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Learn more: PMC Disclaimer | PMC Copyright Notice Sci Rep . 2026 Mar 2;16:11768. doi: 10.1038/s41598-026-40974-w Search in PMC Search in PubMed View in NLM Catalog Add to search Propofol and dexmedetomidine sedation share the similar functional activity but distinct functional synchronization Jian Minyu Jian Minyu 1 Department of Anesthesiology, Beijing Tiantan Hospital, Capital Medical University, No. 119, Southwest 4th Ring Road, Fengtai District, Beijing, 100070 China Find articles by Jian Minyu 1 , Zhang Jiayi Zhang Jiayi 2 School of Artificial Intelligence, Beijing University of Posts and Telecommunications, Beijing, China Find articles by Zhang Jiayi 2 , Li Guiyu Li Guiyu 3 Department of Anesthesiology, Qinghai University Affiliated Hospital, Qinghai University, Xining, Qinghai China Find articles by Li Guiyu 3 , Han Ruquan Han Ruquan 1 Department of Anesthesiology, Beijing Tiantan Hospital, Capital Medical University, No. 119, Southwest 4th Ring Road, Fengtai District, Beijing, 100070 China Find articles by Han Ruquan 1 , Wang Chengwei Wang Chengwei 1 Department of Anesthesiology, Beijing Tiantan Hospital, Capital Medical University, No. 119, Southwest 4th Ring Road, Fengtai District, Beijing, 100070 China Find articles by Wang Chengwei 1 , Liang Fa Liang Fa 1 Department of Anesthesiology, Beijing Tiantan Hospital, Capital Medical University, No. 119, Southwest 4th Ring Road, Fengtai District, Beijing, 100070 China Find articles by Liang Fa 1 , Ma Bo Ma Bo 1 Department of Anesthesiology, Beijing Tiantan Hospital, Capital Medical University, No. 119, Southwest 4th Ring Road, Fengtai District, Beijing, 100070 China Find articles by Ma Bo 1 , Li Yang Li Yang 1 Department of Anesthesiology, Beijing Tiantan Hospital, Capital Medical University, No. 119, Southwest 4th Ring Road, Fengtai District, Beijing, 100070 China Find articles by Li Yang 1 , Wang Xuejun Wang Xuejun 4 Department of Anesthesiology, Qinghai Red Cross Hospital, Xining, Qinghai China Find articles by Wang Xuejun 4 , Zong Fangrong Zong Fangrong 2 School of Artificial Intelligence, Beijing University of Posts and Telecommunications, Beijing, China Find articles by Zong Fangrong 2 , Liu Haiyang Liu Haiyang 1 Department of Anesthesiology, Beijing Tiantan Hospital, Capital Medical University, No. 119, Southwest 4th Ring Road, Fengtai District, Beijing, 100070 China Find articles by Liu Haiyang 1, ✉ Author information Article notes Copyright and License information 1 Department of Anesthesiology, Beijing Tiantan Hospital, Capital Medical University, No. 119, Southwest 4th Ring Road, Fengtai District, Beijing, 100070 China 2 School of Artificial Intelligence, Beijing University of Posts and Telecommunications, Beijing, China 3 Department of Anesthesiology, Qinghai University Affiliated Hospital, Qinghai University, Xining, Qinghai China 4 Department of Anesthesiology, Qinghai Red Cross Hospital, Xining, Qinghai China ✉ Corresponding author. Received 2025 Oct 14; Accepted 2026 Feb 17; Collection date 2026. © The Author(s) 2026 Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/ . PMC Copyright notice PMCID: PMC13066524 PMID: 41772048 Abstract There is insufficient unified research on the effects of propofol and dexmedetomidine on brain functional activity and synchronization. We collected resting-state functional magnetic resonance imaging data from 21 healthy subjects in four different levels of consciousness induced by propofol (awake, mild sedation, deep sedation, and recovery), and other 21 healthy subjects in three different levels of consciousness induced by dexmedetomidine (awake, mild sedation and recovery). The results showed that with the increasing of sedation levels of propofol or dexmedetomidine, fractional amplitude of low-frequency fluctuations and regional homogeneity values decreased in the frontal lobe, while they increased in the superior temporal gyrus and paracentral lobule. Under propofol sedation, functional connectivity (FC) decreased both within and between sensorimotor network and attention network, and within and between the frontoparietal network (FPN) and default mode network (DMN). Simultaneously, a small number of increased connections were observed between the FPN, DMN, and other networks. Under dexmedetomidine sedation, generally decreased FC was observed in the whole brain. This study shows consistent effects on brain functional activity, but distinct impacts on functional synchronization, providing new insights