According to the reward-prediction error hypothesis of dopamine, the phasic activity of dopaminergic neurons in the midbrain signals a discrepancy between the predicted and currently experienced reward of a particular event. It can be claimed that this hypothesis is deep, elegant and beautiful, representing one of the largest successes of computational neuroscience. This paper examines this claim, making two contributions to existing literature. First, it draws a comprehensive historical account of the main steps that led to the formulation and subsequent (...) success of the RPEH. Second, in light of this historical account, it explains in which sense the RPEH is explanatory and under which conditions it can be justifiably deemed deeper than the incentive salience hypothesis of dopamine, which is arguably the most prominent contemporary alternative to the RPEH. (shrink)

A developing neurobiological/psychological theory of positive motivation gives a key causal role to reward events in the brain which can be directly activated by electrical stimulation (ESB). In its strongest form, this Reward Event Theory (RET) claims that all positive motivation, primary and learned, is functionally dependent on these reward events. Some of the empirical evidence is reviewed which either supports or challenges RET. The paper examines the implications of RET for the concepts of 'motivation', 'desire' and 'reward' or 'pleasure'. (...) It is argued (1) that a 'causal base' as opposed to a functional' concept of motivation has theoretical advantages; (2) that a causal distinction between the focus' and the 'anchor' of desire suggests an ineliminable 'opacity' of desire; and (3) that some affective concept, such as 'pleasure', should play a key role in psychological explanation, distinct from that of motivational (or cognitive) concepts. A concept of 'reward' or 'pleasure' as intrinsically positive affect is defended, and contrasted with the more 'operational' definitions of 'reward' in some of the hypotheses of Roy Wise. (shrink)

By the late 1990s, several converging trends in economics, psychology, and neuroscience had set the stage for the birth of a new scientific field known as “neuroeconomics”. Without the availability of an extensive variety of experimental designs for dealing with individual and social decision-making provided by experimental economics and psychology, many neuroeconomics studies could not have been developed. At the same time, without the significant progress made in neuroscience for grasping and understanding brain functioning, neuroeconomics would have never seen the (...) light of day. The paper is an overview of the main significant advances in the knowledge of brain functioning by neuroscience that have contributed to the emergence of neuroeconomics and its rise over the past two decades. These advances are grouped over three non-independent topics referred to as the “emo-rational” brain, “social” brain, and “computational” brain. For each topic, it emphasizes findings considered as critical to the birth and development of neuroeconomics while highlighting some of prominent questions about which knowledge should be improved by future research. In parallel, it shows that the boundaries between neuroeconomics and several recent sub-fields of cognitive neuroscience, such as affective, social, and more generally, decision neuroscience, are rather porous. (shrink)

Evidence abounds of a close relation between ingestive and affective processes in rats and in humans. Emotional distress alters food intake and body weight; conversely, alterations in eating and weight influence emotional health. Thorough experimental analysis of the ingestion-affect relation may clarify the mechanisms of anxiety and depression. A strategy is proposed for examination of environmental and dispositional determinants of ingestive processes, emotionality, and responses to stress.

Pleasure, in the inclusive usages most important in moral psychology, ethical theory, and the studies of mind, includes all joy and gladness — all our feeling good, or happy. It is often contrasted with similarly inclusive pain, or suffering, which is similarly thought of as including all our feeling bad. Contemporary psychology similarly distinguishes between positive affect and negative affect.[1..

(1983). Consciousness and complexity: Evolutionary perspectives on the mind-body problem. Australasian Journal of Philosophy: Vol. 61, No. 4, pp. 378-395.

For decades, psychostimulants have been the gold standard pharmaceutical treatment for attention-deficit/hyperactivity disorder (ADHD). In the United States, an astounding 9% of all boys and 4% of girls will be prescribed stimulant drugs at some point during their childhood. Recent meta-analyses have revealed that individuals with ADHD have reduced brain volume loss later in life (>60 y.o.) compared to the normal aging brain, which suggests that either ADHD or its treatment may be neuroprotective. Crucially, these neuroprotective effects were significant in (...) brain regions (e.g., hippocampus, amygdala) where severe volume loss is linked to cognitive impairment and Alzheimer’s disease. Historically, the ADHD diagnosis and its pharmacotherapy came about nearly simultaneously, making it difficult to evaluate their effects in isolation. Certain evidence suggests that psychostimulants may normalize structural brain changes typically observed in the ADHD brain. If ADHD itself is neuroprotective, perhaps exercising the brain, then psychostimulants may not be recommended across the lifespan. Alternatively, if stimulant drugs are neuroprotective, then this class of medications may warrant further investigation for their therapeutic effects. Here, we take a bottom-up holistic approach to review the psychopharmacology of ADHD in the context of recent models of attention. We suggest that future studies are greatly needed to better appreciate the interactions amongst an ADHD diagnosis, stimulant treatment across the lifespan, and structure-function alterations in the aging brain. (shrink)

Animal research suggests that central serotonergic neurons are involved in behavioral suppression, particularly anxiety-related inhibition. The hypothesis linking decreased serotonin transmission to reduced anxiety as the mechanism in the anxiolytic activity of benzodiazepines conflicts with most clinical observations. Serotonin antagonists show no marked capacity to alleviate anxiety. On the other hand, clinical signs of reduced serotonergic transmission (low 5-HIAA levels in the cerebrospinal fluid) are frequently associated with aggressiveness, suicide attempts, and increased anxiety. The target article attempts to reconcile such (...) human and animal findings by investigating whether anxiety reduction or increased impulsivity is more Likely to account for animal behavioral changes associated with decreased serotonergic transmission. The effects of manipulating central serotonin in experimental anxiety paradigms in animals (punishment, extinction, novelty) are reviewed and compared with the effects of antianxiety drugs. Anxiety seems neither necessary nor sufficient to induce control by serotonergic neurons on behavior. Further evidence suggests that behavioral effects of anxiolytics thought to be mediated by decreases in anxiety are not caused by the ability of these drugs to reduce serotonin transmission. Blockade of serotonin transmission, especially at the level of the substantia nigra, results in a shift of behavior toward facilitation of responding. This behavioral shift is particularly marked when there is competition between acting and restraining response tendencies and when obstacles prevent the immediate attainment of an anticipated reward. It is proposed that serotonergic neurons are involved not only in behavioral arousal but also in enabling the organism to arrange or tolerate delay before acting. Decreases in serotonin transmission seem to be associated with the increased performance of behaviors that are usually suppressed, though not necessarily because of the alleviation of anxiety, which might contribute to the suppression. (shrink)