Qian-Qian M.S. Wang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Qian-Qian M.S. Wang has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
Cheng-Wei B.S. Med Zhang
School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian 350108, China
1 shared publicationLei M.S. Zhang
Department of Pharmacology, School of Pharmacy, Fujian Medical University, Fuzhou, Fujian 350108, China
1 shared publication- Li Chen
Department of Pharmacology, School of Pharmacy, Fujian Medical University, Fuzhou, China
1 shared publication - Li-Li M.S. Duan
Department of Pharmacology, School of Pharmacy, Fujian Medical University, Fuzhou, Fujian 350108, China
1 shared publication Mai-Jie B.S. Med Zhang
School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian 350108, China
1 shared publication- Ping Cai
Fujian Province Key Laboratory of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou, Fujian 350108, China
1 shared publication
Latest Publications
- Open Access
- 2 June 2025
- Published by Wolters Kluwer Health in Anesthesiology
- Vol. 143 (4) , 944-967
Role of the Supramammillary Nucleus–Medial Septum Glutamatergic Pathway in Mediating the Effects of Isoflurane Anesthesia
Background: Glutamatergic neurons in the supramammillary nucleus (SuM) have been recently identified as a key node in arousal system, yet their role in regulating general anesthesia remains unclear. The aim of the current study is to examine the role of the glutamatergic supramammillary neurons and their projections to the medial septum in mediating the effects of isoflurane anesthesia. Methods: Fiber photometry recording was used to determine the changes in calcium signals of glutamatergic neurons in the SuM during isoflurane anesthesia. Optogenetic and chemogenetic approaches were employed to manipulate SuM glutamatergic neuron activity, and the effects on cortical activity, behavioral responses, and physiologic parameters—including pupil diameter, respiratory rate, and blood pressure—were examined in anesthetized mice. Both male and female mice were used in this study. Results: The activities of SuM glutamatergic neurons decreased during isoflurane anesthesia and recovered after the emergence. Optogenetic activation of these neurons enhanced cortical activity, decreasing electroencephalogram delta power (mean ± SD, prestimulation vs. stimulation: 51.35 ± 7.26% vs. 32.08 ± 10.48%, n = 8, P = 0.002) and burst suppression ratio (81.82 ± 7.83% vs. 44.53 ± 28.62%, n = 8, P = 0.002). Furthermore, optogenetic activation altered physiologic parameters including enlarged pupil diameter (prestimulation vs. stimulation: 1.05 ± 0.08% vs. 1.95 ± 0.46%, n = 8, P < 0.001), increased respiratory rate (0.98 ± 0.08% vs. 1.57 ± 0.39%, n = 10, P < 0.001) and elevated blood pressure and induced behavioral responses including increased arousal scores and accelerated emergence (light off vs. light on, 171.40 ± 56.39 s to 59.88 ± 27.18 s, n = 8, P = 0.007). Moreover, chemogenetic activation produced similar effects, whereas inhibition led to opposite effects. Finally, optogenetically activating SuM glutamatergic terminals projecting to the medial septum mimicked the effects of activating SuM glutamatergic soma and increased the activity of medial septum glutamatergic neurons. Conclusions: This study identifies glutamatergic neurons of the SuM as key neural substrates regulating isoflurane anesthesia and facilitating emergence through their projections to the medial septum.
- 2 June 2025
- Published by Wolters Kluwer Health in Anesthesiology
- Vol. 143 (4) , 944-967
Open AccessRole of the Supramammillary Nucleus–Medial Septum Glutamatergic Pathway in Mediating the Effects of Isoflurane Anesthesia
Background: Glutamatergic neurons in the supramammillary nucleus (SuM) have been recently identified as a key node in arousal system, yet their role in regulating general anesthesia remains unclear. The aim of the current study is to examine the role of the glutamatergic supramammillary neurons and their projections to the medial septum in mediating the effects of isoflurane anesthesia. Methods: Fiber photometry recording was used to determine the changes in calcium signals of glutamatergic neurons in the SuM during isoflurane anesthesia. Optogenetic and chemogenetic approaches were employed to manipulate SuM glutamatergic neuron activity, and the effects on cortical activity, behavioral responses, and physiologic parameters—including pupil diameter, respiratory rate, and blood pressure—were examined in anesthetized mice. Both male and female mice were used in this study. Results: The activities of SuM glutamatergic neurons decreased during isoflurane anesthesia and recovered after the emergence. Optogenetic activation of these neurons enhanced cortical activity, decreasing electroencephalogram delta power (mean ± SD, prestimulation vs. stimulation: 51.35 ± 7.26% vs. 32.08 ± 10.48%, n = 8, P = 0.002) and burst suppression ratio (81.82 ± 7.83% vs. 44.53 ± 28.62%, n = 8, P = 0.002). Furthermore, optogenetic activation altered physiologic parameters including enlarged pupil diameter (prestimulation vs. stimulation: 1.05 ± 0.08% vs. 1.95 ± 0.46%, n = 8, P < 0.001), increased respiratory rate (0.98 ± 0.08% vs. 1.57 ± 0.39%, n = 10, P < 0.001) and elevated blood pressure and induced behavioral responses including increased arousal scores and accelerated emergence (light off vs. light on, 171.40 ± 56.39 s to 59.88 ± 27.18 s, n = 8, P = 0.007). Moreover, chemogenetic activation produced similar effects, whereas inhibition led to opposite effects. Finally, optogenetically activating SuM glutamatergic terminals projecting to the medial septum mimicked the effects of activating SuM glutamatergic soma and increased the activity of medial septum glutamatergic neurons. Conclusions: This study identifies glutamatergic neurons of the SuM as key neural substrates regulating isoflurane anesthesia and facilitating emergence through their projections to the medial septum.