Figure 6.

Programmed and experienced delays to reinforcement AcbC-lesioned rats experienced slightly longer response-delivery delays (the delay between the most recent active lever press and pellet delivery) than shams in the 20 s condition, and slightly longer response-collection delays (the delay between the most recent active lever press and pellet collection) in the 10 s and 20 s conditions. (a) Mean experienced response-delivery delays (one value calculated per subject). When the programmed delay was 0 s, reinforcers were delivered immediately so no data are shown. There was a lesion × programmed delay interaction (F1,26 = 12.0, p = .002): when the programmed delay was 10 s, the experienced delays did not differ between groups (F < 1, NS), but when the programmed delay was 20 s, AcbC-lesioned rats experienced longer response-delivery delays (one-way ANOVA, F1,13 = 19.0, ** p = .001). (b) Mean experienced response-collection delays (one value calculated per subject). There was a lesion × programmed delay interaction (F2,38 = 7.14, p = .002): AcbC-lesioned rats did not experience significantly different delays when the programmed delay was 0 s (F < 1, NS) or 10 s (F1,13 = 4.52, p = .053), but experienced significantly longer response-collection delays when the programmed delay was 20 s (F1,13 = 15.4, ** p = .002). (c) Distribution of experienced response-delivery delays. All experienced delays for a given subject were aggregated across all sessions, and the proportion falling into different 2 s ranges were calculated to give one value per range per subject; the graphs show means ± SEMs of these values. The interval notation '[a, b)' indicates that a given delay x falls in the range a x <b. There were no differences in the distribution of delays experienced by AcbC-lesioned and sham rats in the 10 s condition (lesion and lesion × range, Fs < 1, NS), but in the 20 s condition AcbC-lesioned rats experienced slightly fewer short delays and slightly more long delays (lesion × range, F2.1,27.7 = 6.60, = .213, p = .004). (d) Distribution of experienced response-collection delays, displayed in the same manner as (c). There were no differences in the distribution of delays experienced by AcbC-lesioned and sham rats in the 0 s condition (lesion and lesion × range, Fs < 1, NS). In the 10 s condition, AcbC-lesioned rats experienced a slightly higher proportion of long response-collection delays and a slightly lower proportion of short response-collection delays (lesion, F1,13 = 6.36, p = .036, though the lesion × range interaction was not significant, F2.6,34.3 = 1.74, = .139, p = .181). Similarly, in the 20 s condition, AcbC-lesioned rats experienced a slightly higher proportion of long response-collection delays and a slightly lower proportion of short response-collection delays than shams (lesion × range, F4.2,54.8 = 6.65, = .222, p < .001).

Cardinal and Cheung BMC Neuroscience 2005 6:9   doi:10.1186/1471-2202-6-9
Download authors' original image