Incentive Cues Research Articles

Bupropion increases activation in nucleus accumbens during anticipation of monetary reward.

Bupropion is used for major depressive disorder, smoking cessation aid, and obesity. It blocks reuptake of dopamine and noradrenaline and antagonizes nicotinic acetylcholine receptor. Animal studies showed that bupropion enhanced rewarding effects. In addition, bupropion has the potential to treat patients with reward processing dysfunction. However, neural substrates underlying the bupropion effects on reward function in human subjects are not fully understood. We investigated single-dose administration of bupropion on neural response of reward anticipation in healthy subjects using a monetary incentive delay (MID) task by functional magnetic resonance imaging (fMRI), especially focusing on nucleus accumbens (NAc) activity to non-drug reward stimuli under bupropion treatment. We used a randomized placebo-controlled within-subject crossover design. Fifteen healthy adults participated in two series of an fMRI study, taking either placebo or bupropion. The participants performed the MID task during the fMRI scanning. The effects of bupropion on behavioral performance and blood oxygenation level-dependent (BOLD) signal in NAc during anticipation of monetary gain were analyzed. We found that bupropion significantly increased BOLD responses in NAc during monetary reward anticipation. The increased BOLD responses in NAc were observed with both low and high reward incentive cues. There was no significant difference between placebo and bupropion in behavioral performance. Our findings provide support for the notion that bupropion enhances non-drug rewarding effects, suggesting a possible mechanism underlying therapeutic effects for patients with motivational deficit.

Brain responses to anticipating and receiving beer: Comparing light, at-risk, and dependent alcohol users.

Impaired brain processing of alcohol‐related rewards has been suggested to play a central role in alcohol use disorder. Yet, evidence remains inconsistent and mainly originates from studies in which participants passively observe alcohol cues or taste alcohol. Here, we designed a protocol in which beer consumption was predicted by incentive cues and contingent on instrumental action closer to real life situations. We predicted that anticipating and receiving beer (compared with water) would elicit activity in the brain reward network and that this activity would correlate with drinking level across participants.The sample consisted of 150 beer‐drinking males, aged 18 to 25 years. Three groups were defined based on alcohol use disorders identification test (AUDIT) scores: light drinkers (n = 39), at‐risk drinkers (n = 64), and dependent drinkers (n = 47). fMRI measures were obtained while participants engaged in the beer incentive delay task involving beer‐ and water‐predicting cues followed by real sips of beer or water.During anticipation, outcome notification and delivery of beer compared with water, higher activity was found in a reward‐related brain network including the dorsal medial prefrontal cortex, orbitofrontal cortex, and amygdala. Yet, no activity was observed in the striatum, and no differences were found between the groups.Our results reveal that anticipating, obtaining, and tasting beer activates parts of the brain reward network, but that these brain responses do not differentiate between different drinking levels.

Biasing Actions by Incentive Valence in an Approach/Avoidance Task

The present study investigates interactions between incentive valence and action, which mirror well-known valence-action biases in the emotional domain. In three joystick experiments, incentive valence (win/loss) and action type (approach/avoid) were signaled by distinct orthogonal stimulus features. By combining several design aspects, i.e., the use of bi-directional joystick movements, the inclusion of no-incentive baseline trials, and cue-locked versus target-locked valence and action signals, we tried to bridge between paradigms used in the emotional and motivational domain, and to understand previous, partly inconsistent results. In the first task variant (Experiment 1), we observed performance benefits for compatible mappings (win-approach; loss-avoid) relative to incompatible ones (loss-approach; win-avoid) when valence and action signals were target-locked, consistent with a fairly automatic response activation that can benefit or impair task performance. In contrast, cue-locked valence signals led to response facilitation (relative to a no-incentive baseline) more or less independent of actual valence (win/loss) and action type (approach/avoid), which is reminiscent of general facilitation effects of incentive cues across diverse cognitive tasks. Slight design variations did not change this main result pattern, indicating that it was neither driven by the close proximity between target and performance feedback (Experiment 2), nor by mere temporal coincidence of valence and action signals (Experiment 3), but rather by differences between preparatory (cued) and immediate (non-cued) effects of incentive valence. The present study provides novel insights regarding the nature of valence-action biases in the motivational domain and helps to integrate previous, partly inconsistent findings across domains.

