Also, since patients with DS exhibit a blunted ventilatory response to CO2 (i.e., central chemoreflex) (7) and a mouse model of DS identified chemosensitive neurons in the retrotrapezoid nucleus (RTN) as a potential substrate responsible for breathing problems in DS (8), we determined how genetic loss and pharmacological rescue of Scn1a function impacts baseline activity and CO2/H+ sensitivity of RTN neurons. This evidence concerns the gene SCN1A and Dravet syndrome.