Dorsal medial prefrontal cortex (MPFC) circuitry in rodent models of cocaine use: implications for drug addiction therapies.

Although the importance of the medial prefrontal cortex (MPFC) in cocaine addiction is well established, its precise contribution to cocaine seeking, taking and relapse remains incompletely understood. In particular, across two different models of cocaine self-administration, pharmacological or optogenetic activation of the dorsal MPFC has been reported to sometimes promote and sometimes inhibit cocaine seeking. We highlight important methodological differences between the two experimental paradigms and propose a framework to potentially reconcile the apparent discrepancy.

Factors modulating neural reactivity to drug cues in addiction: a survey of human neuroimaging studies.

Human neuroimaging studies suggest that neural cue reactivity is strongly associated with indices of drug use, including addiction severity and treatment success. However, little is known about factors that modulate cue reactivity. The goal of this review, in which we survey published fMRI and PET studies on drug cue reactivity in cocaine, alcohol, and tobacco cigarette users, is to highlight major factors that modulate brain reactivity to drug cues.

Dual role of nicotine in addiction and cognition: a review of neuroimaging studies in humans.

Substantial evidence demonstrates both nicotine's addiction liability and its cognition-enhancing effects. However, the neurobiological mechanisms underlying nicotine's impact on brain function and behavior remain incompletely understood. Elucidation of these mechanisms is of high clinical importance and may lead to improved therapeutics for smoking cessation as well as for a number of cognitive disorders such as schizophrenia.

Task difficulty modulates the impact of emotional stimuli on neural response in cognitive-control regions.

Both heightened reactivity to emotional stimuli and impaired cognitive control are key aspects of depression, anxiety, and addiction. But the impact of emotion on cognitive-control processes, and the factors that modulate this impact, are still not well understood. We examined the effects of threat and reward distracters on the neural correlates of cognitive control using functional MRI (fMRI) and the Multi-Source Interference Task (MSIT).

Impulsivity and inhibitory control deficits are associated with unhealthy eating in young adults.

Heightened impulsivity and inefficient inhibitory control are increasingly recognized as risk factors for unhealthy eating and obesity but the underlying processes are not fully understood. We used structural equation modeling to investigate the relationships between impulsivity, inhibitory control, eating behavior, and body mass index (BMI) in 210 undergraduates who ranged from underweight to obese. We demonstrate that impulsivity and inhibitory control deficits are positively associated with several facets of unhealthy eating, including overeating in response to external food cues and in response to negative emotional states, and making food choices based on taste preferences without consideration of health value.

An imaging genetics approach to understanding social influence.

Normative social influences shape nearly every aspect of our lives, yet the biological processes mediating the impact of these social influences on behavior remain incompletely understood. In this Hypothesis, we outline a theoretical framework and an integrative research approach to the study of social influences on the brain and genetic moderators of such effects. First, we review neuroimaging evidence linking social influence and conformity to the brain's reward system.

Influence of threat and serotonin transporter genotype on interference effects.

Emotion-cognition interactions are critical in goal-directed behavior and may be disrupted in psychopathology. Growing evidence also suggests that emotion-cognition interactions are modulated by genetic variation, including genetic variation in the serotonin system. The goal of the current study was to examine the impact of threat-related distracters and serotonin transporter promoter polymorphism (5-HTTLPR/rs25531) on cognitive task performance in healthy females.

Serotonin transporter gene, stress and raphe-raphe interactions: a molecular mechanism of depression.

Reports of gene-environment interactions (GxE) between the serotonin transporter gene and stress on risk of depression have generated both excitement and controversy. The controversy persists in part because a mechanistic account of this GxE on serotonergic neurotransmission and risk of depression has been lacking. In this Opinion, we draw on recent discoveries in the functional neuroanatomy of the serotonergic dorsal raphe nucleus (DR) to propose such a mechanistic account.

Amygdala response to smoking-cessation messages mediates the effects of serotonin transporter gene variation on quitting.

The amygdala is critically involved in detecting emotionally salient stimuli and in enhancing memory for emotional information. Growing evidence also suggests that the amygdala plays a crucial role in addiction, perhaps by strengthening associations between emotionally-charged drug cues and drug-seeking behavior. In the current study, by integrating functional MRI (fMRI), genetics, and outcome data from a large group of smokers who completed a smoking-cessation intervention and attempted to quit, we show that the amygdala also plays a role in quitting.

Self-related neural response to tailored smoking-cessation messages predicts quitting.

Tailored health interventions can be more effective in eliciting positive behavior change than generic interventions, but the underlying neural mechanisms are not yet understood. Here, 91 smokers participated in a functional magnetic resonance imaging session and a tailored smoking-cessation program. We found that increases in activation in self-related processing regions, particularly dorsomedial prefrontal cortex, to tailored messages predicted quitting during a 4-month follow-up.