What is your brain doing while your mind is wandering? This study used a within-subjects experience-sampling design to test whether episodes of mind-wandering during a demanding cognitive task are associated with increases in EEG alpha power. Alpha refers to cyclic oscillations in EEG activity at 8-12 Hz, and has been previously correlated with internally rather than externally directed cognition. Participants completed a speeded performance task with more than 800 trials while EEG was recorded. Intermittent experience-sampling probes asked participants to indicate whether their mind was wandering or on-task. Participants reported mind-wandering in response to approximately half of the probes. EEG alpha power was significantly higher preceding probes to which participants reported mind-wandering, compared with probes to which participants reported being on task. These findings imply that dynamic changes in alpha power may prove a valuable tool in studying momentary fluctuations in mind-wandering.

Arousal evoked by detecting a performance error may provide a mechanism by which error detection leads to either adaptive or maladaptive changes in attention and performance. By pairing EEG data acquisition with simultaneous measurements of pupil diameter, which is thought to reflect norepinephrinergic arousal, this study tested whether transient changes in EEG oscillations in the alpha frequency range (8–12 Hz) following performance mistakes may reflect error‐evoked arousal. In the inter‐trial interval following performance mistakes (approximately 8% of trials), pupil diameter increased and EEG alpha power decreased, compared to the inter‐trial interval following correct responses. Moreover when trials were binned based on pupil diameter on a within‐subjects basis, trials with greater pupil diameter were associated with lower EEG alpha power during the inter‐trial interval. This pattern of association suggests that error‐related alpha suppression, like pupil dilation, reflects arousal in response to error commission. Errors were also followed by worse next‐trial performance, implying that error‐evoked arousal may not always be beneficial for adaptive control.

No abstract

Background: Estrogen increases dramatically during pregnancy, but quickly drops below prepregnancy levels at birth and remains suppressed during the postpartum period. Clinical and rodent work suggests that this postpartum drop in estrogen results in an "estrogen withdrawal" state that is related to changes in affect, mood, and behavior. Most studies examining the effect of estrogen withdrawal on the brain have focused solely on the hippocampus. Methods: We used a hormone-simulated pseudopregnancy model in Syrian hamsters, a first for this species.Ovariectomized females were given daily injections to approximate hormone levels during gestation and then withdrawn from estrogen to simulate postpartum estrogen withdrawal.Subjects were tested for behavioral assays of anxiety and anhedonia during estrogen withdrawal. Following sacrifice, neuroplasticity in oxytocin-producing neurons in the paraventricular nucleus of the hypothalamus (PVH) and its efferent targets was measured.Results: Estrogen-withdrawn females had increased anxiety-like behaviors in the elevated plus and open field, but did not differ from controls in sucrose preference. Furthermore, estrogenwithdrawn females had more oxytocin-immunoreactive cells and oxytocin mRNA in the PVH, as well as an increase in oxytocin receptor density in the dorsal raphe nucleus (DRN). Finally, blocking oxytocin receptors in the DRN during estrogen withdrawal prevented the high-anxiety behavioral phenotype in estrogen-withdrawn females. Conclusions: Estrogen withdrawal alters oxytocin signaling in the PVH and DRN to increase anxiety-like behavior during the postpartum period. More broadly, these experiments suggest Syrian hamsters as a novel organism in which to model the effects of postpartum estrogen withdrawal on the brain and anxiety-like behavior.

No abstract