Sevoflurane triggers immediate-early gene expression and low-threshold spike bursting in the mouse paraventricular thalamus
Abstract
Introduction. Thalamocortical rhythms have long been hypothesized to underlie both waking and anaesthesia states. Recent immunohistochemical and imaging methods now allow in rodent models to identify brain regions activated under general anaesthesia to target them with state-of-the-art electrophysiological recording. We used this strategy to explore the behaviour of the paraventricular thalamus nucleus (PVT) under sevoflurane anaesthesia. We implemented a computational model to explain the effects of sevoflurane on the PVT's neurophysiology. Methods. C57Bl/6J mice were submitted to sevoflurane anaesthesia. Immediate early gene c-Fos' expression was quantified with immunohistochemistry performed both in whole cleared brains and paraventricular thalamus slices. In vivo multi-unit electrophysiological recordings were carried out using 32-channels silicon probes implanted in the PVT. A conductance-based computational model of PVT neuron was implemented with the TASK background potassium conductance, altered by halogenated gas, to run direct simulations. Results. c-Fos overexpression under sevoflurane anaesthesia was located in a number of specific cortical areas and subcortical nuclei, including the paraventricular thalamus. c-Fos positive cell counting showed an increase under anaesthesia compared to both pure oxygen and anaesthesia induction followed by waking. Neuropeptide galanin-positive cells were overrepresented in the c-Fos-positive cell population under anaesthesia. Electrophysiological recordings showed a decrease in single spikes and low-threshold spike bursts mean frequency. The latter displayed increased number of spikes per burst. These changes resulted in an overall qualitative change of the PVT electrophysiology, switching from tonic to phasic under anaesthesia. Computational modelling allowed to explain these changes with an increase in the TASK potassium conductance by sevoflurane. Conclusion. We report evidence that PVT galanin neurons express cFos under sevoflurane anaesthesia. We show that PVT neurophysiology switches from tonic to phasic firing, and that this modification can be explained by a direct neuromodulatory effect of sevoflurane on a background potassium conductance.
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BibTeX
@misc{areias2026sevoflurane,
title = {{Sevoflurane triggers immediate-early gene expression and low-threshold spike bursting in the mouse paraventricular thalamus}},
author = {Julie Areias and Yan Chastagnier and Jérémie Naudé and Mathieu Desroches and Julie Perroy and Vivien Szabo},
howpublished = {HAL},
year = {2026},
month = sep,
url = {https://inria.hal.science/hal-05763179v1},
note = {CC BY 4.0},
}
RIS
TY - UNPB
TI - Sevoflurane triggers immediate-early gene expression and low-threshold spike bursting in the mouse paraventricular thalamus
AU - Julie Areias
AU - Yan Chastagnier
AU - Jérémie Naudé
AU - Mathieu Desroches
AU - Julie Perroy
AU - Vivien Szabo
PY - 2026
DA - 2026/09/24
PB - HAL
UR - https://inria.hal.science/hal-05763179v1
AB - Introduction. Thalamocortical rhythms have long been hypothesized to underlie both waking and anaesthesia states. Recent immunohistochemical and imaging methods now allow in rodent models to identify brain regions activated under general anaesthesia to target them with state-of-the-art electrophysiological recording. We used this strategy to explore the behaviour of the paraventricular thalamus nucleus (PVT) under sevoflurane anaesthesia. We implemented a computational model to explain the effects of sevoflurane on the PVT's neurophysiology. Methods. C57Bl/6J mice were submitted to sevoflurane anaesthesia. Immediate early gene c-Fos' expression was quantified with immunohistochemistry performed both in whole cleared brains and paraventricular thalamus slices. In vivo multi-unit electrophysiological recordings were carried out using 32-channels silicon probes implanted in the PVT. A conductance-based computational model of PVT neuron was implemented with the TASK background potassium conductance, altered by halogenated gas, to run direct simulations. Results. c-Fos overexpression under sevoflurane anaesthesia was located in a number of specific cortical areas and subcortical nuclei, including the paraventricular thalamus. c-Fos positive cell counting showed an increase under anaesthesia compared to both pure oxygen and anaesthesia induction followed by waking. Neuropeptide galanin-positive cells were overrepresented in the c-Fos-positive cell population under anaesthesia. Electrophysiological recordings showed a decrease in single spikes and low-threshold spike bursts mean frequency. The latter displayed increased number of spikes per burst. These changes resulted in an overall qualitative change of the PVT electrophysiology, switching from tonic to phasic under anaesthesia. Computational modelling allowed to explain these changes with an increase in the TASK potassium conductance by sevoflurane. Conclusion. We report evidence that PVT galanin neurons express cFos under sevoflurane anaesthesia. We show that PVT neurophysiology switches from tonic to phasic firing, and that this modification can be explained by a direct neuromodulatory effect of sevoflurane on a background potassium conductance.
ER -