01). However, rather than being maintained in subsequent compound sessions, as would be expected selleck chemicals if it were a sensory phenomenon, the ratio gradually decreased (Figure 3K; ANOVA, p < 0.01), returning to near unity

by the last compound session. After compound training, the rats were trained in an extinction probe session (PB in Figure 1A). This single session consisted of additional compound training (PB 1/2) followed by extinction training, in which A1 and the other auditory cues were presented alone and unreinforced. During the compound training, the rats continued to exhibit elevated responding to the cues predictive of reward (PB 1/2 in Figure 4A); at this point, responding to A1/V and A2 did not differ statistically (ANOVA, F(1,27) = 0.33; p = 0.57). However, when A1 was separated from V at the start of extinction, rats showed a sudden and selective decline in responding to A1, which persisted throughout extinction (Figure 4A). A two-factor ANOVA (cue X trial) comparing conditioned responding to the cues during extinction revealed significant main effects check details of cue (F(2,54) = 114.7; p < 0.01) and trial (F(7,189) = 37.8; p < 0.01), and a significant interaction (F(14,378) = 12.3; p < 0.01). Post-hoc comparisons revealed significantly less responding to A1 than A2 (F(1,27) = 93.6; p < 0.01). We

recorded 140 neurons in these extinction probe sessions, 61 of which exhibited an excitatory phasic response

Parvulin to at least one of the cues. Firing in response to A1/V and A2 in these neurons was similar during the compound phase (PB 1/2, Figures 4B and 4C), but then spontaneously declined to A1, but not A2, at the start of extinction training (PB 1T; Figures 4B and 4C). A two-factor ANOVA comparing average firing to A1 and A2 (cue X phase) revealed significant main effects of both cue (F(1,60) = 9.95; p < 0.01) and phase (F(1,60) = 20.5; p < 0.01), and a significant interaction between them (F(1,60) = 27.1; p < 0.01; Figure 4C). Direct comparisons revealed a significant reduction of firing on the first trial of the probe phase compared to firing in the compound phase for A1 (F(1,60) = 51.9; p < 0.01), but not for A2 (F(1,60) = 0.26; p = 0.61). Similar effects were evident in the distribution of index scores comparing firing of each neuron to A1 and A2 at the end of compound training versus the first trial in extinction. The distribution of these scores was shifted significantly below zero for A1 (Figure 4D; Wilcoxon signed-rank test, p < 0.01), but not for A2 (Figure 4E; p = 0.97), and the distribution of these scores differed significantly between A1 and A2 (Mann-Whitney U test, p < 0.01). Interestingly, firing to A1/V at the end of compound training remained larger than the sum of the activity to the two individual cues presented at that same time (Figure 4F; p < 0.01).