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These burst spikes then stimulate the nRT neurons to generate low-threshold burst spikes attributable to Ca\textsubscript{v}3.2/Ca\textsubscript{v}3.3 activation.  Bursting in the nRT then sends another inhibitory hyperpolarization through the TC neurons, completing the oscillatory cycle.  These oscillations spread through the cortex via the cortical connections of the TC neurons leading to the familiar slow wave patterns that chracterize the NREM sleep state. \textcolor{red}{Citation for this theory?}  Consistent with this model, mice lacking Ca\textsubscript{v}3.1 lack slow wave oscillations and show reduced and unstable sleep\cite{Lee:2004ey}. \textcolor{red}{What about the role of the other two channels in the nRT? No citations for that?}  On the other hand, some studies have suggested that T-type Ca\textsuperscript{2+} channels are able to be associated with the wake-promoting mechanism as following.  In wake-up call hypothesis, the low-threshold burst spikes depending on activation of T-type Ca\textsuperscript{2+} channel has a strong post-synaptic impact and thereby stimulating the cortex efficiently\cite{swadlow:2001aa}, which may help the sensation or attention to specific sensory stimuli at the cortex.