Early Life Trauma Has Lifelong Consequences for Sleep And Behavior

Lewin, Monica; Lopachin, Jenna; Delorme, James; Opendak, Maya; Sullivan, Regina M.; Wilson, Donald A.

doi:10.1038/s41598-019-53241-y

Cited by 25 publications

(13 citation statements)

References 89 publications

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“…The analyses of slow-wave bouts included the mean percent time in slow-wave over 24 h, mean slow-wave bout duration, and the mean number of slow-wave bout transitions/h of slow-wave activity. The accuracy of slow-wave sleep scoring was also confirmed in a small set of animals with simultaneous visual scoring over 1–2 h periods ( n = 4) to ensure scored sleep epochs corresponded to behavioral sleep periods ( Lewin et al, 2019 ).…”

Section: Methodsmentioning

confidence: 96%

Somatostatin neuron contributions to cortical slow wave dysfunction in adult mice exposed to developmental ethanol

Wilson

Fleming²,

Williams³

et al. 2023

Front. Neurosci.

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IntroductionTransitions between sleep and waking and sleep-dependent cortical oscillations are heavily dependent on GABAergic neurons. Importantly, GABAergic neurons are especially sensitive to developmental ethanol exposure, suggesting a potential unique vulnerability of sleep circuits to early ethanol. In fact, developmental ethanol exposure can produce long-lasting impairments in sleep, including increased sleep fragmentation and decreased delta wave amplitude. Here, we assessed the efficacy of optogenetic manipulations of somatostatin (SST) GABAergic neurons in the neocortex of adult mice exposed to saline or ethanol on P7, to modulate cortical slow-wave physiology.MethodsSST-cre × Ai32 mice, which selectively express channel rhodopsin in SST neurons, were exposed to ethanol or saline on P7. This line expressed similar developmental ethanol induced loss of SST cortical neurons and sleep impairments as C57BL/6By mice. As adults, optical fibers were implanted targeting the prefrontal cortex (PFC) and telemetry electrodes were implanted in the neocortex to monitor slow-wave activity and sleep-wake states.ResultsOptical stimulation of PFC SST neurons evoked slow-wave potentials and long-latency single-unit excitation in saline treated mice but not in ethanol mice. Closed-loop optogenetic stimulation of PFC SST neuron activation on spontaneous slow-waves enhanced cortical delta oscillations, and this manipulation was more effective in saline mice than P7 ethanol mice.DiscussionTogether, these results suggest that SST cortical neurons may contribute to slow-wave impairment after developmental ethanol.

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Section: Methodsmentioning

confidence: 96%

Somatostatin neuron contributions to cortical slow wave dysfunction in adult mice exposed to developmental ethanol

Wilson

Fleming²,

Williams³

et al. 2023

Front. Neurosci.

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“…Several studies have linked childhood trauma exposure to post-exposure insomnia, nightmare-related distress, and types of sleep disorders ( 28 , 29 ). Sleep disorders, such as subjectively experienced difficulty falling asleep, easy awakening, and shortened sleep time, are common symptoms after trauma exposure in the short and long term ( 30 , 31 ). The effects of adverse childhood experiences on sleep are also observed in adolescents ( 32 ).…”

Section: Introductionmentioning

confidence: 99%

Sleep disorders mediate the link between childhood trauma and depression severity in children and adolescents with depression

