The nucleus accumbens (NAc) is thought to contribute to motivated behavior by signaling the value of reward-predicting cues and the delivery of anticipated reward. The NAc is subdivided into core and shell, with each region containing different populations of neurons that increase or decrease firing to rewarding events. While there are numerous theories of functions pertaining to these subregions and cell types, most are in the context of reward processing, with fewer considering that the NAc might serve functions related to action selection more generally. We recorded from single neurons in the NAc as rats of both sexes performed a STOP-change task that is commonly used to study motor control and impulsivity. In this task, rats respond quickly to a spatial cue on 80% of trials (GO) and must stop and redirect planned movement on 20% of trials (STOP). We found that the activity of reward-excited neurons signaled accurate response direction on GO, but not STOP, trials and that these neurons exhibited higher precue firing after correct trials. In contrast, reward-inhibited neurons significantly represented response direction on STOP trials at the time of the instrumental response. Finally, the proportion of reward-excited to reward-inhibited neurons and the strength of precue firing decreased as the electrode traversed the NAc. We conclude that reward-excited cells (more common in core) promote proactive action selection, while reward-inhibited cells (more common in shell) contribute to accurate responding on STOP trials that require reactive suppression and redirection of behavior.

Historically, the orbitofrontal cortex (OFC) has been implicated in a variety of behaviors ranging from reversal learning and inhibitory control to more complex representations of reward value and task space. While modern interpretations of the OFC\'s function have focused on a role in outcome evaluation, these cognitive processes often require an organism to inhibit a maladaptive response or strategy. Single-unit recordings from the OFC in rats performing a stop-change task show that the OFC responds strongly to STOP trials. To investigate the role that the OFC plays in stop-change performance, we expressed halorhodopsin (eNpHR3.0) in excitatory neurons in the OFC and tested rats on the stop-change task. Previous work suggests that the OFC differentiates between STOP trials based on trial sequence (i.e., gS trials: STOP trials preceded by a GO vs sS trials: STOP trials preceded by a STOP). We found that yellow light activation of the eNpHR3.0-expressing neurons significantly decreased accuracy only on STOP trials that followed GO trials (gS trials). Further, optogenetic inhibition of the OFC speeded reaction times on error trials. This suggests that the OFC plays a role in inhibitory control processes and that this role needs to be accounted for in modern interpretations of OFC function.

The ability to inhibit an already initiated response is crucial for navigating the environment. However, it is unclear which characteristics make stop-signals more likely to be processed efficiently. In three consecutive studies, we demonstrate that stop-signal modality and location are key factors that influence reactive response inhibition. Study 1 shows that tactile stop-signals lead to better performance compared to visual stop-signals in an otherwise visual choice-reaction task. Results of Study 2 reveal that the location of the stop-signal matters. Specifically, if a visual stop-signal is presented at a different location compared to the visual go-signal, then stopping performance is enhanced. Extending these results, study 3 suggests that tactile stop-signals and location-distinct visual stop-signals retain their performance enhancing effect when visual distractors are presented at the location of the go-signal. In sum, these results confirm that stop-signal modality and location influence reactive response inhibition, even in the face of concurrent distractors. Future research may extend and generalize these findings to other cross-modal setups.

