The depth and quality of deep sleep correlates with resilience to stress.

I'm finding that as I grow older my resilience and recovery from stressful situations depends crucially on the depth and quality of my deep sleep (as measured by an apple watch and Oura ring). Consonent with my experience, Sebastian et al. show in electrophysiological studies of male mice that the depth and quality of slow-wave (non-REM), i.e. deep, sleep in the limbic prefrontal cortex before a stressful social encounter predicts which animals prove resilient afterward and which are more likely to become susceptible to lasting behavioral changes. Sleep quality is a hidden variable in resilience, not just a downstream casualty of stress. Here are the significance statement and technical abstract from the Journal of Neuroscience article:

Significance Statement The biological mechanisms driving resilience—the ability to overcome stressful conditions—remain poorly understood. While non-rapid eye movement sleep promotes resilience, the cortical mechanisms underlying sleep’s actions are unclear. Here, we demonstrate that local sleep within the prelimbic cortex—specifically neuronal silence—predicts stress resilience. Using single-unit recordings, we show that neuronal silence is coupled with slow-waves, the hallmark of non-rapid eye movement sleep, and this relationship is strengthened in resilient mice. Furthermore, resilience is associated with a post-stress reorganization of neuronal silence and a redistribution of cortical firing rates. These findings suggest that behavioral resilience is predicted by the prefrontal cortex’s capacity for reorganization during sleep and provide a framework for understanding how sleep-dependent circuit plasticity protects against stress.

Abstract

Understanding the biological mechanisms responsible for resilience to stress—the ability to overcome adverse conditions—remains a major challenge. While sleep is a known regulator of resilience, the localized cortical dynamics that facilitate this process remain unclear. We hypothesized that resilience to social stress is determined by local sleep changes within the prelimbic cortex (PrL), a region critical for top-down control of stress-responsive circuits. To test this, we conducted longitudinal single-unit and local field potential (LFP) recordings in the prelimbic (PrL) cortex of male mice before and after a five-day social defeat stress paradigm. Our results demonstrate that population-wide neuronal silences, or "OFF-periods," primarily occur during NREM sleep and strongly correlate with the local slow-waves. Notably, resilient mice exhibit significantly higher baseline coupling between OFF-period density and the number of slow-waves compared to susceptible animals. Following stress, resilient mice showed a unique reorganization of cortical silence patterns, characterized by an increase in shorter OFF-periods and a more uniform temporal distribution across NREM sleep. Furthermore, social stress was associated with a widespread, stochastic-like redistribution of cortical firing rates that was most pronounced in the resilient phenotype. These findings suggest that behavioral resilience is predicted by the capacity for flexible network redistribution and heightened synchronization during local NREM sleep. Furthermore, this study identifies pre-existing, localized sleep-dependent signatures— specifically a stronger coupling between OFF-period density and slow-wave activity —that serve as potential predictors of resilience prior to stress.

 

How nature nurtures

MindBlog has passed on a number of articles on how exposure to nature reduces stress (see a sample list below). Here is a further contribution from Sudimac et al., who show amygdala activity decreases as the result of a one-hour walk in nature:

Since living in cities is associated with an increased risk for mental disorders such as anxiety disorders, depression, and schizophrenia, it is essential to understand how exposure to urban and natural environments affects mental health and the brain. It has been shown that the amygdala is more activated during a stress task in urban compared to rural dwellers. However, no study so far has examined the causal effects of natural and urban environments on stress-related brain mechanisms. To address this question, we conducted an intervention study to investigate changes in stress-related brain regions as an effect of a one-hour walk in an urban (busy street) vs. natural environment (forest). Brain activation was measured in 63 healthy participants, before and after the walk, using a fearful faces task and a social stress task. Our findings reveal that amygdala activation decreases after the walk in nature, whereas it remains stable after the walk in an urban environment. These results suggest that going for a walk in nature can have salutogenic effects on stress-related brain regions, and consequently, it may act as a preventive measure against mental strain and potentially disease. Given rapidly increasing urbanization, the present results may influence urban planning to create more accessible green areas and to adapt urban environments in a way that will be beneficial for citizens’ mental health.

A few previous MindBlog posts on this topic:

Blue Mind - looking at water improves your health and calm 

Pictures of green spaces make you happier. 

More green space in childhood, fewer psychiatric disorders in adulthood.

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 (The above is a repost of MindBlog's 9/26/2022 post)

 

How ketamine breaks through anhedonia - reigniting desire

When chronic depression has not been relieved by behavioral therapies such as meditation or cognitive therapy ketamine is sometimes found to provide relief. Lucan at all probe brain changes in mice given a single expose to ketamine that rescues then from chronic stress inducted anhedonia.  Here is their summary of the paper:

Ketamine is recognized as a rapid and sustained antidepressant, particularly for major depression unresponsive to conventional treatments. Anhedonia is a common symptom of depression for which ketamine is highly efficacious, but the underlying circuits and synaptic changes are not well understood. Here, we show that the nucleus accumbens (NAc) is essential for ketamine’s effect in rescuing anhedonia in mice subjected to chronic stress. Specifically, a single exposure to ketamine rescues stress-induced decreased strength of excitatory synapses on NAc-D1 dopamine receptor-expressing medium spiny neurons (D1-MSNs). Using a cell-specific pharmacology method, we establish the necessity of this synaptic restoration for the sustained therapeutic effects of ketamine on anhedonia. Examining causal sufficiency, artificially increasing excitatory synaptic strength onto D1-MSNs recapitulates the behavioral amelioration induced by ketamine. Finally, we used opto- and chemogenetic approaches to determine the presynaptic origin of the relevant synapses, implicating monosynaptic inputs from the medial prefrontal cortex and ventral hippocampus.