Differential modulations of reward expectation on implicit facial emotion processing: ERP evidence.

Implicit emotional processing refers to the preferential processing of emotional content even if it is task irrelevant. Given that motivation enhances executive control by biasing attentional resources toward target stimuli, here we investigated the effects of reward expectation on implicit facial emotional processing in two experiments using ERPs. A precue signaling additional monetary reward for fast and accurate response for the upcoming trial (incentive condition; relative to a cue indicating no such additional reward, i.e., nonincentive condition) was followed by the presentation of a happy, angry, or neutral face. Participants had to determine the gender of the face in Experiment 1 and decide whether a number superimposed on the face was even or odd in Experiment 2. In both experiments, incentive cues elicited larger P3 and contingent negative variation responses, and the targets following incentive cues elicited more positive-going ERPs (200-700ms), compared with the nonincentive condition. Importantly, the N2 responses (200-280ms) to the target exhibited differential patterns of Reward × Emotion interaction: relative to the nonincentive condition, the N2 amplitude differences between emotional (i.e., happy and/or angry) and neutral faces increased in the incentive condition in Experiment 1, but diminished in Experiment 2. These results indicate that reward expectation can differentially modulate implicit processing of facial expressions, with increased sensitivity to emotions when the processing of whole faces is required, but with reduced sensitivity when the processing of faces is distractive. This study enriches the evidence for interactions between reward-related executive control and implicit emotional processing.

Haste or Speed? Alterations in the Impact of Incentive Cues on Task Performance in Remitted and Depressed Patients With Bipolar Disorder.

A variety of evidence suggests that bipolar disorder is associated with disruptions of reward related processes, although the properties, and scope of these changes are not well understood. In the present study, we aimed to address this question by examining performance of patients with bipolar disorder (30 depressed bipolar; 35 euthymic bipolar) on a motivated choice reaction time task. We compared performance with a group of healthy control individuals (n = 44) and a group of patients with unipolar depression (n = 41), who were matched on several demographic variables. The task consists of an “odd-one-out” discrimination, in the presence of a cue signaling the probability of reward on a given trial (10, 50, or 90%) given a sufficiently fast response. All groups showed similar reaction time (RT) performance, and similar shortening of RT following the presentation of a reward predictive cue. However, compared to healthy individuals, the euthymic bipolar group showed a relative increase in commission errors during the high reward compared to low condition. Further correlational analysis revealed that in the healthy control and unipolar depression groups, participants tended either to shorten RTs for the high rather than low reward cue a relatively large amount with an increase in error rate, or to shorten RTs to a lesser extent but without increasing errors to the same degree. By contrast, reward-related speeding and reward-related increase in errors were less well coupled in the bipolar groups, significantly so in the BPD group. These findings suggest that although RT performance on the present task is relatively well matched, there may be a specific failure of individuals with bipolar disorder to calibrate RT speed and accuracy in a strategic way in the presence of reward-related stimuli.

Age differences in the neural response to negative feedback

ABSTRACTAffective processing is one domain that remains relatively intact in healthy aging. Investigations into the neural responses associated with reward anticipation have revealed that older and younger adults recruit the same midbrain reward regions, but other evidence suggests this recruitment may differ depending on the valence (gain, loss) of the incentive cue. The goal of the current study was to examine functional covariance during gain and loss feedback in younger and healthy older adults. A group of 15 older adults (mean age = 68.5) and 16 younger adults (mean age = 25.4) completed a revised Monetary Incentive Delay task (rMID; Knutson, Westdorp, Kaiser, & Hommer, 2000) while in the fMRI scanner. The rMID is a reaction time task where successful performance, either gaining a reward or avoiding a loss, is defined by hitting a button during the brief presentation of a visual target. Participants receive gain and loss anticipation cues before each trial and feedback after each trial with four possible outcomes: +$5.00, +0.00, -$5.00, and -$0.00. Using seed-voxel partial least squares analyses, with seed voxels in the caudate and ventromedial prefrontal cortex, whole-brain functional covariance revealed that younger and older adults engage the same network of regions to support general feedback processing. However, older adults engaged two additional networks to support processing of negative feedback, gain_miss (+0), loss_miss (-$5), and loss_hit (−0), specifically. These findings are in line with theories of a positivity effect in aging and may have implications for reward-stimulus learning and decision making following performance-contingent negative feedback.

