Training-induced behavioral and brain plasticity in inhibitory control

Abstract

Deficits in inhibitory control, the ability to suppress ongoing or planned motor or cognitive processes, contribute to many psychiatric and neurological disorders. The rehabilitation of inhibition-related disorders may therefore benefit from neuroplasticity-based training protocols aiming at normalizing inhibitory control proficiency and the underlying brain networks. Current literature on training-induced behavioral and brain plasticity in inhibitory control suggests that improvements may follow either from the development of automatic forms of inhibition or from the strengthening of top-down, controlled inhibition. Automatic inhibition develops in conditions of consistent and repeated associations between inhibition-triggering stimuli and stopping goals. Once established, the stop signals directly elicit inhibition, thereby bypassing slow, top-down executive control and accelerating stopping processes. In contrast, training regimens involving varying stimulus-response associations or frequent inhibition failures prevent the development of automatic inhibition and thus strengthen top-down inhibitory processes rather than bottom-up ones. We discuss these findings in terms of developing optimal inhibitory control training regimens for rehabilitation purposes.

Keywords: frontal; inhibitory control; plasticity; rehabilitation; training.

Figure 1

Two mechanisms of training-induced plasticity of inhibitory control. Inhibition stimuli are conveyed to sensory areas processing stimuli features at ca. 80 ms within parietal brain regions (Hyde et al., ; Spierer et al., 2008). (A) In conditions of stable S-R mapping, as for the Go/NoGo task, participants switch from a controlled to an automatic inhibition mode with training. Automatic inhibition develops in parietal areas at ca. 80 ms and shortcuts top-down inputs from the IFG (green arrow; although see Lenartowicz et al., for evidence of a role for the IFG in automatic inhibition; blue arrows) in turn leading to faster inhibition (ca. 150 ms; calculated as the mean RT −100 ms which corresponds to the latency of M1 initiation before motor execution; Thorpe and Fabre-Thorpe, 2001). (B) When S-R mapping varies (as in e.g., SST), top-down, controlled inhibition is modulated by training around 200 ms in the IFG. The IFG then activates subcortical basal ganglia (red arrow) which in turn inhibits the thalamocortical output and suppresses motor execution in M1. Error commission allows shifting from fast automatic to slow top-down controlled forms of inhibition. PAR, parietal; M1, primary motor cortex; IFG, inferior frontal gyrus; BG, basal ganglia; THAL, thalamus; S-R mapping, stimulus-response mapping. Arrows indicate excitatory connections and rounds inhibitory connections. Full lines indicate cortical structures and dashed lines indicate subcortical structures.