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Background: The medial prefrontal cortex plays a crucial role in regulating consciousness. However, the specific functions of its excitatory and inhibitory networks during anesthesia remain uncertain. Here we explored the hypothesis that somatostatin interneurons in the medial prefrontal cortex enhance the effects of sevoflurane anesthesia by increasing GABA transmission to pyramidal neurons., Methods: EEG was utilized to reflect the depth of anesthesia. Immunostaining and fiber photometry were employed to assess neuronal activities and GABA delivery. The regulation of neuronal activity was achieved by chemogenetics and optogenetics., Results: The expression of c-Fos was increased in somatostatin neurons of the medial prefrontal cortex during sevoflurane anesthesia (air versus sevoflurane: 26.4 ± 6.5 % versus 48 ± 6.2 %, P=0.0007, n=5 mice). Chemogenetic inhibition or activation of somatostatin neurons in the medial prefrontal cortex reduced (from 84 ± 24 s to 51 ± 18 s, P=0.008, n=7 mice) or prolonged (from 97 ± 31 s to 140 ± 30 s, P=0.006, n=7 mice) the sevoflurane anesthesia recovery time. Increased GABA input to pyramidal neurons in the medial prefrontal cortex precedes sevoflurane-induced loss of consciousness (ΔF/F: from 0.46 ± 0.57 % to 2.25 ± 1.42 %, P=0.031, n=10 mice). Activation of somatostatin neurons in the medial prefrontal cortex, leading to a significant reduction in calcium signals within local pyramidal neurons (ΔF/F: from -0.14 ± 0.52 % to -10.08 ± 4.44 %, P=0.002, n=10 mice), and GABA input on pyramidal neurons increased (ΔF/F: from -0.001 ± 0.001 % to 0.28 ± 0.03 %, P=0.002, n=7 mice) in a time-locked manner. Chemogenetic inhibition of pyramidal neurons prolonged the recovery from sevoflurane anesthesia in mice (from 101 ± 46 s to 136 ± 54 s, P=0.017, n=19 mice)., Conclusions: Cortical somatostatin neurons may inhibit local pyramidal neurons by enhancing GABA transmission, which increases the effectiveness of sevoflurane anesthesia., Competing Interests: Conflicts of Interest: The authors declare no competing interests., (Copyright © 2025 American Society of Anesthesiologists. All Rights Reserved.)

The fabrication of α-FAPbI 3 perovskite films usually requires high temperature annealing above 150 °C, and the residual tensile strain in the films seriously affects the stability of α-FAPbI 3 by converting to δ-phase FAPbI 3 . Here, we use MASCN surface treatment of FAPbI 3 films to induce a rotation of the coplanar octahedron [PbI 6 ] 4- to the metric octahedron for the strong interaction of SCN - with Pb 2+ , converting δ-FAPbI 3 into α-FAPbI 3 highly crystalline films at room temperature. The optimized FAPbI 3 films have high stability due to releasing residual tensile strains after MASCN treatment. The efficiency of the MASCN-treated unannealed FAPbI 3 PSC is 19.03%, while the optimized FAPbI 3 annealed at 100 °C shows a maximum PCE of 21.95% on a small area. The solar cell stability for humidity, light, and thermal stability are significantly improved. The MASCN treated FAPbI 3 achieves a PCE of 15.32% on a PSC module with an effective area of 9.6 cm 2 and maintains an initial efficiency of 94.1% after 100 days of ageing at 85 °C and 85% humidity.

SnO 2 is widely used as the electron transport layer (ETL) in n-i-p perovskite solar cells. However, the deep-level defects at the interface between SnO 2 and the perovskite film will lead to energy loss, reducing the open-circuit voltage. Therefore, the interface optimization is essential to raise the efficiency and enhance the stability of perovskite solar cells. In this work, we introduce NH 4 F into the SnO 2 electron transport layers, and the optimized SnO 2 films reduce the interface defect density, improve the charge extraction, and reveal a better energy-level arrangement. Compared to the conventional SnO 2 perovskite solar cell, the average V oc is improved by 70 mV with the champion efficiency up to 22.12%. Moreover, the unencapsulated F-doped SnO 2 perovskite solar cells show better thermal stability (maintained 86.2%) and humidity stability (maintained 80.8%) after 35 days.

Purpose: The aim of the current study was to explore the role of the basal forebrain (BF) in propofol anaesthesia., Methods: In the present study, we observed the neural activities of the BF during propofol anaesthesia using calcium fibre photometry recording. Subsequently, ibotenic acid was injected into the BF to verify the role of the BF in propofol anaesthesia. Finally, to test whether GABA A receptors in the BF were involved in modulating propofol anaesthesia, muscimol (GABA A receptor agonist) and gabazine (GABA A receptor antagonist) were microinjected into the BF. Cortical electroencephalogram (EEG), time to loss of righting reflex (LORR), and recovery of righting reflex (RORR) under propofol anaesthesia were recorded and analysed., Results: The activity of BF neurons was inhibited during induction of propofol anaesthesia and activated during emergence from propofol anaesthesia. In addition, non-specifical lesion of BF neurons significantly prolonged the time to RORR and increased delta power in the frontal cortex under propofol anaesthesia. Next, microinjection of muscimol into the BF delayed emergence from propofol anaesthesia, increased delta power of the frontal cortex, and decreased gamma power under propofol anaesthesia. Conversely, infusion of gabazine accelerated emergence times and decreased EEG delta power., Conclusions: The basal forebrain is involved in modulating frontal cortex delta activity and emergence from propofol anaesthesia. Additionally, the GABA A receptors in the basal forebrain are involved in regulating emergence propofol anaesthesia.