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Frontal asymmetry in alpha oscillations is assumed to be associated with psychopathology and individual differences in emotional responding. Brain-activity-based feedback is a promising tool for the modulation of cortical activity. Here, we validated a neurofeedback protocol designed to change relative frontal asymmetry based on individual alpha peak frequencies, including real-time average referencing and eye-correction. Participants ( N  = 60) were randomly assigned to a right, left or placebo neurofeedback group. Results show a difference in trainability between groups, with a linear change in frontal alpha asymmetry over time for the right neurofeedback group during rest . Moreover, the asymmetry changes in the right group were frequency and location specific, even though trainability did not persist at 1 week and 1 month follow-ups. On the behavioral level, subjective stress on the second test day was reduced in the left and placebo neurofeedback groups, but not in the right neurofeedback group. We found individual differences in trainability that were dependent on training group, with participants in the right neurofeedback group being more likely to change their frontal asymmetry in the desired direction. Individual differences in trainability were also reflected in the ability to change frontal asymmetry during the feedback .

Rationale Dopamine is well known to play an important role in learning and motivation. Recent animal studies have implicated dopamine in the reinforcement of stimulus–response habits, as well as in flexible, goal-directed action. However, the role of dopamine in human action control is still not well understood. Objectives We present the first investigation of the effect of reducing dopamine function in healthy volunteers on the balance between habitual and goal-directed action control. Methods The dietary intervention of acute dietary phenylalanine and tyrosine depletion (APTD) was adopted to study the effects of reduced global dopamine function on action control. Participants were randomly assigned to either the APTD or placebo group ( n s = 14) to allow for a between-subjects comparison of performance on a novel three-stage experimental paradigm. In the initial learning phase, participants learned to respond to different stimuli in order to gain rewarding outcomes. Subsequently, an outcome-devaluation test and a slips-of-action test were conducted to assess whether participants were able to flexibly adjust their behaviour to changes in the desirability of the outcomes. Results APTD did not prevent stimulus–response learning, nor did we find evidence for impaired response–outcome learning in the subsequent outcome-devaluation test. However, when goal-directed and habitual systems competed for control in the slips-of-action test, APTD tipped the balance towards habitual control. These findings were restricted to female volunteers. Conclusions We provide direct evidence that the balance between goal-directed and habitual control in humans is dopamine dependent. The results are discussed in light of gender differences in dopamine function and psychopathologies.

Placebo analgesia can be primarily explained by the Pavlovian conditioning paradigm in which a passively applied cue becomes associated with less pain. In contrast, instrumental conditioning employs an active paradigm that might be more similar to clinical settings. In the present study, an instrumental conditioning paradigm involving a modified trust game in a simulated clinical situation was used to induce placebo analgesia. Additionally, Bayesian modeling was applied to predict the placebo responses of individuals based on their choices. Twenty-four participants engaged in a medical trust game in which decisions to receive treatment from either a doctor (more effective with high cost) or a pharmacy (less effective with low cost) were made after receiving a reference pain stimulus. In the conditioning session, the participants received lower levels of pain following both choices, while high pain stimuli were administered in the test session even after making the decision. The choice-dependent pain in the conditioning session was modulated in terms of both intensity and uncertainty. Participants reported significantly less pain when they chose the doctor or the pharmacy for treatment compared to the control trials. The predicted pain ratings based on Bayesian modeling showed significant correlations with the actual reports from participants for both of the choice categories. The instrumental conditioning paradigm allowed for the active choice of optional cues and was able to induce the placebo analgesia effect. Additionally, Bayesian modeling successfully predicted pain ratings in a simulated clinical situation that fits well with placebo analgesia induced by instrumental conditioning.

