No abstract

Selective attention enhances behaviorally important information and suppresses distracting information. Research on the neural basis of selective attention has largely focused on sensory enhancement, with less focus on sensory suppression. Enhancement and suppression can operate through a push-pull relationship that arises from competitive interactions among neural populations. There has been considerable debate, however, regarding (i) whether suppression can also operate independent of enhancement and (ii) whether neural processes associated with the voluntary deployment of suppression can occur prior to distractor onset. We provide further behavioral and electrophysiological evidence of independent suppression at cued distractor locations while humans performed a visual search task. We specifically utilize two established EEG markers of suppression: alpha power (~8-15 Hz) and the distractor positivity (PD). Increased alpha power has been linked with attenuated sensory processing, while the PD, a component of event-related potentials, has been linked with successful distractor suppression. The present results demonstrate that cueing the location of an upcoming distractor speeded responding and led to an earlier onset PD, consistent with earlier suppression due to strategic use of a spatial cue. We further demonstrate that higher pre-distractor alpha power contralateral to distractors was generally associated with successful suppression on both cued and non-cued trials. However, there was no consistent change in alpha power associated with the spatial cue, meaning cueing effects on behavioral and neural measures occurred independent of alpha- related gating of sensory processing. These findings reveal the importance of pre-distractor neural processes for subsequent distractor suppression.

Background: Goal-directed attention involves the selective processing of behaviorally relevant sensory information. This selective processing is thought to be supported by glutamatergic and noradrenergic systems. Pharmacotherapies that simultaneously target these systems could therefore be effective treatments for impaired attention. Aims: We first tested an N-methyl-D-aspartate (NMDA) receptor co-agonist (D-serine) for effects on attention (processing speed and attentional lapses). NMDA receptor activation is thought to support noradrenergic effects on sensory processing; therefore, we tested a combination treatment comprising D-serine and a norepinephrine reuptake inhibitor (atomoxetine). Methods: D-serine was first tested in rats performing a two-choice visuospatial discrimination task. Combination treatments comprising relatively low doses of D-serine and atomoxetine were then tested in a separate group. Results: In experiment 1, D-serine reduced the skew of initiation time (IT) distributions (IT devmode) at the highest dose tested (300 mg/kg). In experiment 2, low-dose D-serine (125 mg/kg) had no effect, while low-dose atomoxetine (0.3 mg/kg) reduced IT devmode and slowed movement speed. Importantly, the combination of these relatively low doses of D-serine and atomoxetine reduced IT devmode more than either drug alone without further slowing movement speed. Conclusions: IT devmode is thought to reflect attentional lapses; therefore, D-serine’s effects on IT devmode suggest that NMDA receptors are involved in the preparatory deployment of attention. Greater effects following a combination of D-serine and atomoxetine suggest that preparatory attention can be facilitated by targeting glutamatergic and noradrenergic systems simultaneously. These results could inform the development of improved treatments for individuals with ADHD who experience abnormally high attentional lapses.