into the understanding of anesthetic mechanisms. Supplementary Information The online version contains supplementary material available at 10.1038/s41598-026-40974-w. Keywords: Propofol, Dexmedetomidine, Functional activity, Functional synchronization, Functional magnetic resonance imaging Subject terms: Medical research, Neurology, Neuroscience Introduction Despite advances in the understanding of the mechanisms for a variety of anesthetics, the specifics of why anesthesia cause unconsciousness remain unclear. Propofol and dexmedetomidine are commonly used in clinical anesthesia. Propofol is a gamma-aminobutyric acidergic drug that increases inhibitory tone in neurons 1 – 3 . Dexmedetomidine is an alpha-2 adrenergic agonist that activates endogenous sleep pathways 4 , 5 . The mechanisms of the two anesthetics are different, and research on their effects on brain function is still insufficient. Resting-state functional magnetic resonance imaging (rsfMRI) is ideally suited for exploring brain function of participants who are incapable of following instructions of goal-directed tasks 6 . Anesthetics induce different states of consciousness by altering the functional activity of specific brain regions and the functional connectivity (FC) 7 . Common measures of brain function include amplitude of low-frequency fluctuations (fALFF), regional homogeneity (ReHo) and FC. The fALFF are defined as the ratio of power spectrum of low frequency to that of the entire frequency range to reflect brain neural activity during rest 8 . ReHo detects the local synchronization of low-frequency oscillations using Kendall’s coefficient of concordance. It represents the similarity between the time series of a given voxel and that of its nearest neighbors 9 . FC is defined as the temporal correlation between pairs of time series extracted from regions of interest or voxels. Previous studies have shown that the impact of propofol on the brain is described as the changes in prefrontal activity as well as alterations in FC 10 , 11 . Similarly, dexmedetomidine can also regulate FC within and between resting state networks and affect low frequency fluctuation amplitude (ALFF) 12 , 13 . Electroencephalogram (EEG)-based studies have shown that both dexmedetomidine-induced unconsciousness and propofol-induced unconsciousness are associated with slow/delta oscillations 14 . However, there is still a lack of unified studies on the effects of propofol and dexmedetomidine on brain functional activity and FC. In this study, we acquired rsfMRI data from 21 healthy subjects in four states of consciousness induced by propofol (awake, mild sedation, deep sedation, and recovery) and other 21 healthy subjects in three states of consciousness (awake, mild sedation, and recovery) induced by dexmedetomidine. fALFF, ReHo and FC were measured for a unified study, aiming to explore the effects of propofol and dexmedetomidine on brain functional activity and synchronization through comprehensive analysis of these indicators. Results Demographic data There was no significant difference in age, gender, education level, nationality, and Body Mass Index (BMI) between two groups ( p > 0.05) (Table 1 ). The vital signs among different sedation states showed no significant difference under propofol and dexmetomidine sedition, respectively ( p > 0.05) (see Supplementary Table S1 and S2 ). The propofol effect-site target concentration at different levels of sedation during the study period were also shown in Supplementary Table S1 . Table 1. Demographic data between propofol group and dexmedetomidine group. Measurements Propofol group( n = 21) Dexmedetomidine group( n = 21) p value Gender, n (%) 0.912 Male 18(85.7) 16(76.2) Female 3(14.3) 5(23.8) Age(years) 25.6 ± 2.4 25.4 ± 2.9 0.907 Nationality, n (%) > 0.999 Non-han nationality 0(0) 0(0) Han nationality 21(100) 21(100) Education level, n (%) 0.751 Senior high school and below 9(42.9) 7(33.3) Senior high school and above 12(57.1) 14(66.7) BMI(kg/m 2 ) 25.88 ± 0.55 25.74 ± 0.57 0.865 Open in a new tab The fALFF values changes under different sedation states induced by propofol In the mild sedation state induced by propofol, compared to the awake state, the fALFF values in the frontal regions (including the superior frontal gyrus and middle frontal gyrus), supramarginal gyrus and cerebellum significantly decreased, while the superior temporal gyrus, calcarine, paracentral lobule and middle occipital gyrus showed a significant increase. In the deep sedation state induced