Social information influences decision-making through an integration of information derived from individual experience with that derived from observing the actions of others. This raises the question as to which extent one should utilize social information. One strategy is to make use of uncertainty estimates, leading to a copy-when-uncertain strategy that weights information from individual and social sources based on their respective reliabilities. Here, we investigate this integration process by extending models of Bayes optimal integration of sensory information to a social decision context. We then use a key parameter of our behavioral model in conjunction with functional magnetic resonance imaging to identify the neural substrate that is specifically linked to the fidelity of this integration process. We show that individuals behave near Bayes optimal when integrating two distinct sources of social information but systematically deviate from Bayes optimal choice when integrating individual with social information. This systematic behavioral deviation from optimality is linked to activity of left inferior frontal gyrus. Thus, an ability to optimally exploit social information depends on processes that overcome an egocentric bias, and this regulatory role involves the left inferior prefrontal cortex. The findings provide a mechanistic explanation for observations wherein individuals neglect the benefits from exploiting social information.

Transient reductions in serotonin levels during tryptophan depletion (TD) are thought to impair reward processing in healthy volunteers, while another facet of the serotonergic system, the serotonin transporter (5-HTTLPR) short allele polymorphism, is implicated in augmented processing of aversive stimuli. We examined the impact and interactions of TD and the serotonin promoter polymorphism genotype on reward and punishment via two forms of instrumental learning: passive avoidance and response reversal. In this study, healthy volunteers (n=35) underwent rapid TD or control procedures and genotyping (n=26) of the 5-HTTLPR for long and short allele variants. In the passive avoidance task, tryptophan-depleted volunteers failed to respond sufficiently to rewarded stimuli compared to the control group. Additionally, long allele homozygous individuals (n=11) were slower to learn to avoid punished stimuli compared to short allele carriers (n=15). TD alone did not produce measurable deficits in probabilistic response reversal errors. However, a significant drug group by genotype interaction was found indicating that in comparison to short allele carriers, tryptophan-depleted individuals homozygous for the long allele failed to appropriately use punishment information to guide responding. These findings extend prior reports of impaired reward processing in TD to include instrumental learning. Furthermore, they demonstrate behavioral differences in responses to punishing stimuli between long allele homozygotes and short allele carriers when serotonin levels are acutely reduced.

A sizable fraction of granule cells convey information about the expectation of reward, with different populations responding to reward delivery, anticipation and omission, with some responses evolving over time with learning. Reward response in granule cells Classical theories suggest that granule cells in the cerebellum carry sensory and motor signals, enabling downstream Purkinje cells to sense fine contextual changes relating to movement. Using two-photon calcium imaging in behaving mice, Liqun Luo and colleagues also show that a sizable fraction of granule cells convey information about the expectation of reward. Different populations responded to reward delivery, anticipation and omission and some responses evolved over time with learning. The discovery of reward-related signals in granule cells has implications for both models of sensorimotor learning and of cognitive processing in the cerebellum. The human brain contains approximately 60 billion cerebellar granule cells 1 , which outnumber all other brain neurons combined. Classical theories posit that a large, diverse population of granule cells allows for highly detailed representations of sensorimotor context, enabling downstream Purkinje cells to sense fine contextual changes 2 , 3 , 4 , 5 , 6 . Although evidence suggests a role for the cerebellum in cognition 7 , 8 , 9 , 10 , granule cells are known to encode only sensory 11 , 12 , 13 and motor 14 context. Here, using two-photon calcium imaging in behaving mice, we show that granule cells convey information about the expectation of reward. Mice initiated voluntary forelimb movements for delayed sugar-water reward. Some granule cells responded preferentially to reward or reward omission, whereas others selectively encoded reward anticipation. Reward responses were not restricted to forelimb movement, as a Pavlovian task evoked similar responses. Compared to predictable rewards, unexpected rewards elicited markedly different granule cell activity despite identical stimuli and licking responses. In both tasks, reward signals were widespread throughout multiple cerebellar lobules. Tracking the same granule cells over several days of learning revealed that cells with reward-anticipating responses emerged from those that responded at the start of learning to reward delivery, whereas reward-omission responses grew stronger as learning progressed. The discovery of predictive, non-sensorimotor encoding in granule cells is a major departure from the current understanding of these neurons and markedly enriches the contextual information available to postsynaptic Purkinje cells, with important implications for cognitive processing in the cerebellum.

