This study addresses the relationship between trait impulsivity and inhibitory control, two features known to be impaired in a number of psychiatric conditions. While impulsivity is often measured using psychometric self-report questionnaires, the inhibition of inappropriate, impulsive motor responses is typically measured using experimental laboratory tasks. It remains unclear, however, whether psychometrically assessed impulsivity and experimentally operationalized inhibitory performance are related to each other. Therefore, we investigated the relationship between these two traits in a large sample using correlative and latent variable analysis. A total of 504 healthy individuals completed the Barratt Impulsiveness Scale (BIS-11) and a battery of four prepotent response inhibition paradigms: the antisaccade, Stroop, stop-signal, and go/no-go tasks. We found significant associations of BIS impulsivity with commission errors on the go/no-go task and directional errors on the antisaccade task, over and above effects of age, gender, and intelligence. Latent variable analysis (a) supported the idea that all four inhibitory measures load on the same underlying construct termed "prepotent response inhibition" and (b) revealed that 12% of variance of the prepotent response inhibition construct could be explained by BIS impulsivity. Overall, the magnitude of associations observed was small, indicating that while a portion of variance in prepotent response inhibition can be explained by psychometric trait impulsivity, the majority of variance remains unexplained. Thus, these findings suggest that prepotent response inhibition paradigms can account for psychometric trait impulsivity only to a limited extent. Implications for studies of patient populations with symptoms of impulsivity are discussed.
The human dopamine transporter (DAT) gene (SLC6A3) contains a 40-bp variable number of tandem repeats (VNTR) polymorphism. A number of studies have investigated the association of this VNTR with striatal DAT availability in humans using single photon emission computed tomography (SPECT). However, the results are not consistent. Therefore, we carried out a meta-analysis of the association between the SLC6A3 VNTR and striatal DAT binding measured in human SPECT studies. The meta-analysis of five samples of healthy individuals failed to find a significant difference in DAT availability between SLC6A3 9-repeat carriers and 10-repeat homozygotes (P = 0.22) although the 9R carriers had nominally higher striatal DAT levels (g = 0.66). The results remained nonsignificant after the inclusion of patient samples, namely schizophrenia, attention deficit hyperactivity disorder, and Parkinson's disease (four samples; all P > 0.18). To conclude, this meta-analysis provides no evidence to support the hypothesis that the SLC6A3 VNTR is significantly associated with interindividual differences in DAT availability in the human striatum. Further work is needed to clarify the molecular mechanisms by which this polymorphism may affect cognition and psychiatric disorders, if not through altered expression as measured by molecular imaging.
Methylphenidate (MPH) is an indirect dopaminergic and noradrenergic agonist that is used to treat attention deficit hyperactivity disorder and that has shown therapeutic potential in neuropsychiatric diseases such as depression, dementia, and Parkinson's disease. While effects of MPH on task-induced brain activation have been investigated, little is known about how MPH influences the resting brain. To investigate the effects of 40 mg of oral MPH on intrinsic functional connectivity, we used resting state fMRI in 54 healthy male subjects in a double-blind, randomized, placebo-controlled study. Functional connectivity analysis employing ICA revealed seven resting state networks (RSN) of interest. Connectivity strength between the dorsal attention network and the thalamus was increased after MPH intake. Other RSN located in association cortex areas, such as the left and right frontoparietal networks and the executive control network, showed MPH-induced connectivity increase to sensory-motor and visual cortex regions and connectivity decrease to cortical and subcortical components of cortico-striato-thalamo-cortical circuits (CST). RSN located in sensory-motor cortex areas showed the opposite pattern with MPH-induced connectivity increase to CST components and connectivity decrease to sensory-motor and visual cortex regions. Our results provide evidence that MPH does not only alter intrinsic connectivity between brain areas involved in sustained attention, but that it also induces significant changes in the cortico-cortical and cortico-subcortical connectivity of many other cognitive and sensory-motor RSN.
Methylphenidate (MPH) is a catecholamine transporter blocker, with dopamine agonistic effects in the basal ganglia. Response inhibition, error detection, and its mediating frontostriatal brain activation are improved by MPH in patients with attention-deficit/hyperactivity disorder. However, little is known about the effects of MPH on response inhibition and error processing or its underlying brain function in healthy individuals. Therefore, this study employed functional magnetic resonance imaging (fMRI) and 2 response inhibition tasks in 52 healthy males. Subjects underwent fMRI during a go/no-go task and a tracking stop-signal task after administration of 40 mg MPH and placebo in a double-blind, placebo-controlled, repeated-measures design. Results revealed task- and condition-specific neural effects of MPH: it increased activation in the putamen only during inhibition errors but not during successful inhibition and only in the go/no-go task. We speculate that task specificity of the effect might be due to differences in the degree of error saliency in the 2 task designs, whereas errors were few in the go/no-go task and thus had high saliency and the stop-signal task was designed to elicit 50% of errors in all subjects, diminishing the error saliency effect. The findings suggest that neural MPH effects interact with the saliency of the behavior under investigation.
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