et al. 2022

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BackgroundChildhood trauma is closely related to the onset of depression and more severe depressive symptoms; however, the specific mechanisms are unclear. We aimed to examine the relationship between childhood trauma and sleep disorders in children and adolescents with depression and to explore further the role of sleep disorders in the relationship between childhood trauma and depression severity.MethodsA total of 285 children and adolescents with depression completed all scale assessments, including the Childhood Trauma Questionnaire, Self-Reported Insomnia Severity Index and Epworth Sleepiness Scale, and the Center for Epidemiologic Studies Depression Scale. A simple mediation model was used as a theoretical model to examine whether sleep disorders could mediate the relationship between childhood trauma and depression severity.ResultsAmong children and adolescents with depression, childhood trauma is about 78.9%. Compared with patients without childhood trauma, patients with childhood trauma had a higher incidence of sleep disorders (Z = 17.59, P < 0.001), which were characterized by insomnia (Z = 14.45, P < 0.001), not hypersomnia (Z = 2.77, P = 0.096). Different childhood trauma subtypes significantly affected sleep disorders and insomnia (all P < 0.05). Insomnia partially mediated the relationship between childhood trauma and depression severity, and the mediating effect accounted for 35.90%.ConclusionThis study found a high rate of concurrent childhood trauma and insomnia among children and adolescents with depression. Insomnia, as a mediator between childhood trauma and depression severity, partially mediates the relationship.

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“…Typically, LB models last for 7 days, while MS models last for 18 days, and it is, therefore, possible that the difference in duration of adversity contributes to the disparity observed between adversity types. MS stress may lend itself more to isolation stress, while LB may lead to more aversive stress, as modified LB methods have been related to abusive maternal care (e.g., Lewin et al, 2019 ). It is possible that the types of stress elicited by the models differ, leading to unique changes in PV.…”

Section: Introductionmentioning

confidence: 99%

Sex Differences in Affective Dysfunction and Alterations in Parvalbumin in Rodent Models of Early Life Adversity

Ellis

Ganguly

2021

Front. Behav. Neurosci.

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The early life environment markedly influences brain and behavioral development, with adverse experiences associated with increased risk of anxiety and depressive phenotypes, particularly in females. Indeed, early life adversity (ELA) in humans (i.e., caregiver deprivation, maltreatment) and rodents (i.e., maternal separation, resource scarcity) is associated with sex-specific emergence of anxious and depressive behaviors. Although these disorders show clear sex differences in humans, little attention has been paid toward evaluating sex as a biological variable in models of affective dysfunction; however, recent rodent work suggests sex-specific effects. Two widely used rodent models of ELA approximate caregiver deprivation (i.e., maternal separation) and resource scarcity (i.e., limited bedding). While these approaches model aspects of ELA experienced in humans, they span different portions of the pre-weaning developmental period and may therefore differentially contribute to underlying mechanistic risk. This is borne out in the literature, where evidence suggests differences in trajectories of behavior depending on the type of ELA and/or sex; however, the neural underpinning of these differences is not well understood. Because anxiety and depression are thought to involve dysregulation in the balance of excitatory and inhibitory signaling in ELA-vulnerable brain regions (e.g., prefrontal cortex, amygdala, hippocampus), outcomes are likely driven by alterations in local and/or circuit-specific inhibitory activity. The most abundant GABAergic subtypes in the brain, accounting for approximately 40% of inhibitory neurons, contain the calcium-binding protein Parvalbumin (PV). As PV-expressing neurons have perisomatic and proximal dendritic targets on pyramidal neurons, they are well-positioned to regulate excitatory/inhibitory balance. Recent evidence suggests that PV outcomes following ELA are sex, age, and region-specific and may be influenced by the type and timing of ELA. Here, we suggest the possibility of a combined role of PV and sex hormones driving differences in behavioral outcomes associated with affective dysfunction following ELA. This review evaluates the literature across models of ELA to characterize neural (PV) and behavioral (anxiety- and depressive-like) outcomes as a function of sex and age. Additionally, we detail a putative mechanistic role of PV on ELA-related outcomes and discuss evidence suggesting hormone influences on PV expression/function which may help to explain sex differences in ELA outcomes.

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Early Life Trauma Has Lifelong Consequences for Sleep And Behavior

Cited by 25 publications

References 89 publications

Somatostatin neuron contributions to cortical slow wave dysfunction in adult mice exposed to developmental ethanol

Somatostatin neuron contributions to cortical slow wave dysfunction in adult mice exposed to developmental ethanol

Sleep disorders mediate the link between childhood trauma and depression severity in children and adolescents with depression

Sex Differences in Affective Dysfunction and Alterations in Parvalbumin in Rodent Models of Early Life Adversity

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