Control of response interference: caudate nucleus contributes to selective inhibition

Abstract

While the role of cortical regions in cognitive control processes is well accepted, the contribution of subcortical structures (e.g., the striatum), especially to the control of response interference, remains controversial. Therefore, the present study aimed to investigate the cortical and particularly subcortical neural mechanisms of response interference control (including selective inhibition). Thirteen healthy young participants underwent event-related functional magnetic resonance imaging while performing a unimanual version of the Simon task. In this task, successful performance required the resolution of stimulus–response conflicts in incongruent trials by selectively inhibiting interfering response tendencies. The behavioral results show an asymmetrical Simon effect that was more pronounced in the contralateral hemifield. Contrasting incongruent trials with congruent trials (i.e., the overall Simon effect) significantly activated clusters in the right anterior cingulate cortex, the right posterior insula, and the caudate nucleus bilaterally. Furthermore, a region of interest analysis based on previous patient studies revealed that activation in the bilateral caudate nucleus significantly co-varied with a parameter of selective inhibition derived from distributional analyses of response times. Our results corroborate the notion that the cognitive control of response interference is supported by a fronto-striatal circuitry, with a functional contribution of the caudate nucleus to the selective inhibition of interfering response tendencies.

Psychopathic tendency in violent offenders is associated with reduced aversive Pavlovian inhibition of behavior and associated striatal BOLD signal

“…The key finding is that this association was completely reversed in the violent offenders, so that the across-participant pattern of caudate nucleus signal resembled that in their putamen. In line with evidence from work with experimental rodents, evidence in humans (Balleine and O'Doherty, 2009) implicates the caudate nucleus [together with the ventromedial prefrontal cortex (Valentin et al, 2007)] in the instrumental control of behavior (Tanaka et al, 2008;de Wit et al, 2012) as well as response inhibition (Watanabe and Munoz, 2010;Schmidt et al, 2020). Accordingly, one might speculate, based on our neural findings, that aversive Pavlovian disinhibition in psychopathy is accompanied by a failure of the caudate nucleus to exhibit the Pavlovian inhibition computations that it exhibits normally, as suggested by the negative relation in healthy controls.…”

A circuit-based approach to repair hypersexuality in Parkinson’s disease

“…Such top-down dysfunctional connection (based on dynamic causal modelling) was linked to an anatomical increase (based on fractional anisotropy tracts) in PD+HS (approaching significance values). Ultimately, opposite correlations between patients were seen between the pre-SMA-caudate tract and SSRT, which altogether suggests a dual neurobiological problem (local and descending pre-SMA connectivity) in the cognitive control network 91,92 . Thus, reductions in top-down control rely upon paradoxical increases of white matter integrity, a possible neural compensatory response previously reported in Parkinson’s disease and ICD 72,93,94 .…”

Atrophy in subcortical gray matter in adult patients with moyamoya disease

“…The thalamus is considered as a relay simply transferring information from the periphery to the neocortex or one cortical/subcortical region to another; however, accumulating evidence indicates that the thalamus also plays a key role in higher-order cognition, such as learning and memory, shaping mental representations, and flexible adaptation [29]. Recent neuroimaging studies have provided further support for the involvement of the basal ganglia in aspects of working memory, executive function, cognitive flexibility, and response interference control [30][31][32][33]. In the present study, volumetric decreases in subcortical areas were observed across several regions, but only 15.49% of patients with MMD manifested significant cognitive impairments.…”