Ventral pallidal encoding of reward-seeking behavior depends on the underlying associative structure.

Despite its being historically conceptualized as a motor expression site, emerging evidence suggests the ventral pallidum (VP) plays a more active role in integrating information to generate motivation. Here, we investigated whether rat VP cue responses would encode and contribute similarly to the vigor of reward-seeking behaviors trained under Pavlovian versus instrumental contingencies, when these behavioral responses consist of superficially similar locomotor response patterns but may reflect distinct underlying decision-making processes. We find that cue-elicited activity in many VP neurons predicts the latency of instrumental reward seeking, but not of Pavlovian response latency. Further, disruption of VP signaling increases the latency of instrumental but not Pavlovian reward seeking. This suggests that VP encoding of and contributions to response vigor are specific to the ability of incentive cues to invigorate reward-seeking behaviors upon which reward delivery is contingent.

Transient and sustained incentive effects on electrophysiological indices of cognitive control in younger and older adults.

Preparing for upcoming events, separating task-relevant from task-irrelevant information and efficiently responding to stimuli all require cognitive control. The adaptive recruitment of cognitive control depends on activity in the dopaminergic reward system as well as the frontoparietal control network. In healthy aging, dopaminergic neuromodulation is reduced, resulting in altered incentive-based recruitment of control mechanisms. In the present study, younger adults (18-28 years) and healthy older adults (66-89 years) completed an incentivized flanker task that included gain, loss, and neutral trials. Event-related potentials (ERPs) were recorded at the time of incentive cue and target presentation. We examined the contingent negative variation (CNV), implicated in stimulus anticipation and response preparation, as well as the P3, which is involved in the evaluation of visual stimuli. Both younger and older adults showed transient incentive-based modulation of CNV. Critically, cue-locked and target-locked P3s were influenced by transient and sustained effects of incentives in younger adults, while such modulation was limited to a sustained effect of gain incentives on cue-P3 in older adults. Overall, these findings are in line with an age-related reduction in the flexible recruitment of preparatory and target-related cognitive control processes in the presence of motivational incentives.

Incentives facilitate developmental improvement in inhibitory control by modulating control-related networks

Adolescence is a period of heightened sensitivity to incentives and relatively weak cognitive control, which may contribute to risky behaviors. Studies of brain activity have generally identified greater activation of the ventral striatum to rewards and less activation of prefrontal regions during control tasks in adolescents compared to adults. Little is known, however, about age-related changes in the functional brain networks underlying incentive processing and cognitive control. This cross-sectional study characterized the effects of incentives on inhibitory control during an oculomotor task using whole-brain functional connectivity analyses. During an fMRI scan, one hundred forty typically developing individuals completed an incentivized antisaccade task consisting of incentive cue, preparation, and response phases. We found that task modulation of control networks increased gradually from childhood to adulthood, whereas a network including ventral striatum and ventromedial prefrontal cortex displayed an adolescent-specific peak in response to the receipt of outcomes, consistent with dual-systems models. Notably, however, greater modulation of salience and motor networks during the preparation phase mediated age-related improvements in antisaccade accuracy, whereas adolescent enhancement of value-related circuitry did not. Relative to neutral cues, both reward and loss cues enhanced task-related connectivity of the salience network when preparing to inhibit a saccade. Altogether, our findings suggest that incentives facilitate inhibitory control by enhancing the salience of one's responses and that over development, the recruitment of functional networks involved in saliency and motor preparation supports better performance.

