Swallow & Jiang (2011) delineated several hypotheses to explain the attentional boost

effect. The first is attentional cueing, which is based on an orienting response to the target leading to a concurrently enhanced processing of the background scene. Attentional cueing may occur concurrently with perceptual learning when target and scene are assembled into a single object (Driver & Baylis, 1989). Based on our findings, however, a simple attentional cueing does not sufficiently explain attentional boost because we did not find any connection with alerting and orienting of visual attention. In a similar paradigm to that used in the present study, Enzalutamide in vitro Leclercq & Seitz (2012) found poor memorization for scenes that were preceded by an auditory alerting cue. However, for target-paired scenes, memory was enhanced when an alerting cue preceded the target, but only when the cue was available only on a subset of trials

(Leclercq & Seitz, 2012). Another possibility high throughput screening is that the target elicits a reward/salience signal because the proper identification and recall of the target letter was the main purpose of the task, and therefore it was indirectly reinforced in the experimental conditions (Seitz & Watanabe, 2009; Swallow & Jiang, 2011; but see also Tosoni et al., 2013). In the present study, we used a direct reward. This reward might ‘widen the window of attention’ facilitating the encoding of the background scene. The hippocampal formation may play a pivotal role in this encoding process because individuals with hippocampal atrophy had weak attentional boost (Szamosi et al., 2013). Shohamy & Wagner (2008) showed that the interaction between midbrain dopaminergic centers (ventral tegmental area/substantia Dichloromethane dehalogenase nigra) and the hippocampal formation

is essential for associative encoding (see also Wimmer et al., 2012). There is evidence that in the hippocampus dopaminergic modulation of attention is important in the selection of relevant and salient information (Muzzio et al., 2009). We propose that similar mechanisms may be implicated in attentional boost, which is intact in early-stage PD when dopaminergic loss is not pronounced in the midbrain-hippocampal system (Foerde et al., 2013). If dopaminergic medications are used in this stage of the disease, patients will demonstrate enhanced attentional boost outperforming healthy unmedicated individuals. An intriguing finding was that patients with PD receiving dopaminergic medications displayed enhanced attentional boost not only in the case of rewarded targets, but also in the case of distractors. In other words, they might encode scenes not only at behaviorally rewarded points of time, but also at behaviorally inhibited occasions when central stimuli (distractors) had to be ignored. In contrast, at behaviorally neutral points (scenes alone), there were no such effects.