Furthermore, there is general agreement that inhibitory processes involve frontal regions of the IWR-1 nmr brain, more specifically lateral regions of the right prefrontal cortex [1]. Interest in the neural bases of inhibitory processing is high because these processes have been found to be disrupted in a number of psychiatric disorders, including ADHD [2] and substance abuse disorders [3]. This review focuses on two issues that recently have spurred debate. While there is agreement that right lateral prefrontal regions play a prominent role in inhibitory control, the exact nature

of the specific computation or process that is being implemented by this region, especially that of the right inferior frontal gyrus (rIFG), is being debated (see Figure 1). The second issue Afatinib purchase revolves around the degree to which ‘inhibition’ is a unitary construct, which relies on a central

shared brain mechanism regardless of the domain — motoric, cognitive, or emotional — in which inhibition is exerted, or whether there are separate neural mechanisms for inhibitory control in each of these domains. Typically, inhibitory control is indexed by asking an individual to override, interrupt, or suppress an ongoing cognitive, emotional or behavioral response. Classically this ability has been measured by paradigms that assess inhibition in the motoric domain, such as the Go/No-Go paradigm, which induces a prepotent bias to respond, and which must be overridden when certain specific stimuli are present. Similarly, in the Stop-Signal paradigm, individuals Y-27632 2HCl make a forced-choice decision on the majority of trials, but on a minority a specific sensory signal

(e.g., auditory tone, perceptual cue) indicates that an ongoing process of responding must be aborted or interrupted [4]. Approximately a decade ago, it was proposed that the rIFG (also sometimes referred to as right ventrolateral cortex) plays a prominent role in inhibiting motor responses by sending a signal to the subthalamic nucleus of the basal ganglia, which in turn suppresses thalamocortical output so as to preclude motor responding [5•]. Since that time, compelling work using a variety of converging methods including that performed with patients with focal lesions, alteration of brain activation (rTMS, tDCS), neuroimaging and electrophysiological evidence has supported such a viewpoint [6••]. An expansion of this viewpoint suggests two distinct forms of motor inhibition, one invoked for stopping all responses, and another that is more selective, only stopping certain responses but not others [7]. It has been proposed that the global stopping mechanisms may be mediated by a hyperdirect pathway from the rIFG → STN → Globus Pallidus → Thalamus.