Glutamatergic neurons in paraventricular nucleus of the thalamus regulate the recovery from isoflurane anesthesia

Objectives Previous studies have demonstrated that the paraventricular nucleus of the thalamus (PVT) is a key wakefulness-controlling nucleus in the thalamus. Therefore, PVT may also be involved in the process of general anesthesia. This study intends to explore the role of PVT in isoflurane anesthesia. Methods In the present study, we used the expression of c-Fos to observe the neuronal activity of PVT neurons under isoflurane anesthesia. We further recorded the effect of isoflurane anesthesia on the calcium signal of PVT glutamatergic neurons in real time with the help of calcium fiber photometry. We finally used chemogenetic technology to specifically regulate PVT glutamatergic neurons, and observed its effect on isoflurane anesthesia and cortical electroencephalography (EEG) in mice. Results We found that glutamatergic neurons of PVT exhibited high activity during wakefulness and low activity during isoflurane anesthesia. Activation of PVT glutamatergic neuronal caused an acceleration in emergence from isoflurane anesthesia accompanied with a decrease in EEG delta power (1-4 Hz). Whereas suppression of PVT glutamatergic neurons induced a delay recovery of isoflurane anesthesia, without affecting anesthesia induction. Conclusions Assuming a pharmacokinetic explanation for results can be excluded, these results demonstrate that the PVT is involved in regulating anesthesia emergence.

Automated summary

This study investigated the role of the paraventricular nucleus of the thalamus (PVT) in isoflurane anesthesia. The results showed that glutamatergic neurons in the PVT were highly active during wakefulness but had low activity during isoflurane anesthesia. Activation of PVT glutamatergic neurons accelerated emergence from isoflurane anesthesia, while suppression of these neurons delayed the recovery from anesthesia.