Fatigue is a disabling symptom in patients with multiple sclerosis and Parkinson’s Disease, and is also common in patients with traumatic brain injury, cancer, and inflammatory disorders. Little is known about the neurobiology of fatigue, in part due to the lack of an approach to induce fatigue in laboratory animals. Fatigue is a common response to systemic challenge by pathogens, a response in part mediated through action of the pro-inflammatory cytokine interleukin-1 beta (IL-1β). We investigated the behavioral responses of mice to IL-1β. Female C57Bl/6J mice of 3 ages were administered IL-1β at various doses i.p. Interleukin-1β reduced locomotor activity, and sensitivity increased with age. Further experiments were conducted with middle-aged females. Centrally administered IL-1β dose-dependently reduced locomotor activity. Using doses of IL-1β that caused suppression of locomotor activity, we measured minimal signs of sickness, such as hyperthermia, pain or anhedonia (as measured with abdominal temperature probes, pre-treatment with the analgesic buprenorphine and through sucrose preference, respectively), all of which are responses commonly reported with higher doses. We found that middle-aged orexin-/- mice showed equivalent effects of IL-1β on locomotor activity as seen in wild-type controls, suggesting that orexins are not necessary for IL-1β -induced reductions in wheel-running. Given that the availability and success of therapeutic treatments for fatigue is currently limited, we examined the effectiveness of two potential clinical treatments, modafinil and methylphenidate. We found that these treatments were variably successful in restoring locomotor activity after IL-1β administration. This provides one step toward development of a satisfactory animal model of the multidimensional experience of fatigue, a model that could allow us to determine possible pathways through which inflammation induces fatigue, and could lead to novel treatments for reversal of fatigue.
Sleep spindles, defining oscillations of non‐rapid eye movement stage 2 sleep (N2), mediate memory consolidation. Spindle density (spindles/minute) is a stable, heritable feature of the sleep electroencephalogram. In schizophrenia, reduced spindle density correlates with impaired sleep‐dependent memory consolidation and is a promising treatment target. Measuring sleep spindles is also important for basic studies of memory. However, overnight sleep studies are expensive, time consuming and require considerable infrastructure. Here we investigated whether afternoon naps can reliably and accurately estimate nocturnal spindle density in health and schizophrenia. Fourteen schizophrenia patients and eight healthy controls had polysomnography during two overnights and three afternoon naps. Although spindle density was lower during naps than nights, the two measures were highly correlated. For both groups, naps and nights provided highly reliable estimates of spindle density. We conclude that naps provide an accurate, reliable and more scalable alternative to measuring spindle density overnight.
Results: Out of the 310 students who participated in the study, 298 (96.1%) returned an appropriately completed questionnaire (Male-56%). The prevalence of poor sleep quality was 48.0%. A significant majority (77.7%) had moderate to high level of perceived stress and the mean CGPA (SD) was 3.84 (2.03). About one-fourth had a high risk for psychopathology. The global sleep quality score was positively correlated with perceived stress level (R=0.187, p=0.001) and risk of psychopathology (R=0.453, p <0.001 Introduction: Sleep disturbance is common within psychosis, and it is found to be predictive of future diagnoses of schizophrenia and bipolar disorder. However, there has been no comprehensive synthesis of non-clinical psychosis-like and hypomanic-like experiences and sleep disturbances. The present review aimed to identify and assess the causal nature of sleep disturbances within non-clinical psychosis-like and hypomanic-like experiences. Methods: On September 2016, a systematic literature review of MedLine and PsycInfo identified studies in the general population which reported a validated measure of sleep and psychosis-like or hypomanic-like experiences. A total of 5643 manuscripts were identified in the initial search and 45 were retained for this review. Effect sizes were calculated to assess the magnitude of associations between sleep and circadian variables and psychosis-like and hypomanic-like experiences. However, a full meta-analysis was not appropriate given heterogeneity of study designs. Results:The results showed that insomnia was associated with all individual psychosis-like and hypomania-like experiences reviewed. Parasomnias, nightmare frequency, nightmare distress and individual sleep stages were associated with psychosis-like experiences but there was evidence of variation in magnitude between individual experiences. Sleep manipulation studies highlighted a potential causal link between sleep loss and psychosis-like experiences but limitations in methodology made it hard to draw definite conclusions at this time. Finally, a dysregulation of circadian rhythms was found in the hypomania-like but not psychosis-like experiences. However, gaps in the literature made it difficult to make strong comparisons between these two non-clinical experience clusters. Conclusion:The review found that sleep disturbances were linked to non-clinical psychosis-like experiences but there are currently gaps in the literature which makes it hard to make direct comparisons between individual psychosis-like experiences. Introduction: Sleep spindle density has shown good test-retest reliability in nocturnal sleep and in naps. Additionally, both nocturnal sleep and naps enhance memory consolidation. However, research on the reliability of spindle density and memory enhancement between nocturnal sleep and naps is lacking. If naps provide reliable estimates of nocturnal sleep spindle density and overnight memory consolidation, future studies of spindles and sleep-dependent memory consolidation can be tested using naps rathe...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.