e., more active with larger reward) and negative type neurons (i.e., more active with smaller reward). The positive VP neurons, specifically, seem to represent the worthiness of an action by combining expected values and expected costs. Such sustained activity would be highly useful for the sensorimotor system because it could directly modulate the preparatory processes of the goal-directed action. In fact, the activity of VP neurons during the period preceding a saccade

was well associated with the latency and velocity of the saccade, as the saccade performance changed across blocks of trials due to changes in reward amount. These data raised the possibility that the VP neuronal activity is used for modulating impending motor actions based on expected reward values, in addition to learning the value of behavioral find protocol context. If so, the removal of the VP

neuronal signals should reduce the reward-based modulation of motor actions. To test this prediction, we reversibly inactivated the VP and tested its effects on reward-oriented behavior. Bilateral VP inactivation had little effect on the basic sensorimotor processes underlying saccadic eye movements, Angiogenesis inhibitor but caused a rapid and dramatic deficit in reward-based biases in saccade initiation. Furthermore, unilateral inactivations of the VP had little effect, suggesting that the VP on both sides conjointly contributes to the reward expectation-dependent modulation of motor actions. Notably, the bilateral VP inactivation led to shortening of saccade latencies on small-reward trials while the saccade latencies on large-reward trials remained short. However, this may seem odd since a majority of reward-related VP neurons were positive type, and blocking their activity may be expected to dampen the initiation of saccades on large-reward trials. We propose two mechanisms that, together, might explain this Mephenoxalone phenomenon. First, reward negative VP neurons, though a minority,

might exert comparatively strong behavioral effects, suppressing the initiation of saccades on small-reward trials. If so, blocking their activity would remove the suppressive effect on small-reward trials. However, this mechanism alone may not explain our results, because the response of VP neurons was bidirectional. On large-reward trials, the negative VP neurons were inhibited and therefore saccades would be facilitated (i.e., disinhibited). Blocking this effect would remove the facilitatory effect, leading to an increase in saccade latency. Such an effect was not observed clearly. However, the above argument is focused on the reward-biased phasic responses of VP neurons. Actually, a majority of VP neurons fire tonically, and this may act as a second mechanism. Thus, VP neurons might exert general inhibitory effects on the target motor areas in addition to the reward-biased phasic effect. The inactivation of VP neurons would then lead to a removal of the inhibitory effects, thus causing general shortening of saccade latencies.