Individuals may differ systematically in their applied decision strategies, which has critical implications for decision neuroscience but is yet scarcely studied. Our study's main focus was therefore to investigate the neural mechanisms underlying compensatory versus noncompensatory strategies in risky choice. Here, we compared people using a compensatory expected value maximization with people using a simplified noncompensatory loss-minimizing choice strategy. To this end, we used a two-choice paradigm including a set of “simple”

The ability to stop ongoing motor responses in a split-second is a vital element of human cognitive control and flexibility that relies in large part on prefrontal cortex. We used the stop-signal paradigm to elucidate the engagement of primary motor cortex (M1) in inhibiting an ongoing voluntary motor response. The stop-signal paradigm taps the ability to flexibly countermand ongoing voluntary behavior upon presentation of a stop signal. We applied single-pulse TMS to M1 at several intervals following the stop signal to track the time course of excitability of the motor system related to generating and stopping a manual response. Electromyography recorded from the flexor pollicis brevis allowed quantification of the excitability of the corticospinal tract and the involvement of intracortical GABA B ergic circuits within M1, indexed respectively by the amplitude of the motor-evoked potential and the duration of the late part of the cortical silent period (SP). The results extend our knowledge of the neural basis of inhibitory control in three ways. First, the results revealed a dynamic interplay between response activation and stopping processes at M1 level during stop-signal inhibition of an ongoing response. Second, increased excitability of inhibitory interneurons that drives SP prolongation was evident as early as 134 msec following the instruction to stop. Third, this pattern was followed by a stop-related reduction of corticospinal excitability implemented around 180 after the stop signal. These findings point to the recruitment of GABA B ergic intracortical inhibitory circuits within M1 in stop-signal inhibition and support the notion of stopping as an active act of control.

The aim of the present study was to specify the involvement of the basal ganglia in motor response selection and response inhibition. Two samples were studied. The first sample consisted of patients diagnosed with Parkinson's disease (PD) who received deep-brain stimulation (DBS) of the subthalamic nucleus (STN). The second sample consisted of patients who received DBS for the treatment of PD or essential tremor (ET) in the ventral intermediate nucleus of the thalamus (Vim). Stop-signal task and go/no-go task performances were studied in both groups. Both groups performed these tasks with ( on stimulation) and without ( off stimulation) DBS to address the question of whether stimulation is effective in improving choice reaction time (RT) and stop-signal RT. The results show that DBS of the STN was associated with significantly enhanced inhibitory control, as indicated by shorter stop-signal RTs. An additional finding is that DBS of the STN led to significantly shorter choice RT. The effects of DBS on responding and response inhibition were functionally independent. Although DBS of the Vim did not systematically affect task performance in patients with ET, a subgroup of Vim-stimulated PD patients showed enhanced stop-signal RTs in on stimulation versus off stimulation. This result suggests that the change in performance to stop signals may not be directly related to STN function, but rather results from a change in PD function due to DBS in general. The findings are discussed in terms of current functional and neurobiological models that relate basal ganglia function to the selection and inhibition of motor responses.