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Walton D. Jones added knockdown.tex
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\subsection*{Pan-neuronal knock-down of DmCa\textsubscript{v}3 increases sleep}
We examined whether neuronal T-type channel is responsible for increased sleep of DmCa\textsubscript{v}3 mutants.
Pan-neuronal knockdown of DmCa\textsubscript{v}3 using elav-gal4 driven DmCa\textsubscript{v}3 RNAi expression increased sleep both LD and DD, showing neuronal T-type Ca\textsuperscript{2+} channel is responsible for sleep regulation (Fig \ref{fig:5}A and B).
Knockdown of DmCa\textsubscript{v}3 with DmCa\textsubscript{v}3\textsuperscript{Gal4} driver also showed increased sleep after third day of continuous dark phase ensuring that gal4 expression of DmCa\textsubscript{v}3\textsuperscript{Gal4} represents endogenous DmCa\textsubscript{v}3 expression (Fig. \ref{fig:S4}).
Next, we wondered if any specific brain area is responsible for sleep regulating role of DmCa\textsubscript{v}3.
We knock downed DmCa\textsubscript{v}3 using broad neuronal gal4 drivers as well as specific gal4 drivers that cover previously known sleep regulating centers.
Most gal4 drivers did not increase sleep both in LD and DD, except Vglut-gal4 (Fig. \ref{fig:6}A and \ref{fig:S5}).
Knock-down of DmCa\textsubscript{v}3 driven by Vglut-gal4 increased sleep in DD (Fig. \ref{fig:6}B), suggesting glutamatergic neurons involve in DmCa\textsubscript{v}3 mediated sleep regulation.