Interactions between incentive valence and action information in a cued approach–avoidance task

Environmental stimuli can provoke specific response tendencies depending on their incentive valence. While some studies report positive-approach and negative-avoidance biases, others find no such mappings. To further illuminate the relationship between incentive valence and action requirement, we combined a cued monetary incentive paradigm with an approach/avoidance joystick task. Incentive type was manipulated between groups: The reward group won money, while the punishment group avoided losing money for correct and fast responses to targets following incentive cues. Depending on their orientations, targets had to be 'approached' or 'avoided'. Importantly, incentive valence (signaled by cue color) was orthogonal to action requirement (target orientation). Moreover, targets could carry valence-associated information or not (target color), which was, however, task-irrelevant. First, we observed that both valence cues (reward/punishment) improved performance compared to neutral cues, independent of the required action (approach/avoid), suggesting that advance valence cues do not necessarily produce specific action biases. Second, task-irrelevant valence associations with targets promoted action biases, with valence-associated targets facilitating approach and impairing avoid responses. Importantly, this approach bias for valence-associated targets was observed in both groups and hence occurred independently of absolute valence ('unsigned'). This rather unexpected finding might be related to the absence of a direct contrast between positive valence and negative valence within groups and the common goal to respond fast and accurately in all incentive trials. Together, our results seem to challenge the notion that monetary incentives trigger 'hard-wired' valence-action biases in that specific design choices seem to modulate the presence and/or direction of valence-action biases.

Does the Effort of Processing Potential Incentives Influence the Adaption of Context Updating in Older Adults?

A number of aging studies suggest that older adults process positive and negative information differently. For instance, the socioemotional selectivity theory postulates that older adults preferably process positive information in service of emotional well-being (Reed and Carstensen, 2012). Moreover, recent research has started to investigate whether incentives like gains or losses can influence cognitive control in an ongoing task. In an earlier study (Schmitt et al., 2015), we examined whether incentive cues, indicating potential monetary gains, losses, or neutral outcomes for good performance in the following trial, would influence older adults’ ability to exert cognitive control. Cognitive control was measured in an AX-Continuous-Performance-Task (AX-CPT) in which participants had to select their responses to probe stimuli depending on a preceding context cue. In this study, we did not find support for a positivity effect in older adults, but both gains and losses led to enhanced context processing. As the trial-wise presentation mode may be too demanding on cognitive resources for such a bias to occur, the main goal of the present study was to examine whether motivational mindsets, induced by block-wise presentation of incentives, would result in a positivity effect. For this reason, we examined 17 older participants (65–76 years) in the AX-CPT using a block-wise presentation of incentive cues and compared them to 18 older adults (69–78 years) with the trial-wise presentation mode from our earlier study (Schmitt et al., 2015). Event-related potentials were recorded to the onset of the motivational cue and during the AX-CPT. Our results show that (a) older adults initially process cues signaling potential losses more strongly, but later during the AX-CPT invest more cognitive resources in preparatory processes like context updating in conditions with potential gains, and (b) block-wise and trial-wise presentation of incentive cues differentially influenced cognitive control. When incentives were presented block-wise, the above described valence effects were consistently found. In contrast, when incentives were presented trial-wise, the effects were mixed and salience as well as valence effects can be obtained. Hence, how positive and negative incentive cues influence cognitive control in older adults is dependent on demands of cue processing.

Electrocortical components of anticipation and consumption in a monetary incentive delay task.

