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 will obviously be associated with a large amount of dendritic Ca2+ influx. This hints at the possibility that whilst mAchR-induced HT bursting may perform a simple electrical pacemaker role (Lörincz et al. 2008), mGluR-induced bursting may also be associated with profound biochemical changes within the neuron, potentially leading to alterations in synaptic strength and gene expression.
