Introduction Evidence suggests that individuals with generalized anxiety disorder exhibit decreases in slow-wave sleep (SWS). Because SWS has been shown to be modifiable, it is imperative to better understand the relationship between symptoms of anxiety and amount of SWS to inform treatment development. This study aimed to explore the relationship between anxiety and SWS, and to investigate the impact of slow-wave sleep disruption on state anxiety. Methods Twenty-seven participants’ (mean age 30.9) were recruited as part of an ongoing study examining the relationship between SWS and depression. Participants spent two nights in the laboratory: baseline (BL) and slow-wave disruption (SWD), where SWS was disrupted using auditory stimulation. Anxiety was measured using the State-Trait Anxiety Inventory (STAI). Both trait and state anxiety (BL, SWD) measures were collected. Repeated measures ANOVA was used to determine the impact of SWD on state anxiety. Results Participants’ trait anxiety scores were significantly correlated with percent N3, such that greater anxiety was associated with less N3 (r = -0.43; p<0.05). Individuals were then categorized as either high-anxiety (HA) or low-anxiety (LA) by median split (M=46.5). Results of the repeated measures showed a significant main effect of group (F=43.963; p<0.001), with HA individuals showing greater state anxiety than LA individuals. A significant interaction of group*condition was also found (F(1,24)=4.703; p=0.40). LA participants showed a significant increase in state anxiety following SWD (t=-2.539; p=0.028), while HA participants showed no change. Conclusion The current findings replicate previous research showing that anxious individuals have a reduced amount of SWS and demonstrate that decreases in SWS may exacerbate anxiety in individuals with low anxiety. Further, this work suggests that individuals with high anxiety may be more resilient to changes in anxiety state than individuals with low anxiety when SWS is reduced. Support (If Any) Goldschmied: K23MH118580 (NIMH)

Introduction Irritability has been proposed to be a core symptom of male-specific major depressive disorder (MDD), with a greater propensity to experiencing anger attacks and overreacting to minor annoyances compared to females with MDD. Males with MDD have also been shown to exhibit a pattern of reduced slow-wave sleep (SWS) that is not characteristic of females. Because SWS has been implicated in the homeostatic regulation of neuroplasticity, it is possible that this mood dysfunction in males is a result of SWS alterations via impairments in neuroplasticity. Therefore, in this study we aimed to manipulate SWS and examine its impact on mood. Methods 19 individuals (11 F) with MDD were recruited for an ongoing clinical trial. Participants spent two nights in the sleep laboratory one week apart: a baseline (BL) night, and a night of slow-wave sleep disruption (SWD) utilizing auditory stimulation. Irritability was assessed in the morning following each overnight visit using the 5-item Brief Irritability Test (BITe). Repeated measures ANOVA was used to evaluate the change in irritability following SWD with condition (BL, SWD) as the within-subject factor and sex (M, F) as the between-subjects factor. Results Results revealed a significant Condition x Sex interaction (F(1,17) =10.1, p=.006) for change in irritability scores, with post-hoc t-tests indicating that males with MDD showed a significant decrease in irritability following SWD, t(7)=2.22, p<.05 while women showed a significant increase in irritability, t(10)=-2.34, p<.05. Changes in irritability were not found to be associated with changes in N3. Conclusion These data demonstrate that experimentally reducing SWS decreases irritability, a core symptom of mood dysfunction, in males with MDD. As SWS has been theorized to facilitate synaptic downscaling, these results may indicate that maintaining waking levels of synaptic strength in males improves depressive symptomatology and may point to the importance of sex differences in sleep and psychopathology. Moreover, these results suggest that the modulation of neuroplasticity via sleep manipulation may be a potential therapeutic target. Support (If Any) K23MH118580 (JG)

Introduction Research has demonstrated that sleep deprivation may alter emotion recognition. Given that emotion recognition is critical for effective human communication, it is essential to understand how sleep is involved in this process. Slow-wave sleep (SWS) has been suggested to be important for the consolidation and processing of emotional memories and neuroplasticity. This study aimed to examine the impact of experimental disruption of SWS on emotion recognition to further understand the contribution of SWS. Methods 31 participants (20 individuals diagnosed with Major Depressive Disorder (MDD), 11 healthy controls (HC)) completed two overnight sleep studies spaced one week apart. One night served as baseline (BL) and on the other night participants underwent slow-wave disruption (SWD), where SWS was disrupted using auditory stimulation. In the morning following each overnight visit, participants completed an emotion recognition task. Accuracy scores were computed as the percentage correct in each of 10 categories of emotions (anger, contempt, disgust, embarrassment, fear, joy, neutral, pride, sadness, and surprise). Repeated measures ANOVA was used to assess the impact of SWD on emotion recognition with group (HC, MDD) as the between subjects factor and condition (BL, SWD) as the within subjects factor. Results Results revealed a significant main effect of condition for disgust (F=13.72, p< .001), embarrassment (F=6.23, p=.019), and surprise (F=8.06, p=.008), with follow-up t-tests demonstrating that accuracy for the recognition of disgust and embarrassment decreased following SWD and accuracy for surprise increasing following SWD. No significant interactions were found for group*condition (ps>.105). Conclusion These results suggest that while SWD decreases the ability to recognize certain negative emotions, it also increases the ability to recognize surprise, which is in line with previous research examining acute total sleep deprivation. Interestingly, there appears to be no difference in the ability to recognize emotions between individuals with and without depression. Slow-wave sleep deficits, common in disorders such as depression and schizophrenia, may therefore contribute to poor communication abilities through decreased ability to recognize emotions, increasing the risk of interpersonal distress and mental health problems. Support (If Any) Goldschmied: K23MH118580 (NIMH)

No abstract

Introduction Individuals with Major Depressive Disorder (MDD) exhibit reductions in slow-wave sleep (SWS) and impairments in neuroplasticity. For example, decreased executive functioning, including poorer response inhibition compared to healthy controls, has been reported. SWS has been implicated in the homeostatic regulation of neuroplasticity, however it is unclear if the cognitive deficits seen in MDD are directly associated with SWS. In this study, we aimed to examine if disrupting SWS, thereby altering neuroplasticity, could improve response inhibition in patients with MDD. Methods Participants in this study (n=29) included 19 individuals with depression and 10 healthy controls. Data were collected after two overnight sleep studies separated by one week. During one of the two nights, participants’ slow-wave sleep was disrupted via auditory tones. In the morning following each night, participants completed a neurocognitive task battery including an auditory Go/No-Go task. Accuracy scores were calculated as the percentage of trials on which the participant responded correctly to the “Go” or “No-Go” stimulus. Repeated measures ANOVA and paired t-tests were then performed to examine changes from baseline to SWD, assessing the role of SWD on response inhibition. Results Following SWD, depressed participants’ performance on the Go/No-Go task was significantly more accurate (t=-2.067, p=.027) than following baseline sleep, while healthy controls showed no significant change between nights (t=-.231, p=.411). The interaction between group (MDD vs. healthy control) and condition (baseline vs. SWD) did not reach statistical significance (p=.175). Conclusion In a sample of individuals with depression, accuracy on the Go/No-Go task improved significantly after undergoing SWD compared to following baseline sleep, indicating improved response inhibition. However, healthy controls did not exhibit this same improvement in accuracy. These findings highlight a possible disparity in the role that SWS plays in the regulation of neuroplasticity in those with depression and those without. Support (If Any) Goldschmied: K23MH118580 (NIMH)