In order to improve our understanding of the components that reflect functionally important processes during reward anticipation and consumption, we used principle components analyses (PCA) to separate and quantify averaged ERP data obtained from each stage of a modified monetary incentive delay (MID) task. Although a small number of recent ERP studies have reported that reward and loss cues potentiate ERPs during anticipation, action preparation, and consummatory stages of reward processing, these findings are inconsistent due to temporal and spatial overlap between the relevant electrophysiological components. Our results show three components following cue presentation are sensitive to incentive cues (N1, P3a, P3b). In contrast to previous research, reward-related enhancement occurred only in the P3b, with earlier components more sensitive to break-even and loss cues. During feedback anticipation, we observed a lateralized centroparietal negativity that was sensitive to response hand but not cue type. We also show that use of PCA on ERPs reflecting reward consumption successfully separates the reward positivity from the independently modulated feedback-P3. Last, we observe for the first time a new reward consumption component: a late negativity distributed over the left frontal pole. This component appears to be sensitive to response hand, especially in the context of monetary gain. These results illustrate that the time course and sensitivities of electrophysiological activity that follows incentive cues do not follow a simple heuristic in which reward incentive cues produce enhanced activity at all stages and substages.

Chronic Nicotine Alters Corticostriatal Plasticity in the Striatopallidal Pathway Mediated By NR2B-Containing Silent Synapses.

Smoking is the leading cause of preventable death in the United States and success rates for quitting remain low. High relapse rates are attributed to pervasive nicotine-reinforced associative learning of incentive cues that is highly resistant to extinction. Why such learning is so persistent is poorly understood but may arise as a consequence of neuroadaptations in synaptic plasticity induced by chronic nicotine. We used whole-cell patch clamp recording to investigate the effect of chronic nicotine (cNIC) on synaptic plasticity in dopamine D2 receptor-expressing medium-spiny neurons in the indirect, striatopallidal pathway in dorsolateral striatum. Mice exposed to cNIC exhibited long-term potentiation in response to high-frequency stimulation instead of the expected depression. cNIC decreased baseline AMPA/NMDA ratio, arising from increased NMDA currents enriched in the NR2B subunit with a concomitant upregulation of NMDA-only, silent synapses. These data demonstrate that cNIC can increase silent synapses in MSNs, as observed with cocaine and opiates, and alter the regulation of corticostriatal plasticity. Prior work has characterized cocaine- and morphine-induced upregulation of silent synapses in the ventral striatum; we show it can occur in the dorsal striatum, a region associated with later stages of addiction, craving, and cue-induced relapse.

Neuronal Network and Awareness Measures of Post-Decision Wagering Behavior in Detecting Masked Emotional Faces

Awareness can be measured by investigating the patterns of associations between discrimination performance (first-order decisions) and confidence judgments (knowledge). In a typical post-decision wagering (PDW) task, participants judge their performance by wagering on each decision made in a detection task. If participants are aware, they wager advantageously by betting high whenever decisions are correct and low for incorrect decisions. Thus, PDW—like other awareness measures with confidence ratings—quantifies if the knowledge upon which they make their decisions is conscious. The present study proposes a new method of assessing the association between advantageous wagering and awareness in the PDW task with a combination of log-linear (LLM) modeling and neural network simulation to reveal the computational patterns that establish this association. We applied the post-decision wagering measure to a backward masking experiment in which participants made first-order decisions about whether or not a masked emotional face was present, and then used imaginary or real monetary stakes to judge the correctness of their initial decisions. The LLM analysis was then used to examine whether advantageous wagering was aware by testing a hypothesis of partial associations between metacognitive judgments and accuracy of first-order decisions. The LLM outcomes were submitted into a feed-forward neural network. The network served as a general approximator that was trained to learn relationships between input wagers and the output of the corresponding log-linear function. The simulation resulted in a simple network architecture that successfully accounted for wagering behavior. This was a feed-forward network unit consisting of one hidden neuron layer with four inputs and one output. In addition, the study indicated no effect of the monetary incentive cues on wagering strategies, although we observed that only low-wager input weights of the neural network considerably contributed to advantageous wagering.

