sleep disruption
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The role of the complement pathway in post-traumatic sleep disruption and epilepsy
While traumatic brain injury (TBI) acutely disrupts the cortex, most TBI-related disabilities reflect secondary injuries that accrue over time. The thalamus is a likely site of secondary damage because of its reciprocal connections with the cortex. Using a mouse model of mild cortical injury that does not directly damage subcortical structures (mTBI), we found a chronic increase in C1q expression specifically in the corticothalamic circuit. Increased C1q expression co-localized with neuron loss and chronic inflammation, and correlated with disruption in sleep spindles and emergence of epileptic activities. Blocking C1q counteracted these outcomes, suggesting that C1q is a disease modifier in mTBI. Single-nucleus RNA sequencing demonstrated that microglia are the source of thalamic C1q. Since the corticothalamic circuit is important for cognition and sleep, which can be impaired by TBI, this circuit could be a new target for treating TBI-related disabilities
A metabolic function of the hippocampal sharp wave-ripple
The hippocampal formation has been implicated in both cognitive functions as well as the sensing and control of endocrine states. To identify a candidate activity pattern which may link such disparate functions, we simultaneously measured electrophysiological activity from the hippocampus and interstitial glucose concentrations in the body of freely behaving rats. We found that clusters of sharp wave-ripples (SPW-Rs) recorded from both dorsal and ventral hippocampus reliably predicted a decrease in peripheral glucose concentrations within ~10 minutes. This correlation was less dependent on circadian, ultradian, and meal-triggered fluctuations, it could be mimicked with optogenetically induced ripples, and was attenuated by pharmacogenetically suppressing activity of the lateral septum, the major conduit between the hippocampus and subcortical structures. Our findings demonstrate that a novel function of the SPW-R is to modulate peripheral glucose homeostasis and offer a mechanism for the link between sleep disruption and blood glucose dysregulation seen in type 2 diabetes and obesity.
Thalamic reticular nucleus dysfunction in neurodevelopmental disorders
The thalamic reticular nucleus (TRN), the major source of thalamic inhibition, is known to regulate thalamocortical interactions critical for sensory processing, attention and cognition. TRN dysfunction has been linked to sensory abnormality, attention deficit and sleep disturbance across multiple neurodevelopmental disorders. Currently, little is known about the organizational principles underlying its divergent functions. In this talk, I will start with an example of how dysfunction of TRN contributes to attention deficit and sleep disruption using a mouse model of Ptchd1 mutation, which in humans cause neurodevelopmental disorder with ASD. Building on these findings, we further performed an integrative single-cell analysis linking molecular and electrophysiological features of the TRN to connectivity and systems-level function. We identified two subnetworks of the TRN with segregated anatomical structure, distinct electrophysiological properties, differential connections to the functionally distinct first-order and higher-order thalamic nuclei, and differential role in regulating sleep. These studies provide a comprehensive atlas for TRN neurons at the single-cell resolution and a foundation for studying diverse functions and dysfunctions of the TRN. Finally, I will describe the newly developed minimally invasive optogenetic tool for probing circuit function and dysfunction.
Chronic unpredictable sleep disruption induces changes in locomotor activity, metabolism, and inflammation in Wistar rats
FENS Forum 2024
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