The finding that an inhibition of BK channels leads to rhythmic bursting at ~40 Hz in TC neurons in vitro is noteworthy because previous in vivo studies utilising single unit extracellular recordings have shown that, during both natural wakefulness and REM sleep, a subset of TC neurons in the cat CL nucleus exhibit rhythmic bursting at ~40 Hz with similar properties to those described here (Steriade and Glenn 1982; Steriade et al. 1993). Indeed, intracellular recordings of these cells obtained during barbiturate anaesthesia revealed that this type of bursting is intrinsic and involves a clear spike ADP which bears a striking resemblance to that seen in our in vitro recordings (Steriade et al. 1993). The additional lack of prominent spike AHP and narrow action potential width in these CL TC neurons led the investigators to speculate that their unusual behaviour arose from a combination of reduced Ca2+-activated K+ current and increased Na+ conductance, a suggestion which, again, is fully in line with our in vitro data. Mirroring these findings from the CL thalamus, we have recently noted that some TC
