From learned value to sustained bias: how reward conditioning changes attentional priority

Attentional bias to reward-associated stimuli can occur even when it interferes with goal-driven behavior. One theory posits that striatal activitydopaminergic siganaling in the striatum during reward conditioning leads to changes in visual cortical and parietal representations of the stimulus used; this in turn sustains attentional bias even when reward is discontinued. However, only a few studies have examined neural activity during both rewarded and unrewarded task phases. In the current study, participants first completed a reward-conditioned conditioning learning phase, during which responses to certain stimuli were associated with monetary reward. These stimuli were then included as non-predictive cues in a spatial cueing task. Participants underwent functional brain imaging during both task phases. Results show that striatal activity during the learning phase predicted increased visual cortical and parietal activity, and decreased ventro-medial prefrontal cortex activity, in response to conditioned stimuli at test. Striatal activity was also associated with anterior cingulate cortex activation when the reward-conditioned stimulus directed attention away from the target. Our findings Findings suggest that striatal activity during reward conditioning predicts the degree to which reward history biases attention through learning-induced changes in visual and parietal activity

Spectrum of Infection and Risk Factors for Human Monkeypox, United States, 2003

Infection is associated with proximity to virus-infected animals and their excretions and secretions

RALA and RALBP1 regulate mitochondrial fission at mitosis

Mitochondria exist as dynamic interconnected networks that are maintained through a balance of fusion and fission(1). Equal distribution of mitochondria to daughter cells during mitosis requires fission(2). Mitotic mitochondrial fission depends upon both the relocalization of large GTPase Drp1 to the outer mitochondrial membrane and phosphorylation of S616 on Drp1 by the mitotic kinase cyclin B/Cdk1(2). We now report that these processes are mediated by the small Ras-like GTPase RalA and its effector RalBP1 (RLIP76/RLIP1/RIP1)(3,4). Specifically, the mitotic kinase Aurora A phosphorylates S194 of RalA, relocalizing it to the mitochondria, where it concentrates RalBP1 and Drp1. Furthermore, RalBP1 associates with cyclin B/Cdk1 kinase activity to foster phosphorylation of Drp1 on S616. Disrupting either RalA or RalBP1 leads to a loss of mitochondrial fission at mitosis, improper segregation of mitochondria during cytokinesis and a decrease in ATP levels and cell number. Thus, the two mitotic kinases Aurora A and cyclin B/Cdk1 converge upon RalA and RalBP1 to promote mitochondrial fission, the appropriate distribution of mitochondria to daughter cells and ultimately proper mitochondrial function