Figure 6. The CSDn does not modulate DA1 odor responses.
(A) DA1 odor responses to cVA with chronic optogenetic stimulation of the CSDn (CSDn-Gal4 > UAS-Chrimson) in saline (red circles) and methysergide (black circles). The CSDn was continuously activated with a 10 Hz sine wave at 660 nm. The sinewave was intrupted temporarily to test DA1 responses to cVA. (B) PSTH showing DA1 spiking response to cVA before (magenta) and during (green) CSDn stimulation in saline. (C) Summary statistics for data in A and B. DA1 responses to cVA were not statistically modulated by optogentically driven CSDn activity. Period 1 vs Period 2 in saline. n = 7, p=0.307. DA1 odor responses also did not change with CSDn stimulation in methysergide. n = 6, p=0.138. (D) DA1 odor responses were sampled at 80 s intervals and the CSDn was stimulated with pulses of ammonia every 10 s (red circles). Ammonia was not presented simultaneoulsy with cVA to avoid fast lateral inhibition and excitation. DA1 resonses to cVA were stable in the absense of intermittent ammonia stimulation (black circles). Period 1 represents timeframe before ammonia stimulation in experimental group and Period 2 represents time frame during ammonia stimulation. (E) PSTH showing DA1 spiking response to cVA before (magenta) and during (green) ammonia presentation. (F) Summary statistics for data in D and E. DA1 responses to cVA were not statistically modulated by ammonia driven CSDn activity. n = 7, Period 1 vs Period 2 with NH3 presentation. p=0.976, paired t-test. DA1 odor responses also did not change without ammonia stimulation. n = 6, p=0.105, paired t-test.