Brain Research Bulletin最新文献

{"title":"An adaptive fMRI paradigm of direction-specific, time-critical grip-force transitions.","authors":"Robert Lubomierski, Verena Dzialas, Sumaya Zaalouki, Thilo van Eimeren","doi":"10.1016/j.brainresbull.2026.112171","DOIUrl":"https://doi.org/10.1016/j.brainresbull.2026.112171","url":null,"abstract":"<p><p>Rapid transitions between force states, including fast increases and rapid releases, are fundamental to voluntary movement and everyday object interaction. Converging evidence from movement disorders suggests that rapid force reduction can be disproportionately impaired relative to force production, motivating the hypothesis that these transition directions rely on partly distinct control mechanisms. Brain imaging studies suggest direction-sensitive neural contributions, but existing paradigms make it difficult to determine whether differences between force production and force reduction reflect transition direction itself or other task-related differences. Here, we present the YANK task, a new open-source grip-force paradigm that manipulates rapid force production and rapid force reduction within the same visuomotor task. As an initial clinical proof-of-concept, pilot data from a single participant with Parkinson's disease demonstrate within-participant, direction-specific modulation of yank. Trials designed to elicit positive yank produced higher peak scaled positive yank (p <.001), whereas trials designed to elicit negative yank produced more peak scaled negative yank (p <.001). The accompanying neuroimaging data demonstrate that the paradigm can be implemented during fMRI and provide qualitative within-subject proof-of-concept evidence of task-evoked BOLD responses in visuomotor and sensorimotor regions. Together, these findings position the YANK task as a novel, neuroimaging-compatible paradigm for investigating direction-specific rapid grip-force transitions.</p>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":" ","pages":"112171"},"PeriodicalIF":4.5,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Harnessing BMSCs for ischemic stroke: Decoding multimodal repair and navigating the path to clinical translation.","authors":"Xinyi Huang, XiaoLing Chen, GuoLiang Zhu, HongWei Deng, YaPeng Lin, JiangMin Li, KeJie Chen, JunLi Hao, QuanDan Tan, Jie Yang","doi":"10.1016/j.brainresbull.2026.112170","DOIUrl":"10.1016/j.brainresbull.2026.112170","url":null,"abstract":"<p><p>Ischemic stroke (IS) is characterized by a high incidence rate, high disability rate and high recurrence rate. The existing treatment methods have limitations such as a narrow time window and limited recovery of neurological function. Bone marrow mesenchymal stem cells (BMSCs) have become a research hotspot in the regenerative treatment of IS due to their multi-directional differentiation potential, paracrine regulation and immune regulation characteristics. This review explores the mechanism of action, strategies for enhancing therapeutic efficacy and the progress of clinical transformation of BMSCs in the treatment of IS. Basic research indicates that BMSCs improve neurological function through multiple mechanisms such as migrating to ischemic foci, secreting neurotrophic factors, promoting angiogenesis, and inhibiting apoptosis of nerve cells. Gene modification technology and the application of exosomes can further potentiate therapeutic efficacy. The optimization of injection routes, cell types, transplantation time Windows and cell doses is crucial to the therapeutic effect. Clinical studies have initially confirmed the safety of BMSCs treatment and some functional improvement effects, but there are still problems such as small sample size and unclear long-term efficacy. In the future, it is necessary to further clarify the treatment mechanism, optimize the treatment plan, and promote the transformation of basic research into clinical practice (Graphical Abstract).</p>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":" ","pages":"112170"},"PeriodicalIF":4.5,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential Mechanisms of N-Methyltyramine in Multitarget Regulation of Mental Disorders via the GPCR-cAMP Pathway.","authors":"Wang Zijian","doi":"10.1016/j.brainresbull.2026.112169","DOIUrl":"https://doi.org/10.1016/j.brainresbull.2026.112169","url":null,"abstract":"<p><p>N-Methyltyramine (NMT) is a tyramine derivative widely distributed in citrus plants and the traditional Chinese medicine Zhishi. Pharmacological studies have confirmed that NMT directly binds to the dopamine D₂ receptor (DRD2; Ki = 31.3µM), inhibits forskolin-induced cAMP accumulation (EC₅₀ ≈ 4µM, Emax = 89%), and dose-dependently antagonizes quinpirole-mediated β-arrestin2 recruitment, exhibiting G protein-biased agonistic properties. Meanwhile, NMT activates the human trace amine-associated receptor 1 (hTAAR1; EC₅₀ ≈ 2µM) to increase cAMP, possesses α₂-adrenergic receptor antagonistic activity (IC₅₀ = 5.53µM), and exhibits blood-brain barrier permeability (logPe = -5.16cm/s). Based on these multi-target receptor profiles, NMT may participate in the regulation of central monoaminergic neurotransmission via the GPCR-cAMP signaling axis, providing a new multi-target lead compound direction for research on neurological disorders such as Alzheimer's disease, depression, and drug addiction. Notably, evidence for direct activation of β₂-adrenergic receptors by NMT remains insufficient, and its therapeutic effects and downstream signal integration mechanisms require NMT-specific experimental validation.