Asset Details
Do you wish to reserve the book?
The Role of Paraventricular Nucleus of Thalamus in Sleep Disturbance Induced by Withdrawal from Repeated Ethanol Exposure
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
The Role of Paraventricular Nucleus of Thalamus in Sleep Disturbance Induced by Withdrawal from Repeated Ethanol Exposure
Do you wish to request the book?
The Role of Paraventricular Nucleus of Thalamus in Sleep Disturbance Induced by Withdrawal from Repeated Ethanol Exposure
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
The Role of Paraventricular Nucleus of Thalamus in Sleep Disturbance Induced by Withdrawal from Repeated Ethanol Exposure
2025
Overview
Sleep disturbance is known to be comorbid with withdrawal from repeated ethanol exposure and could be a negative reinforcement for the majority of people with alcohol use disorder (AUD). The paraventricular nucleus of the thalamus (PVT) has been highlighted for its function in integrating arousal states and associated modulation in sleep homeostasis. However, there is limited understanding of the involvement of PVT neurons in regulating sleep patterns, especially during withdrawal from chronic ethanol exposure. In this study, we investigated the potential function of the PVT in sleep disturbance during ethanol withdrawal using electrophysiology, in vivo calcium imaging, biochemical, and chemogenetic approaches. At 24 hours post-withdrawal from chronic intermittent ethanol exposure (CIE) for four weeks, there is an increase in wake time and a decrease in non-rapid eye movement (NREM) sleep. The calcium transient levels in the PVT neurons are positively correlated with the transition from sleep to wakefulness. CIE elevates the PVT neuronal activity in a subregion-specific manner, resulting in a significant rise in cFos levels in the anterior PVT (aPVT). Temporal suppression of aPVT excitatory neurons via chemogenetics ameliorates the disturbance in sleep patterns generated by CIE. The aPVT has a notable distinction in the expression of the m-type potassium channel subunit, KCNQ2, with a higher expression level compared to the posterior PVT (pPVT). While the expression of KCNQ2 in the aPVT is reduced in CIE mice, the restoration of KCNQ2 expression using viral gene transfer within the aPVT alleviates the sleep disturbances produced by CIE. This data indicates a significant role of the PVT in sleep disturbance during ethanol withdrawal, which may partially be due to the downregulation of M-channels, hence underscoring M-channels in the PVT as a potential therapeutic target for sleep disturbance in alcohol use disorder.
Publisher
Cold Spring Harbor Laboratory
Subject