Research on avoidance conditioning began in the late 1930s as a way to use laboratory experiments to better understand uncontrollable fear and anxiety. Avoidance was initially conceived of as a two-factor learning process in which fear is first acquired through Pavlovian aversive conditioning (so-called fear conditioning), and then behaviors that reduce the fear aroused by the Pavlovian conditioned stimulus are reinforced through instrumental conditioning. Over the years, criticisms of both the avoidance paradigm and the two-factor fear theory arose. By the mid-1980s, avoidance had fallen out of favor as an experimental model relevant to fear and anxiety. However, recent progress in understanding the neural basis of Pavlovian conditioning has stimulated a new wave of research on avoidance. This new work has fostered new insights into contributions of not only Pavlovian and instrumental learning but also habit learning, to avoidance, and has suggested that the reinforcing event underlying the instrumental phase should be conceived in terms of cellular and molecular events in specific circuits rather than in terms of vague notions of fear reduction. In our approach, defensive reactions (freezing), actions (avoidance) and habits (habitual avoidance) are viewed as being controlled by unique circuits that operate nonconsciously in the control of behavior, and that are distinct from the circuits that give rise to conscious feelings of fear and anxiety. These refinements, we suggest, overcome older criticisms, justifying the value of the new wave of research on avoidance, and offering a fresh perspective on the clinical implications of this work.

Addiction treatment has not been appreciably improved by neuroscientific research. One problem is that mechanistic studies using rodent models do not incorporate volitional social factors, which play a critical role in human addiction. Here, using rats, we introduce an operant model of choice between drugs and social interaction. Independent of sex, drug class, drug dose, training conditions, abstinence duration, social housing, or addiction score in Diagnostic & Statistical Manual IV-based and intermittent access models, operant social reward prevented drug self-administration. This protection was lessened by delay or punishment of the social reward but neither measure was correlated with the addiction score. Social-choice-induced abstinence also prevented incubation of methamphetamine craving. This protective effect was associated with activation of central amygdala PKCδ-expressing inhibitory neurons and inhibition of anterior insular cortex activity. These findings highlight the need for incorporating social factors into neuroscience-based addiction research and support the wider implantation of socially based addiction treatments.

Current models of conditioned fear expression and extinction involve the basolateral amygdala (BLA), ventral medial prefrontal cortex (vmPFC), and the hippocampus (HPC). There is some disagreement with respect to the specific roles of these structures, perhaps due to subregional differences within each area. For example, growing evidence suggests that infralimbic (IL) and prelimbic (PL) subregions of vmPFC have opposite influences on fear expression. Moreover, it is the ventral HPC (vHPC), rather than the dorsal HPC, that projects to vmPFC and BLA. To help determine regional specificity, we used small doses of the GABA A agonist muscimol to selectively inactivate IL, PL, BLA, or vHPC in an auditory fear conditioning and extinction paradigm. Infusions were performed prior to extinction training, allowing us to assess the effects on both fear expression and subsequent extinction memory. Inactivation of IL had no effect on fear expression, but impaired the within-session acquisition of extinction as well as extinction memory. In contrast, inactivation of PL impaired fear expression, but had no effect on extinction memory. Inactivation of the BLA or vHPC impaired both fear expression and extinction memory. Post-extinction inactivations had no effect in any structure. We suggest a model in which amygdala-dependent fear expression is modulated by inputs from PL and vHPC, whereas extinction memory requires extinction-induced plasticity in IL, BLA, and/or vHPC.

This article reviews recent research on the extinction of instrumental (or operant) conditioning from the perspective that it is an example of a general retroactive interference process. Previous discussions of interference have focused primarily on findings from Pavlovian conditioning. The present review shows that extinction in instrumental learning has much in common with other examples of retroactive interference in instrumental learning (e.g., omission learning, punishment, second-outcome learning, discrimination reversal learning, and differential reinforcement of alternative behavior). In each, the original learning can be largely retained after conflicting information is learned, and behavior is cued or controlled by the current context. The review also suggests that a variety of stimuli can play the role of context, including room and apparatus cues, temporal cues, drug state, deprivation state, stress state, and recent reinforcers, discrete cues, or behaviors. In instrumental learning situations, the context can control behavior through its direct association with the reinforcer or punisher, through its hierarchical relation with response-outcome associations, or its direct association (inhibitory or excitatory) with the response. In simple instrumental extinction and habit learning, the latter mechanism may play an especially important role.