursting into regular tonic firing (Hughes et al. 2004; Crunelli et al. 2006). Because the mGluR subtype that is responsible for inducing HT bursting (i.e. mGluR1a; (Hughes et al. 2004) is located at distal sites on TC neurons (Godwin et al. 1996; Erisir et al. 1997b) and thought to be negatively coupled to leak K+ channels (von Krosigk et al. 1999; Turner and Salt 2000; Hughes et al. 2002), it is reasonable to assume that mGluR-dependent HT bursting is reliant on a strong suppression of dendritic K+ conductance which in turn facilitates the generation of