by propofol, compared to the mild sedation state, fALFF values significantly increased in the temporal, parietal lobes and cerebellum, along with a significant decrease in the calcarine region. In the deep sedation state induced by propofol, compared to the awake state, the fALFF values significantly decreased and the regions showing significant fALFF changes expanded within the frontal cortex, with a peak at left middle frontal gyrus. The area with a significant increase in fALFF values in the temporal gyrus expanded. The fALFF values in the supramarginal gyrus, angular gyrus decreased significantly, while it in paracentral lobule significantly increased. Calcarine’s fALFF values no longer increased. The fALFF of the cerebellum has both increased and decreased. In the recovery state induced by propofol, compared to the deep sedation state, the fALFF values in the temporal gyrus and parietal gyrus significantly decreased, while the fALFF values in the frontal regions and calcarine significantly increased (Fig. 1 ). Fig. 1. Open in a new tab Paired t-test of fALFF between awake, mild sedation induced by propofol, deep sedation induced by propofol and recovery. Warm colors indicate higher fALFF in the second state of each paired comparison. Cool colors indicate higher fALFF in the frist state of each paired comparison. The significance of results is reported at p < 0.05. There was no significant difference between awake and recovery after propofol sedation. Detailed results are presented in the supplementary Table S3 . The fALFF values changes under different sedation states induced by dexmedetomidine In the mild sedation state induced by dexmedetomidine, compared to the awake state, the fALFF values in the frontal regions with a peak at frontal inferior orbital gyrus, cerebellum and middle temporal pole significantly decreased, while the temporal, parietal and occipital regions (with a peak at fusiform) showed a significant increase. In the recovery state induced by dexmedetomidine, compared to the mild sedation state, the fALFF values in the middle occipital gyrus, middle temporal gyrus and fusiform significantly decreased (Fig. 2 ). Fig. 2. Open in a new tab Paired t-tests of fALFF between awake, mild sedation induced by dexmedetomidine and recovery. Warm colors indicate higher fALFF in the second state of each paired comparison. Cool colors indicate higher fALFF in the first state of each paired comparison. The significance of results is reported at p < 0.05. There was no significant difference between awake and recovery after dexmedetomidine sedation. Detailed results are presented in the supplementary Table S4 . The ReHo values changes under different sedation states induced by propofol The trend of ReHo value changes under mild sedation induced by propofol is similar to that of fALFF, with a decrease observed in the frontal gyrus, supramarginal gyrus, and cerebellar regions and an increase in the precuneus, rolandic operculum and lingual gyrus. In the deep sedation state induced by propofol, compared to the mild sedation state, ReHo values significantly increased in the temporal and parietal lobes, along with a significant decrease in the frontal gyrus and calcarine region. As the sedation of propofol deepens, ReHo values significantly decreases in supramarginal gyrus, parietal inferior gyrus, calcarine, cerebellum and the entire frontal region, and an increase in the superior temporal gyrus and paracentral lobule. In the recovery state, the ReHo values in the superior temporal regions and paracentral lobule significantly decreases, while the ReHo values in the frontal regions, calcarine, cerebellum and supramarginal gyrus significantly increases (Fig. 3 ). Fig. 3. Open in a new tab Paired t-tests of ReHo between awake, wakefulness, mild sedation induced by propofol, deep sedation induced by propofol and recovery states. Warm colors indicate higher fALFF in the second state of each paired comparison. Cool colors indicate higher fALFF in the first state of each paired comparison. The significance of results is reported at p < 0.05. There was no significant difference between awake and recovery after propofol sedation. Detailed results are presented in the supplementary Table S5 . The ReHo values changes under different sedation states induced by dexmedetomidine Compared to the awake state, ReHo values decreased in the middle frontal gyrus, temporal pole, middle temporal gyrus, caudate gyrus, precuneus and cerebellar regions, while it increased in the