Role of the paraventricular nucleus of the hypothalamus in sleep–wake regulation

Jiang, Shan; Chen, Lu; Huang, Zhi‐Li; Chen, Changrui

doi:10.26599/bsa.2022.9050017

Cited by 4 publications

(2 citation statements)

References 64 publications

(108 reference statements)

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“…5D). 49–52 Thus, the long-term effect of TBI on the hypothalamus may explain the sleep changes in these rmFPI mice. Western blot analysis of GFAP level in the cortex and hippocampus further confirmed this finding (Fig.…”

Section: Resultsmentioning

confidence: 99%

Sleep Disruption in a Mouse Model of Chronic Traumatic Brain Injury

Morris,

Gudenschwager Basso,

Gutierrez-Monreal

et al. 2023

Preprint

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Chronic sleep/wake disturbances are strongly associated with traumatic brain injury (TBI) in patients and are being increasingly recognized. However, the underlying mechanisms are largely understudied and there is an urgent need for animal models of lifelong sleep/wake disturbances. The objective of this study was to develop a chronic TBI rodent model and investigate the lifelong chronic effect of TBI on sleep/wake behavior. We performed repetitive midline fluid percussion injury (rmFPI) in four months old mice and monitored their sleep/wake behavior using the non-invasive PiezoSleep system. The sleep/wake states were recorded before injury (baseline) and then monthly thereafter. We found that TBI mice displayed a significant decrease in sleep duration in both the light and dark phases, beginning at three months post-TBI and continuing throughout the study. Consistent with the sleep phenotype, these TBI mice showed circadian locomotor activity phenotypes and exhibited reduced anxiety-like behavior. TBI mice also gained less weight, and had less lean mass and total body water content, compared to sham controls. Furthermore, TBI mice showed extensive brain tissue loss and increased GFAP and IBA1 levels in the hypothalamus and the vicinity of the injury, indicative of chronic neuropathology. In summary, our study identified a critical time window of TBI pathology and associated circadian and sleep/wake phenotypes. Future studies should leverage this mouse model to investigate the molecular mechanisms underlying the chronic sleep/wake phenotypes following TBI early in life.

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Section: Resultsmentioning

confidence: 99%

Sleep Disruption in a Mouse Model of Chronic Traumatic Brain Injury

Morris,

Gudenschwager Basso,

Gutierrez-Monreal

et al. 2023

Preprint

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show abstract

“…The paraventricular nucleus of the hypothalamus (PVH) is an important hub for regulating neuroendocrine and autonomic functions, complex behaviors and negative emotions after stress [6]. Jiang et al provide a focused and thorough review of emerging anatomical and neuroscience research supporting a critical role of PVH in the promotion and maintenance of wakefulness [7].…”

mentioning

confidence: 99%

New advances in molecular and neural mechanisms of sleep regulation

Liu

2022

Brain Science Advances

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Lifelong Chronic Sleep Disruption in a Mouse Model of Traumatic Brain Injury

Morris,

Gudenschwager Basso,

Gutierrez-Monreal

et al. 2024

Neurotrauma Reports

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Chronic sleep/wake disturbances (SWDs) are strongly associated with traumatic brain injury (TBI) in patients and are being increasingly recognized. However, the underlying mechanisms are largely understudied and there is an urgent need for animal models of lifelong SWDs. The objective of this study was to develop a chronic TBI rodent model and investigate the lifelong chronic effect of TBI on sleep/wake behavior. We performed repetitive midline fluid percussion injury (rmFPI) in 4-month-old mice and monitored their sleep/wake behavior using the non-invasive PiezoSleep system. Sleep/wake states were recorded before injury (baseline) and then monthly thereafter. We found that TBI mice displayed a significant decrease in sleep duration in both the light and dark phases, beginning at 3 months post-TBI and continuing throughout the study. Consistent with the sleep phenotype, these TBI mice showed circadian locomotor activity phenotypes and exhibited reduced anxiety-like behavior. TBI mice also gained less weight, and had less lean mass and total body water content, compared to sham controls. Further, TBI mice showed extensive brain tissue loss and increased glial fibrillary acidic protein and ionized calcium-binding adaptor molecule 1 levels in the hypothalamus and vicinity of the injury, indicative of chronic neuropathology. In summary, our study identified a critical time window of TBI pathology and associated circadian and sleep/wake phenotypes. Future studies should leverage this mouse model to investigate the molecular mechanisms underlying the chronic sleep/wake phenotypes post-TBI early in life.

show abstract

Role of the paraventricular nucleus of the hypothalamus in sleep–wake regulation

Cited by 4 publications

References 64 publications

Sleep Disruption in a Mouse Model of Chronic Traumatic Brain Injury

Sleep Disruption in a Mouse Model of Chronic Traumatic Brain Injury

New advances in molecular and neural mechanisms of sleep regulation

Lifelong Chronic Sleep Disruption in a Mouse Model of Traumatic Brain Injury

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