Salience, Authenticity, Integrity, and Webdesign

“INTRODUCTION: debate continues over the precise causal contribution made by mesolimbic dopamine systems to reward. there are three competing explanatory categories: ‘liking’, learning, and ‘wanting’. does dopamine mostly mediate the hedonic impact of reward (‘liking’)? does it instead mediate learned predictions of future reward, prediction error teaching signals and stamp in associative links (learning)? or does dopamine motivate the pursuit of rewards by attributing incentive salience to reward-related stimuli (‘wanting’)? each hypothesis is evaluated here, and it is suggested that the incentive salience or ‘wanting’ hypothesis of dopamine function may be consistent with more evidence than either learning or ‘liking’. in brief, recent evidence indicates that dopamine is neither necessary nor sufficient to mediate changes in hedonic ‘liking’ for sensory pleasures. other recent evidence indicates that dopamine is not needed for new learning, and not sufficient to directly mediate learning by causing teaching or prediction signals. by contrast, growing evidence indicates that dopamine does contribute causally to incentive salience. dopamine appears necessary for normal ‘wanting’, and dopamine activation can be sufficient to enhance cue-triggered incentive salience. drugs of abuse that promote dopamine signals short circuit and sensitize dynamic mesolimbic mechanisms that evolved to attribute incentive salience to rewards. such drugs interact with incentive salience integrations of pavlovian associative information with physiological state signals. that interaction sets the stage to cause compulsive ‘wanting’ in addiction, but also provides opportunities for experiments to disentangle ‘wanting’, ‘liking’, and learning hypotheses. results from studies that exploited those opportunities are described here. conclusion: in short, dopamine’s contribution appears to be chiefly to cause ‘wanting’ for hedonic rewards, more than ‘liking’ or learning for those rewards.”

“Oxytocin is a nonapeptide that also serves as a neuromodulator in the human central nervous system. over the last decade, a sizeable body of literature has examined its effects on social behavior in humans. these studies show that oxytocin modulates various aspects of social behaviors such as empathy, trust, in-group preference, and memory of socially relevant cues. several theoretical formulations have attempted to explain the effects of oxytocin. the prosocial account argues that oxytocin mainly enhances affiliative prosocial behaviors; the fear/stress theory suggests that oxytocin affects social performance by attenuating stress; and the in-/out-group approach proposes that oxytocin regulates cooperation and conflict among humans in the context of intergroup relations. nonetheless, accumulating evidence reveals that the effects of oxytocin are dependent on a variety of contextual aspects and the individual’s characteristics and can induce antisocial effects including aggression and envy. in an attempt to reconcile these accounts, we suggest a theoretical framework that focuses on the overarching role of oxytocin in regulating the salience of social cues through its interaction with the dopaminergic system. crucially, the salience effect modulates attention orienting responses to external contextual social cues (e.g., competitive vs. cooperative environment) but is dependent on baseline individual differences such as gender, personality traits, and degree of psychopathology. this view could have important implications for the therapeutic applications of oxytocin in conditions characterized with aberrant social behavior.”