Given that TC neurons have the clear capacity to generate Na+ channel-dependent spike ADPs and that a high immunoreactivity specifically for BK channels is present in the dorsal thalamus of the rodent brain (Sausbier et al. 2006), we recently tested whether application of Ibtx to TC neurons of the LGN maintained in vitro could induce FRB. In doing so, we found that Ibtx, applied at 100 nM, was able to consistently and reversibly induce FRB at 20–60 Hz in all TC neurons tested (Fig 4A). Furthermore, as with layer II/III neocortical cells, this type of activity involved a clear spike ADP (Fig 4B) and was preferentially blocked by TTX, being abolished well before a full block of action potentials was achieved (Fig 5). Interestingly, we have found that manipulations which reduce the supply of intracellular Ca2+, either by decreasing [Ca2+]o to 0 mM or chelating intracellular Ca2+ with EGTA or BAPTA (Fig 4C), are also able to induce FRB-like behaviour in TC neurons, in a similar way to that predicted by simulation studies to occur for cortical pyramidal neurons (Traub