postcentral gyrus, occipital regions (with a peak at fusiform) and superior temporal in the mild sedation state induced by dexmedetomidine. In the recovery state, the previously increased ReHo values in the inferior occipital gyrus, middle occipital gyrus, fusiform and postcentral gyrus significantly decreased (Fig. 4 ). Fig. 4. Open in a new tab Paired t-tests of ReHo between awake, mild sedation induced by dexmedetomidine and recovery states. Warm colors indicate higher fALFF in the second state of each paired comparison. Cool colors indicate higher fALFF in the first state of each paired comparison. The significance of results is reported at p < 0.05. There was no significant difference between awake and recovery after dexmedetomidine sedation. Detailed results are presented in the supplementary Table S6 . The FC changes under different sedation states induced by propofol After propofol sedation, the decrease in FC first appears between the SMN and DAN. As the depth of propofol sedation increases, the FC within and between the SMN, DAN, and VAN decreases, and the FC within the FPN and DMN also decreases. At the same time, a small number of increasing connections were observed within FPN and DMN, as well as between FPN, DMN and other networks. The VN network shows a trend of first increasing and then decreasing (Figs. 5 and 6 ). No significant differences were observed between the recovery state and the awake state, nor between the deep sedation state and recovery state. Fig. 5. Open in a new tab Brain maps showing significant differences in FC between awake, mild sedation induced by propofol, deep sedation induced by propofol and recovery states. The red lines indicate higher in connections in the second state of each paired comparison, and the blue lines indicate higher connections in the first state of each paired comparison. Different node colors represent different functional networks. Fig. 6. Open in a new tab Paired t-tests of FC between awake, mild sedation induced by propofol, deep sedation induced by propofol and recovery states. Warm colors indicate higher FC in the second state of each paired comparison. Cool colors indicate higher FC in the first state of each paired comparison. The significance of results is reported at p < 0.01. The FC changes under different sedation states induced by dexmedetomidine In the mild sedation state induced by dexmedetomidine, we observed a general decrease in FC across the entire brain (Fig. 7 ). No significant differences were observed between the recovery state and the awake state, nor between the deep sedation state and recovery state. Fig. 7. Open in a new tab Paired t-tests of FC between awake, mild sedation induced by dexmedetomidine and recovery states. Cool colors indicate higher FC in the first state of each paired comparison. The significance of results is reported at p < 0.01. Discussion This study aims to explore the changes in brain functional activity and synchronization under propofol and dexmedetomidine sedation, explaining the different mechanism of these two anesthetics. Our results suggest that, both anesthetics reduce functional activity in the frontal lobe, while/Section increasing activity in the superior temporal gyrus and paracentral lobule. Furthermore, propofol and dexmedetomidine have distinct effects on functional synchronization between brain regions. Propofol mainly reduces connectivity in the SMN, VAN, FPN and DMN, while dexmedetomidine has a more pronounced impact on FC, leading to a general reduction in FC under mild sedation. Functional activity changes between different states fALFF is the ratio of power spectrum of low frequency to that of the entire frequency range, may effectively suppress non-specific signal components in the rsfMRI, and therefore would significantly improve the sensitivity and specificity in detecting regional spontaneous brain activity 8 . ReHo measures the similarity or synchronization between the time series of a given voxel and its nearest neighbors 9 . These two indicators complement each other and comprehensively reveal the changes in brain function activity after anesthesia. The study found that the effects of propofol and dexmedetomidine on brain functional activity showed similar results. The decrease of frontal functional activity under mild and deep sedation states is worth exploring. The frontal lobes contribute to conscious perception and cognitive functions 15 , 16 . Previous studies have shown that anesthetics preferentially inhibit activity in