Ventral Pallidum Neurons Encode Incentive Value and Promote Cue-Elicited Instrumental Actions

The ventral pallidum (VP) is posited to contribute toreward seeking by conveying upstream signals from the nucleus accumbens (NAc). Yet, very little is known about how VP neuron responses contribute to behavioral responses to incentive cues. Here, we recorded activity of VP neurons in a cue-driven reward-seeking task previously shown to require neural activity in the NAc. We find that VP neurons encode both learned cue value and subsequent reward seeking and that activity in VP neurons is required for robust cue-elicited reward seeking. Surprisingly, the onset of VP neuron responses occurs at a shorter latency than cue-elicited responses in NAc neurons. This suggests that this VP encoding is not a passive response to signals generated in the NAc and that VP neurons integrate sensory and motivation-related information received directly from other mesocorticolimbic inputs.

Role of orbitofrontal cortex in reward sensitivity: evidence from human lesions

BackgroundAn emerging hypothesis from cognitive neuroscience is that the ventromedial prefrontal cortex (vmPFC) is central to the evaluation and expectation of reward. However, there is scant evidence that lesions in this region alter reward processing. Rather, patients with damage in vmPFC have shown many conflicting effects with respect to motivation and affect. We aimed to specifically examine incentivisation by reward after damage to human vmPFC. MethodsWe selected a group of 19 patients with highly focal medial frontal lesions, from a database of 453 patients with subarachnoid haemorrhage, and 32 age-matched healthy controls. We directly tested for sensitivity to incentives using eye movements. Lesions included anterior cingulate, vmPFC, and medial orbitofrontal cortex. The task required participants to make saccadic eye movements to a target while avoiding a distractor, to obtain speed-related rewards. Crucially, before each eye movement, participants heard a reward cue indicating the maximum reward available. We examined the effect of the incentive cue on subsequent saccade velocity, and how this motivational effect was altered by medial frontal damage. FindingsIn healthy people, mean peak saccadic velocity was modulated by the incentive (from 458 degrees per s [SE 15] to 489 [17], p=0·0011), allowing a parametric measure of reward sensitivity. As a group, patients with medial frontal damage had significantly reduced effects of reward on invigorating saccadic velocity (from 443 degrees per s [SE 16] to 459 [19], p=0·038) and autonomic (pupil) responses (z-score traces significantly differed after 653 ms, p<0·05) compared with controls. However at the individual level, some patients showed the opposite effect, with abnormally strong incentivisation effects (3 SD above controls). Voxel-based lesion mapping demonstrated that within the lesion group, increased sensitivity to rewards correlated with damage to vmPFC subregions (144 voxels=1·15 cm3 whole-brain corrected). Lesions to vmPFC were also associated with clinical apathy (p=0·027 in region of interest) suggesting that apathy associated with prefrontal damage is reduced by vmPFC damage. InterpretationThis study found that, although medial frontal lesions could generally reduce reward sensitivity, damage to key subregions paradoxically were protective of this effect. Changes in reward sensitivity caused by altered representation of reward value might be a central link between various facets of behavioural changes seen after medial frontal damage. The results suggest a direct, mechanistic role for prefrontal reward computation in clinical motivation syndromes. FundingWellcome Trust.

Reward anticipation and trait anhedonia: An electrophysiological investigation in subjects with schizophrenia.

Investigate impairment of reward anticipation in subjects with schizophrenia (SCZ) and its association with negative symptom dimensions and hedonic experience. Event-related potentials (ERPs) were recorded, in thirty SCZ and twenty-three matched healthy controls (HC), during a "Monetary Incentive Delay" task in which reward and loss cues (incentive cues of positive and negative value) of different magnitude, as well as neutral cues were presented. anticipatory and consummatory pleasure, trait anhedonia and motivation in all subjects; avolition and expressive deficit in SCZ. SCZ had lower motivation but comparable hedonic experience with respect to HC. In HC, during reward anticipation, the early P3 was larger for large magnitude incentives, irrespective of their valence, while the late P3 was larger for large reward. In SCZ, early P3 did not discriminate the incentive magnitude and the late P3 was larger for large loss. Early P3 amplitude for large magnitude incentives was inversely related to trait social anhedonia but not to negative symptoms dimensions. SCZ are unable to integrate the incentive magnitude and reward value of future events in the context of their ongoing task. P3 abnormalities are associated with trait anhedonia, but not with negative symptoms dimensions. In line with recent studies, our findings indicate that anhedonia and avolition are partially independent constructs.

