Socially isolated mice exhibit a blunted homeostatic sleep response to acute sleep deprivation compared to socially paired mice

Capitanio

2014

Psychological Bulletin

443

351

Social isolation has been recognized as a major risk factor for morbidity and mortality in humans for more than a quarter century. The brain is the key organ of social connections and processes, however, and the same objective social relationship can be experienced as caring and protective or as exploitive and isolating. We review evidence that the perception of social isolation (i.e., loneliness) impacts brain and behavior and is a risk factor for broad-based morbidity and mortality. However, the causal role of loneliness on neural mechanisms and mortality is difficult to test conclusively in humans. Mechanistic animal studies provide a lens through which to evaluate the neurological effects of a member of a social species living chronically on the social perimeter. Experimental studies show that social isolation produces significant changes in brain structures and processes in adult social animals. These effects are not uniform across the brain or across species but instead are most evident in brain regions that reflect differences in the functional demands of solitary versus social living for a particular species. The human and animal literatures have developed independently, however, and significant gaps also exist. The current review underscores the importance of integrating human and animal research to delineate the mechanisms through which social relationships impact the brain, health, and well-being.

Section: Loneliness (Perceived Social Isolation) As a Risk Factor Formentioning

confidence: 74%

Toward a neurology of loneliness.

Capitanio

2014

Psychological Bulletin

443

351

“…Both isolated and pair-housed mice showed increases in EEG delta power in nonrapid eye movement sleep following sleep deprivation, but this increase in EEG delta power did not persist throughout the dark period in socially isolated mice, indicating less deep sleep and poorer sleep quality compared with matched pair-housed mice. This difference was still evident 18 hr after deprivation (Kaushal, Nair, Gozal, & Ramesh, 2012). …”

Section: Loneliness and Self-preservationmentioning

confidence: 87%

Loneliness Across Phylogeny and a Call for Comparative Studies and Animal Models

Cole

et al. 2015

Perspect Psychol Sci

164

140

Loneliness typically refers to the feelings of distress and dysphoria resulting from a discrepancy between a person’s desired and achieved levels of social relations, and there is now considerable evidence that loneliness is a risk factor for poor psychological and physical health. Loneliness has traditionally been conceptualized as a uniquely human phenomenon. However, over millions of years of evolution, efficient and manifold neural, hormonal, and molecular mechanisms have evolved for promoting companionship and mutual protection/assistance and for organizing adaptive responses when there is a significant discrepancy between the preferred and realized levels of social connection. We review evidence suggesting that loneliness is not a uniquely human phenomenon, but, instead, as a scientific construct, it represents a generally adaptive predisposition that can be found across phylogeny. Central to this argument is the premise that the brain is the key organ of social connections and processes. Comparative studies and animal models, particularly when integrated with human studies, have much to contribute to the understanding of loneliness and its underlying principles, mechanisms, consequences, and potential treatments.

“…Sleep-wake states were identified by inspecting both EEG and EMG signals using 4-s epochs, and classified into wakefulness, NREM sleep, and REM sleep, as previously described [33]. Sample EEG-EMG traces of each sleep-wake state are shown in Fig.…”

Section: Methodsmentioning

confidence: 99%

Neuroligin 3 R451C mutation alters electroencephalography spectral activity in an animal model of autism spectrum disorders

et al. 2017

Human studies demonstrate that sleep impairment is a concurrent comorbidity of autism spectrum disorders (ASD), but its etiology remains largely uncertain. One of the prominent theories of ASD suggests that an imbalance in synaptic excitation/inhibition may contribute to various aspects of ASD, including sleep impairments. Following the identification of Nlgn3 R451C mutation in patients with ASD, its effects on synaptic transmission and social behaviours have been examined extensively in the mouse model. However, the contributory role of this mutation to sleep impairments in ASD remains unknown. In this study, we showed that Nlgn3 R451C knock-in mice, an established genetic model for ASD, exhibited normal duration and distribution of sleep/wake states but significantly altered electroencephalography (EEG) power spectral profiles for wake and sleep.