higher-order information processing areas, particularly the frontal lobes 17 . This result suggests that a loss of frontal executive function may be the primary factor in propofol-induced and dexmedetomidine-induced unconsciousness. The fALFF and ReHo in the superior temporal gyrus and paracentral lobule increased significantly with the increase of sedation depth. Research on EEG indicates that the gamma band power in the temporal lobe increases, which may reflect the formation of declarative memory under propofol sedation 18 . Study has also found that under dexmedetomidine sedation, ALFF in the resting state BOLD signals in the somatosensory motor areas significantly increased 12 . We also found an interesting result. After mild propofol sedation, the fALFF and ReHo in the occipital lobe increased. However, after deep propofol sedation, this increase disappeared. Under mild dexmedetomidine sedation, the increase in fALFF and ReHo in the occipital lobe was more pronounced. Therefore, we speculate that in the low-dose phase, the occipital lobe may be temporarily activated. In the future, continuous depth of the same anesthetic should be used for further verification. FC changes between different states In this study, we used the Brainnetome Atlas to evaluate the effect of anesthesia on FC between gray matter regions of the brain, which complements the research on FC based on functional networks. There is currently controversy over the impact of propofol on SMN 19 – 21 . Our study found that under propofol deep sedation, the coordination within and between the SMN and VAN was suppressed. This suggest that propofol-induced disconnection may occur within low-order resting-state functional networks and between high-order networks and low-order networks 10 , 21 , 22 . Furthermore, there has been debates regarding the FC changes within FPN and DMN, as well as with other networks 10 , 19 , 23 , 24 . In this study, many connections within the FPN and DMN, as well as between them and other networks were decreased, while some connections increased. This provides a more detailed observation of the functional synchrony changes in the FPN and DMN. Although previous studies have suggested that disruptions in high-order resting-state functional networks during propofol-induced unresponsive seem to be a hallmark of the unresponsive state 10 , 20 , 25 . Some connections within the FPN, DMN, and between them and other networks were noticeably increased under deep sedation. This may suggest that during propofol deep sedation, the brain still maintains a certain level of functional collaboration. After dexmedetomidine mild sedation, we observed a general decrease in FC across the entire brain. Previous study suggested that FC within and between resting state networks is modulated by dexmedetomidine, and a significant reduction in FC strength, during the wakefulness to unconsciousness 12 , 13 . Although we separately evaluated functional connectivity differences between propofol-induced deep sedation and the recovery state, as well as between dexmedetomidine-induced mild sedation and the recovery state, no statistically significant effects were observed. Similarly, functional connectivity does not differ significantly between the awake and recovery states. Collectively, these results suggest that functional connectivity during the recovery state may represent an intermediate pattern between the awake and sedation states; however, such changes do not reach statistical significance. Another possible explanation for this discrepancy is that we observed significant differences in fALFF and ReHo from deep sedation to the recovery state, yet no statistically significant differences were found in functional connectivity. This may indicate that changes in different sedation states induce alterations in brain functional activity, but the use of different analytical methods leads to divergent results. Limitations In this study, firstly, although we discussed the effects of both propofol and dexmedetomidine on brain function, the inconsistent depths of anesthesia in this study hindered the comparison of the effects of the two anesthetics on brain function directly. Furthermore, the number of datasets in this study is limited. But through meticulous analysis of the limited yet representative data, we have been able to preliminarily reveal the functional activity and FC changes at propofol and dexmedetomidine. Methods This study was conducted at Beijing Tiantan Hospital, Capital Medical