UNASSIGNED: Similar to addictive disorders, deficits on cognitive control might be involved in the onset and development of Binge Eating Disorder (BED). However, it remains unclear whether general or food-related inhibitory control impairments would be basically linked to overeating and binge eating behaviors. This study thus aimed to investigate behavioral performance and electrophysiological correlates of food-related inhibitory control among individuals with binge eating behavior.
UNASSIGNED: Sixty individuals with probable BED (pBED) and 60 well-matched healthy controls (HCs) were assessed using the typical Stop-Signal Task, a revised Go/No Go Task, and a food-related Go/No Go Task. Besides, another separate sample, including 35 individuals with pBED and 35 HCs, completed the food-related Go/No Go Task when EEG signals were recorded with the event-related potentials (ERPs).
UNASSIGNED: The data revealed that the pBED group performed worse with a longer SSRT on the Stop-Signal Task compared with HCs (Cohen\'s d = 0.58, p = 0.002). Moreover, on the food-related Go/No Go Task, the pBED group had a lower success rate of inhibition in no-go trials (Cohen\'s d = 0.47, p = 0.012). The ERPs data showed that in comparison with HCs, the pBED group exhibited increased P300 latency (FC1, FC2, F3, F4, FZ) in the no-go trials of the food-related Go/No Go Task (Cohen\'s d 0.56-0.73, all p < 0.05).
UNASSIGNED: These findings suggested that individuals with binge eating could be impaired in both non-specific and food-related inhibitory control aspects, and the impairments in food-related inhibitory control might be linked to P300 abnormalities, implying a behavioral-neurobiological dysfunction mechanism implicated in BED.

Inhibition is a key cognitive control mechanism humans use to enable goal-directed behavior. When rapidly exerted, inhibitory control has broad, nonselective motor effects, typically demonstrated using corticospinal excitability measurements (CSE) elicited by transcranial magnetic stimulation (TMS). For example, during rapid action-stopping, CSE is suppressed at both stopped and task-unrelated muscles. While such TMS-based CSE measurements have provided crucial insights into the fronto-basal ganglia circuitry underlying inhibitory control, they have several downsides. TMS is contraindicated in many populations (e.g., epilepsy or deep-brain stimulation patients), has limited temporal resolution, produces distracting auditory and haptic stimulation, is difficult to combine with other imaging methods, and necessitates expensive, immobile equipment. Here, we attempted to measure the nonselective motor effects of inhibitory control using a method unaffected by these shortcomings. Thirty male and female human participants exerted isometric force on a high-precision handheld force transducer while performing a foot-response stop-signal task. Indeed, when foot movements were successfully stopped, force output at the task-irrelevant hand was suppressed as well. Moreover, this nonselective reduction of isometric force was highly correlated with stop-signal performance and showed frequency dynamics similar to established inhibitory signatures typically found in neural and muscle recordings. Together, these findings demonstrate that isometric force recordings can reliably capture the nonselective effects of motor inhibition, opening the door to many applications that are hard or impossible to realize with TMS.

Attention deficit hyperactivity disorder (ADHD) is associated with deficits in inhibitory functions including interference control, inhibition of prepotent/automatic responses and suppression of already initiated responses. This study used functional near-infrared spectroscopy (fNIRS) to investigate the neural basis of these three forms of inhibition assessed by a recently developed behavioral protocol combining the Stroop-matching/stop-signal task in twenty-five young adults with inattention, impulsivity and/or hyperactivity symptoms. The severity of ADHD symptoms was measured using the Adult ADHD Self-Report Scale (ASRS). The concentration of oxygenated hemoglobin (HbO) was assessed in the dorsolateral prefrontal cortex (DLPFC), inferior frontal gyrus (IFG) and temporoparietal regions (TP) during the Stroop-matching/stop-signal task. Correlations yielded significant associations between ASRS scores and HbO concentration in frontal regions during blocks with stop-signal tasks, namely the right IFG, the left DLPFC and the left IFG. This study revealed that different types of inhibition involve unique frontal and temporoparietal activities and linked frontal dysfunction during the suppression of ongoing responses to the severity of ADHD symptoms.

The ability to inhibit or adapt unwanted actions or movements is a critical feature of almost all forms of behavior. Many have attributed this ability to frontal brain areas such as the anterior cingulate cortex (ACC) and the medial prefrontal cortex (mPFC), but the exact contribution of each brain region is often debated because their functions are not examined in animals performing the same task. Recently, we have shown that ACC signals a need for cognitive control and is crucial for the adaptation of action selection signals in dorsomedial striatum (DMS) in rats performing a stop-change task. Here, we show that unlike ACC, the prelimbic region of mPFC does not disrupt the inhibition or adaption of an action plan at either the level of behavior or downstream firing in DMS. Instead, lesions to mPFC correlate with changes in DMS signals involved in action initiation and disrupt performance on GO trials while improving performance on STOP trials.