Human ventromedial prefrontal lesions alter incentivisation by reward

Although medial frontal brain regions are implicated in valuation of rewards, evidence from focal lesions to these areas is scant, with many conflicting results regarding motivation and affect, and no human studies specifically examining incentivisation by reward. Here, 19 patients with isolated, focal damage in ventral and medial prefrontal cortex were selected from a database of 453 individuals with subarachnoid haemorrhage. Using a speeded saccadic task based on the oculomotor capture paradigm, we manipulated the maximum reward available on each trial using an auditory incentive cue. Modulation of behaviour by motivation permitted quantification of reward sensitivity. At the group level, medial frontal damage was overall associated with significantly reduced effects of reward on invigorating saccadic velocity and autonomic (pupil) responses compared to age-matched, healthy controls. Crucially, however, some individuals instead showed abnormally strong incentivisation effects for vigour. Increased sensitivity to rewards within the lesion group correlated with damage in subgenual ventromedial prefrontal cortex (vmPFC) areas, which have recently become the target for deep brain stimulation (DBS) in depression. Lesion correlations with clinical apathy suggested that the apathy associated with prefrontal damage is in fact reduced by damage at those coordinates. Reduced reward sensitivity showed a trend to correlate with damage near nucleus accumbens. Lesions did not, on the other hand, influence reward sensitivity of cognitive control, as measured by distractibility. Thus, although medial frontal lesions may generally reduce reward sensitivity, damage to key subregions paradoxically protect from this effect.

Reward favors the prepared: Incentive and task-informative cues interact to enhance attentional control.

The dual mechanisms of control account suggests that cognitive control may be implemented through relatively proactive mechanisms in anticipation of stimulus onset, or through reactive mechanisms, triggered in response to changing stimulus demands. Reward incentives and task-informative cues (signaling the presence/absence of upcoming cognitive demand) have both been found to influence cognitive control in a proactive or preparatory fashion; yet, it is currently unclear whether and how such cue effects interact. We investigated this in 2 experiments using an adapted flanker paradigm, where task-informative and reward incentive cues were orthogonally manipulated on a trial-by-trial basis. In Experiment 1, results indicated that incentives not only speed reaction times, but specifically reduce both interference and facilitation effects when combined with task-informative cues, suggesting enhanced proactive attentional control. Experiment 2 manipulated the timing of incentive cue information, demonstrating that such proactive control effects were only replicated with sufficient time to process the incentive cue (early incentive); when incentive signals were presented close to target onset (late incentive) the primary effect was a speed-accuracy trade-off. Together, results suggest that advance cueing may trigger differing control strategies, and that these strategies may critically depend on both the timing-and the motivational incentive-to use such cues.

How Attention Changes in Response to Incentives.

Although the performance of simple cognitive tasks can be enhanced if an incentive is provided, the mechanisms enabling such motivational control are not known. This study sought to uncover how mechanisms of attention and readiness are altered by reward-associated incentive stimuli. We measured EEG/ERP activity as human adults viewed a high- or low-incentive cue, experienced a short preparation interval, and then performed a simple visual search task to gain the predicted reward. Search performance was faster with high versus low incentives, and this was accompanied by distinct incentive-related EEG/ERP patterns at each phase of the task (incentive, preparation, and search). First, and most surprisingly, attention to high but not low incentive cues was actively suppressed, as indexed by a PD component in response to the incentive display. During the subsequent preparation interval, neural oscillations in the alpha frequency range were reduced after high-incentive cues, indicating heightened visual readiness. Finally, attentional orienting to the target in the search array was deployed with relatively little effort on high-incentive trials, as indexed by a reduced N2pc component. These results reveal the chain of events by which the brain's executive control mechanisms respond to incentives by altering the operation of multiple processing systems to produce optimal performance.