University, Beijing, China, and it was registered at clinicaltrials.gov on 17-09-2017 (registration number, NCT03343873 ). The Institutional Review Board of Beijing Tiantan Hospital has approved the study (KY2017-036-02). This study was performed in accordance with the Declaration of Helsinki. Written informed consent was obtained from all subjects participating in the trial. The study followed the Consolidated Standards of Reporting Trials (CONSORT) 2025 reporting guidelines. Participants Forty-two healthy adult volunteers were assigned into propofol group or dexmedetomidine group, with twenty-one subjects in each group. All participants were native Chinese speakers and had no histories of neurological, psychiatric conditions, or structural brain abnormalities. The exclusion criteria were as follows: (1) metal implants in the body; (2) intracranial lesions or systemic comorbidities; (3) a history of general anesthesia; (4) a history of drug abuse or alcohol abuse; (5) allergy to propofol/dexmedetomidine; (6) claustrophobia; (7) left-handed. Sedation protocol Two certified anesthesiologists were responsible for the monitoring and safety of the volunteers. Subjects were asked to fast for at least 8 h before sedation. Upon arrival, standard American Society of Anesthesiologists monitoring was continuously performed including electrocardiography, heart rate, blood pressure, pulse oxygen saturation, and respiratory rate. A 20-gauge IV cannula was used for fluid and sedation administration. Throughout the sedation and MRI scans, the subjects breathed spontaneously with a nasal catheter of oxygen 5–6 L/min. Dexmedetomidine was administered as a bolus at 1 µg/kg over a period of 15 min; it was then administered at 0.6 µg/kg/h by continuous intravenous infusion to maintain sedation. Target-controlled infusion (TCI) of propofol was delivered by a syringe pump (B. Braun, Germany). The initial effect-site target concentration was set at 0.5ug/ml and increased step-up by every 0.2 ug/ml. The level of consciousness in each group was evaluated every 5 min by using the Observer’s Assessment of Alertness/Sedation (OAA/S) Scale. Subjects wore headphones throughout the experiment and were thus spoken to through an MRI speaker. All communications occurred between MRI acquisitions, and subjects were instructed to respond verbally. No motor response was involved, thus avoiding the introduction of motion artifact. Image acquisition All MRI data were obtained using a 3.0 T MRI system (Siemens Medical Systems Prisma) at Beijing Neurosurgical Institute. Before sedation, images were acquired using a high-resolution three-dimensional T1- weighted brain volume MRI sequence with the following parameters: repetition time, 2300 ms (dexmedetomidine group) /2200 ms (propofol group); echo time, 2.27ms; flip angle, 8°; field of view, 256 × 256 mm 2 ; matrix, 256 × 256; voxel size, 1 × 1 × 1 mm 3 ; slice thickness, 1 mm; and 192 sagittal slices. We then used an echo-planar imaging sequence to perform rsfMRI in different clinical states. In dexmedetomidine group, normal wakefulness (OAA/S Scale score 5), mild sedation (OAA/S Scale score 3–4), and recovery of consciousness (OAA/S Scale score 5) were collected. The typical duration for each state was 15 min. The scanning parameters were as follows: repetition time, 2000 ms; echo time, 30 ms; flip angle, 75°; field of view, 192 × 192 mm 2 ; matrix = 64 × 64; slice thickness, 4 mm; voxel size, 3 × 3 × 4.4 mm 3 ; 32 slices; and 200 volumes. Image preprocessing The functional image preprocessing steps included the following using Brant ( http://brant.brainnetome.org ) 26 . (1) The first ten time points were removed for signal equilibrium and to allow the participants to adapt at to the scanning noise. (2) Slice-time correction. (3) Realignment to the mean functional image. (4) Normalization to the Montreal Neurological Institute space. (5) Regression of nuisance signals, including linear trends, six motion parameters and signals representing cerebrospinal fluid and white matter. (6) Temporal scrubbing using motion “spikes” (threshold of framewise displacement = 0.5) was performed. (7) Band-pass filtering (0.01–0.1 Hz) was performed to reduce non-neuronal contributions to blood oxygen level-dependent (BOLD) fluctuations. (8) Spatial smoothing with a 6 mm Gaussian Kernel. Computation of fALFF, ReHo and FC To quantify the intensity of spontaneous brain activity in a region, fALFF was calculated by using the brant toolbox. The BOLD time series of all brain voxels