Deficits in response inhibition, defined as an inability to stop a behavior that is no longer relevant, are characteristic of posttraumatic stress disorder (PTSD). Given that impaired response inhibition is associated with worse symptom recovery and accumulating evidence pointing to the effectiveness of cognitive control trainings in reducing PTSD symptoms, individuals with moderate to severe PTSD total severity (Posttraumatic Diagnostic Scale total score ≥ 21) and pre-training response inhibition deficits (M ≤ 75% successful inhibition on the Go/No-go) completed a 3-h, adaptive Go/No-go training designed to improve ability to withhold prepotent motor responses. Then forty-nine participants were randomized to an adaptive response inhibition training (n = 24, M = 19.27 years, SD = 0.70) or a waitlist condition (n = 25, M = 18.31 years, SD = 4.80). Behavioral response inhibition and self-reported trauma-related symptoms were assessed at pre- and post-training. Response inhibition training was associated with improved response inhibition on an untrained transfer Stop-Signal task and symptom reduction in PTSD compared to a waitlist group, at post-training. There was, however, reduced inhibition on a modified Go/No-go task from pre-to post-training. Overall, response inhibition deficits and PTSD symptoms are amenable to top-down remediation using response inhibition training. Our study provides preliminary evidence for the feasibility of response inhibition training in a PTSD sample characterized by response inhibition deficits.

During human motor control, the three pathways of motor control coordinate to complete human response and inhibition control, so whether different types of motor skills training will affect the three pathways of motor control is the main question in this study. Magnetic resonance imaging was combined with behavioural evaluation to analyse the effects of different special training sessions on the motor control network of the frontal lobe and basal ganglia and to explore the role of the central nervous system in the regulation of motor behaviour. A Stop-signal paradigm was used to measure reaction and inhibition capacity, functional magnetic resonance imaging was used for whole brain scanning, and resting state data were collected. Compared to the control group, the competitive aerobics athletes had better reflexes while the soccer players had both better reflexes and inhibitory control. Furthermore, we found that training in the two sets of skills resulted in significant differences in different resting state brain function parameters compared with the control group. Additionally, there were significant differences among the three groups in the direct and indirect pathways of motor control in terms of functional connectivity. Open skill training may improve reaction ability while closed skill training improve both reaction and inhibition ability. These results suggest that the strength of the functional connectivity between the right inferior frontal gyrus and the left putamen may be a key to improving the inhibitory, and the left supplementary motor area- bilateral thalamic loop may play an inhibitory role in motor control.

Inhibitory control over thoughts, emotions, and actions is challenging for people with Post-Traumatic Stress Disorder (PTSD). Whether specific aspects of inhibitory control are differentially affected in PTSD remains an open question. Here we examined performance on two popular response inhibition tasks in 28 combat Veterans with PTSD and 27 control Veterans. We used a Hybrid variant that intermixed 75% Go trials, 12.5% NoGo trials, and 12.5% Stop trials. Parameters from an ex-Gaussian race model (Matzke et al., 2017) provided estimates of stopping speed (μ Stop) and stopping variability (τ Stop). Participants with PTSD had higher error rates on NoGo trials, replicating previous results. The estimated probability of \"trigger failures\" (failures to launch inhibitory control) on Stop trials was also higher in PTSD patients, suggesting that sustained attention was a common deficit in the two tasks. Stopping variability was also increased in participants with PTSD, which supports a difficulty with maintaining task goals. Conversely, stopping speed did not differ between patients and controls, suggesting that core inhibitory processes were intact. These results demonstrate a dissociation between the speed and reliability of motor response inhibition in PTSD, and suggest that top-down inhibitory control was deployed less consistently in participants with PTSD.