One example is shown in Figure 6B. Its injection site is shown by a magenta square in Figure 6A. The saccade latency bias, which was present before the

injection (Figure 6B, left), disappeared 10 min after the muscimol injection (Figure 6B, right). We repeated the same experiment (bilateral muscimol injections in the VP) four times, see more and the results were very similar (Table 1). To examine how localized the effects of muscimol injections were, we made bilateral muscimol injections at 12 sites around the VP (Table 1). The reward-dependent saccade latency bias decreased after most injections, but the effects tended to appear later than after the injections in the VP (i.e., longer latencies). We graded the effectiveness of the injection based on the latency (Sakamoto and Hikosaka, 1989): highly effective if the latency was less than 20 min and

weakly effective if the latency was more than 20 min but less than 40 min. Such effective injection sites are depicted by magenta (highly effective) and green (weakly effective) in Figure 6A. As shown in Figure 6A, the highly effective sites were centered on the VP (AC+1), but extended posteriorly into the GPe and GPi, which was 3 mm posterior to the VP (AC-2). At a more anterior level (3 mm anterior to the VP, AC+4) injections into the nucleus accumbens (NAc) had no clear effect selleckchem (n = 2). At a more posterior level (6 mm posterior to the VP, not shown) injections into the subthalamic nucleus (STN)/SNr induced oculomotor effects that prevented the monkey from making saccades to the target, such as involuntary saccades and nystagmic eye movements (Hikosaka and Wurtz, 1985). These data suggest that the effects of muscimol on the reward-dependent saccade latency bias were relatively localized in a region including the VP and possibly the GPe-GPi. Figure 6C shows the population Rolziracetam data based on muscimol injections into the effective sites (n = 11), indicating similarly devastating effects on the reward-dependent saccade latency bias. Crucially, these inactivations selectively affected the motivational

bias, without severe impairments in the sensorimotor control of saccades. If anything, inactivation caused saccade latencies to become shorter, especially on during small-reward trials for on which saccades normally had very long latencies (Figure 6D; Figure S4A). These bilateral muscimol injections also caused changes in saccade peak velocity and the stability of gaze fixation (Figure S4B and S4C). The bias in the saccade peak velocity (i.e., faster when a large reward was expected) disappeared after the injections. After the muscimol injections the monkey broke fixations more frequently before the target came on (error rate of fixation break: p < 0.01 for both small- and large-reward conditions, Wilcoxon signed-rank test). We found that VP neurons encoded the expected value associated with the upcoming action (i.e.