were transformed into the frequency domain through Fourier transform and the power spectrum was calculated. The fALFF index is the total power of the 0.01–0.1 Hz frequency band divided by that of the entire frequency range. Subsequently, the fALFF was smoothed with a smoothing kernel of 6 mm. ReHo is the Kendall’s coefficient of coherence between the seed voxel and its nearest neighboring 26 voxels, representing the degree of spontaneous activity near the seed voxel. The higher the intensity of voxels in the ReHo map, the more similar the time series of adjacent voxels. Since spatial smoothing artificially enhances ReHo and reduces its reliability 27 , the ReHo map was calculated from non-smoothed time series. Subsequently, spatial smoothing was applied using a 6 mm Gaussian kernel. FC between gray matter regions of the brain was calculated based on the Brainnetome Atlas 28 , and a 246 × 246 FC matrix (excluding cerebellum) was obtained. The Pearson correlation between the average time series of any brain region in each subject was then calculated and Fisher’s z-transforms was performed on the correlation matrix. The threshold for FC was set to r > 0.2 to eliminate interference from noise 29 . Statistical analysis To investigate the differences in fALFF and ReHo induced by anesthetic at the group level, paired t-test was performed on fALFF and ReHo maps between different sedation states. The significance threshold was set to p < 0.05 and multiple comparisons correction was performed using the false discovery rate (FDR). Clusters with voxels greater than 50 were selected using the dpabi toolbox 30 . Similarly, the paired t-test was performed on the FC matrices between different sedation states. The significance threshold was set to p < 0.01, and FDR was used for multiple comparisons correction of different connections. Conclusions This study systematically revealed the regulatory mechanisms of propofol and dexmedetomidine on brain functional activity and synchronization. The results showed that these two anesthetics had consistent effects on brain functional activity but exhibited differences in regulating functional connectivity. Specifically, both propofol and dexmedetomidine significantly reduced functional activity in the frontal lobe, while enhancing functional activity in the superior temporal gyrus and paracentral lobule. Notably, in terms of functional synchronization, propofol primarily reduced the connectivity strength between the SMN, VAN, FPN, and DMN networks, while dexmedetomidine induced a widespread decrease in brain-wide connectivity. These findings not only clarify the differential regulatory patterns of different anesthetics on functional activity and functional synchronization but also provide important theoretical evidence for understanding the neural mechanisms of anesthesia-induced loss of consciousness. Supplementary Information Below is the link to the electronic supplementary material. Supplementary Material 1 (30.8KB, docx) Acknowledgements We sincerely appreciate all the participants who took part in this study. Their time, effort, and cooperation were invaluable to this research. Author contributions L.H conceived and designed the study and supervised the entire research process. J.M, L.G, H.R, W.C, L.F, L.Y and W.X collected the raw data and performed the experiments. Z.J and Z.F analyzed the MRI data. J.M, H.R and Z.R secured the funding. J.M and Z.J drafted the manuscript. All authors reviewed and approved the final manuscript and agree to be accountable for all aspects of the work. Funding We acknowledge funding provided by the National Natural Science Foundation of China (No. 82371910, 61901465, 82271284) and the Beijing Hospital Management Center Youth Talent Development Program “Young Sprouts” (QML20230509). Data availability The data that support the findings of this study are available from the corresponding author upon reasonable request. Declarations Competing interests The authors declare no competing interests. Disclosures The authors report no competing interests. Footnotes Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Jian Minyu and Zhang Jiayi have contributed equally to this work. References 1. Brown, E. N., Lydic, R. & Schiff, N. D. General anesthesia, sleep, and coma. N. Engl. J. Med. 363 , 2638–2650 (2010). [ DOI ] [ PMC free article ] [ PubMed ] [ Google Scholar ] 2. Rudolph, U. & Antkowiak, B. Molecular and neuronal substrates for general anaesthetics. 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