No correlation analyses were performed www.selleckchem.com/products/NVP-AUY922.html on the group
of putative interneurons due to the small sample size. To determine the impact of cue-dependent activation of GC on the time course of responses to ExpT, population activity induced by ExpT and UT in putative pyramidal neurons (Figure 6A, gray line and black line, respectively) was compared using PCA. The product of this analysis (Figures 6A–6C) shows that early differences in the response result from the first bin of activity to ExpT (1 gray) moving closer to the second bin evoked by UT (i.e., the time at which taste coding begins; 2 black). The same visualization applied to each tastant (Figure 6B) confirms that the result from the average is general to all stimuli. Responses to ExpT and UT begin to realign 250 ms after delivery of the tastant (Figures 6A–6C). The running correlation between the first bin of responses to ExpT and the time course of responses to UT confirms the results
obtained with PCA (Figure 6D) by showing a broad peak of correlation that similarly involves the first (0–125 ms) and the second Olaparib clinical trial (125–250 ms) bin of the responses to UT (0.74 ± 0.01 and 0.72 ± 0.01, respectively, p = 0.22, n = 28). Figure 6E portrays an example of early responses to ExpT resembling later responses to UT. Figure 6 was obtained analyzing the same population of neurons used for Figure 5 (i.e., putative pyramidal Ketanserin neurons, n = 40). Analyses of the
entire population of nonsomatosensory cue-responsive neurons (n = 58; Figure S6) yielded qualitatively similar results. Differences in responses to UT and ExpT could be related to changes in oro-motor activity induced by expectation. To address this issue, an analysis of mouth movements triggered by cues, UT, and ExpT was performed. Blind visual inspection and automated image analysis of the oral region were performed for each frame to extract the timing of isolated and rhythmic mouth movements (see Experimental Procedures and Figure S7). Auditory cues produced small mouth movements with an average latency of 189 ± 30 ms (n = 10) and a magnitude that was only 21.4% ± 6.5% of the amplitude of taste-induced movements. Automated analysis as well as blind visual inspection of video records revealed that cue-evoked mouth movements did not initiate rhythmic mouth movements, which were only evoked by the tastant. The representative single-trial and trial-averaged traces from Figure S7 confirm this assessment. The average mouth movement recorded for ExpT revealed only a small ramp before self-administration, which is likely the result of cue-evoked movements. The amplitude of the mouth movements prior to self-administration is only 12.8% ± 4.7% of that evoked by ExpT. Tastants, on the other hand, evoked large, rhythmic, and long-lasting movements.
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