Ventral Striatum

Repetitive transcranial magnetic stimulation (rTMS) has recently been assessed as a non-invasive treatment modality for neuropsychiatric disorders. However, the mechanisms underlying the therapeutic effects are still not understood. Studies in rodents revealed lasting effects in limbic-related regions, but species difference in brain structures makes it difficult to infer the regional effect in primate brain. To reveal how rTMS affects primate brain function, we performed positron emission tomography (PET) using 18F-fluorodeoxyglucose (FDG) and 11C-raclopride (RAC) in anaesthetized macaque monkeys. A total of 2000 pulses of 5Hz-rTMS were delivered on the unilateral primary motor cortex using a small coil. Voxel-based analysis revealed statistically robust changes in FDG activity in the motor, cingulate, and orbitofrontal cortices, as well as in binding potential of RAC in the ventral striatum. Interestingly, the change in FDG activity persisted at least 8 days. These results demonstrate that motor cortical rTMS induces dynamic functional changes in motor and limbic associated structures, suggesting its therapeutic effect on dysfunction of motor and motivation system.

Rationale Several lines of evidence suggest that altered serotonin (5-HT) function persists after recovery from anorexia nervosa (AN) and bulimia nervosa (BN). Objectives We compared 11 subjects who recovered (>1 year normal weight, regular menstrual cycles, no bingeing or purging) from restricting-type AN (REC RAN), 7 who recovered from bulimia-type AN (REC BAN), 9 who recovered from BN (REC BN), and 10 healthy control women (CW). Materials and methods Positron emission tomography (PET) imaging with [11C]McN5652 was used to assess the 5-HT transporter (5-HTT). For [11C]McN5652, distribution volume (DV) values were determined using a two-compartment, three-parameter tracer kinetic model, and specific binding was assessed using the binding potential (BP, BP = DVregion of interest/DVcerebellum − 1). Results After correction for multiple comparisons, the four groups showed significant (p < 0.05) differences for [11C]McN5652 BP values for the dorsal raphe and antero-ventral striatum (AVS). Post-hoc analysis revealed that REC RAN had significantly increased [11C]McN5652 BP compared to REC BAN in these regions. Conclusions Divergent 5-HTT activity in subtypes of eating disorder subjects may provide important insights as to why these groups have differences in affective regulation and impulse control.

The nucleus accumbens, a site within the ventral striatum, plays a prominent role in mediating the reinforcing effects of drugs of abuse, food, sex, and other addictions. Indeed, it is generally believed that this structure mandates motivated behaviors such as eating, drinking, and sexual activity, which are elicited by natural rewards and other strong incentive stimuli. This article focuses on sex addiction, but we hypothesize that there is a common underlying mechanism of action for the powerful effects that all addictions have on human motivation. That is, biological drives may have common molecular genetic antecedents, which if impaired, lead to aberrant behaviors. Based on abundant scientific support, we further hypothesize that dopaminergic genes, and possibly other candidate neurotransmitter-related gene polymorphisms, affect both hedonic and anhedonic behavioral outcomes. Genotyping studies already have linked gene polymorphic associations with alcohol and drug addictions and obesity, and we anticipate that future genotyping studies of sex addicts will provide evidence for polymorphic associations with specific clustering of sexual typologies based on clinical instrument assessments. We recommend that scientists and clinicians embark on research coupling the use of neuroimaging tools with dopaminergic agonistic agents to target specific gene polymorphisms systematically for normalizing hyper- or hypo-sexual behaviors.

We considered clinical observations in patients with obsessive-compulsive- and anxiety-disorders, who underwent bilateral anterior capsulotomy, as well as anatomical and pathophysiological findings. Based on these considerations, we choose the shell region of the right nucleus accumbens as target for deep brain stimulation (DBS) in a pilot-series of four patients with severe obsessive-compulsive- and anxiety-disorders. Significant reduction in severity of symptoms has been achieved in three of four patients treated. Clinical results as well as a 15-O-H(2)O-PET study, perfomed in one patient during stimulation, speak in favour of the following hypothesis. As a central relay-structure between amygdala, basal ganglia, mesolimbic dopaminergic areas, mediodorsal thalamus and prefrontal cortex, the accumbens nucleus seems to play a modulatory role in information flow from the amygdaloid complex to the latter areas. If disturbed, imbalanced information flow from the amygdaloid complex could yield obsessive-compulsive- and anxiety-disorders, which can be counteracted by blocking the information flow within the shell region of the accumbens nucleus by deep brain stimulation.

Despite being one of the healthiest developmental periods, morbidity and mortality rates increase dramatically during adolescence, largely due to preventable, risky behaviors. Heightened reward sensitivity, coupled with ineffective cognitive control, has been proposed to underlie adolescents&#39; risk-taking. In the current study, we test whether reward sensitivity can be redirected to promote safe behavior. Adolescents completed a risk-taking task in the presence of their mother and alone during fMRI. Adolescents demonstrated reduced risk-taking behavior when their mothers were present compared to alone, which was associated with greater recruitment of the VLPFC when making safe decisions, decreased activation in the ventral striatum following risky decisions, and greater functional coupling between the ventral striatum and VLPFC when making safe decisions. Importantly, the very same neural circuitry (i.e., ventral striatum) that has been linked to greater risk-taking can also be r...