</p>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":" ","pages":"112169"},"PeriodicalIF":4.5,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isoquercetin targets histone methyltransferase G9a to promote BDNF expression and improve cerebral ischemia-reperfusion injury","authors":"Liming Hong,&nbsp;Hangfei Wang,&nbsp;Xiyuan Lin,&nbsp;Bo Sun,&nbsp;Xianping Lin,&nbsp;Miao Chen","doi":"10.1016/j.brainresbull.2026.112100","DOIUrl":"10.1016/j.brainresbull.2026.112100","url":null,"abstract":"<div><div>Reperfusion therapies following stroke can contribute to further brain injury.Inhibition of G9a has been demonstrated to increase BDNF expression, thereby exerting neuroprotective effects. Isoquercetin (ISO) has shown neuroprotective potential, but its molecular mechanisms are not fully known. This study aimed to investigate the role and mechanism of ISO in improving cerebral ischemia-reperfusion injury, in relation to G9a/H3K9me2/BDNF pathway. A rat middle cerebral artery occlusion (MCAO) model and an oxygen-glucose deprivation/reoxygenation (OGD/R) neuronal model were used. Neurological scores, infarct volume, brain water content, neuronal morphology, apoptosis and cell viability were evaluated. Moreover, a G9a overexpression plasmid was constructed to verify mechanism specificity. G9a and H3K9me2 expression levels were assessed by RT-PCR and western blotting. BDNF levels were measured by ELISA, oxidative stress by ROS assays and H3K9me2 enrichment at the BDNF promoter by chromatin immunoprecipitation. Cerebral I/R injury significantly increased G9a and H3K9me2 expression, leading to reduced BDNF levels and enhanced neuronal apoptosis. ISO treatment decreased G9a/H3K9me2 expression, increased BDNF levels, improved neurological function and reduced neuronal damage both in vivo and in vitro. G9a overexpression reversed these protective effects. Isoquercetin alleviates cerebral I/R injury by inhibiting G9a-mediated histone methylation and promoting BDNF expression, highlighting a novel epigenetic mechanism for stroke therapy</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"245 ","pages":"Article 112100"},"PeriodicalIF":4.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atypical cortical asymmetries in toddlers with congenital heart disease before surgery","authors":"Huijun Li,&nbsp;Xueying Du,&nbsp;Longxian Cheng,&nbsp;Feng Yang,&nbsp;Siyu Ma,&nbsp;Fan lu,&nbsp;Meijiao Zhu,&nbsp;Huiling Wang,&nbsp;Ming Yang,&nbsp;Xuming Mo","doi":"10.1016/j.brainresbull.2026.112130","DOIUrl":"10.1016/j.brainresbull.2026.112130","url":null,"abstract":"<div><h3>Background</h3><div>Patients with congenital heart disease (CHD) may exhibit atypical structural asymmetry in the brain, while the altered structural lateralization and its relationship with cognitive function have not been fully revealed.</div></div><div><h3>Methods</h3><div>We performed a cross-sectional structural imaging study of 109 toddlers of CHD, including 80 with mild CHD, 29 with moderate-severe CHD in our hospital and 56 normal controls (NC). Surface-based image analysis was used to compute lateralization index (LI) for cortical surface area (CSA), cortical thickness (CT), and cortical volume (CV) in CHD groups and NC group across 34 bilateral regions. Group comparisons were conducted using generalized linear models, and partial correlation analyses were performed to examine associations between LIs, clinical variables, and developmental quotients (DQs) assessed by the Gesell Developmental Scale.</div></div><div><h3>Results</h3><div>Compared to the NC group, both the mild and moderate-severe CHD groups showed overlapping altered lateralization regions in the caudal anterior cingulate gyrus, pars opercularis, superior temporal gyrus, cuneus cortex, medial orbitofrontal gyrus, parahippocampal gyrus, and posterior cingulate cortex (<em>p</em>_FDR &lt; 0.05). Moreover, the LI of CT in the pars opercularis was negatively associated with personal-social skills DQ in the CHD group (<em>r</em> = -0.327, <em>p</em>＜0.001 uncorrected; <em>p_</em>FDR = 0.021).</div></div><div><h3>Conclusions</h3><div>Mild and moderate-severe CHD groups showed comparable alterations in cerebral asymmetries, predominantly involving perisylvian and default-mode network regions. Notably, the association between the LI of CT in the pars opercularis and personal-social skills DQ highlights a potential structural correlate of neurodevelopmental risk in CHD.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"245 ","pages":"Article 112130"},"PeriodicalIF":4.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the therapeutic mechanism of leech in vascular dementia: An integrated approach combining network pharmacology and experimental validation","authors":"Yanjiao Li,&nbsp;Xialin Xue,&nbsp;Hongyu Luo,&nbsp;Dan Chen,&nbsp;Shuxian Yang,&nbsp;Xuekuan Huang,&nbsp;Yan Li","doi":"10.1016/j.brainresbull.2026.112131","DOIUrl":"10.1016/j.brainresbull.2026.112131","url":null,"abstract":"<div><h3>Background</h3><div>Vascular dementia (VaD), the second leading cause of dementia following Alzheimer’s disease, results from the reduction in cerebral blood flow. Medicinal leeches (SZ) in traditional Chinese medicine (TCM), a classic remedy for promoting blood circulation and improving blood stasis, have shown capabilities to relieve neuroinflammation and repair the blood-brain barrier (BBB) integrity. However, the efficacy and the underlying mechanisms of medicinal leeches in treating VaD remain unclear.</div></div><div><h3>Objective</h3><div>This study aimed to explore the efficacy of medicinal leeches in treating VaD and its molecular mechanisms.</div></div><div><h3>Methods</h3><div>An <em>in vivo</em> VaD model of rats was created via a two-vessel occlusion (2VO) ischemia protocol. Learning and memory functions in rats were assessed via the water maze test, Y-maze test, and novel object recognition test. The neuronal injury in rat hippocampus was assessed by H&amp;E and Nissl staining. Network pharmacology (NP) and molecular docking depicted a “SZ-Compounds-Targets” network and visualized the binding pattern between core components of medicinal leeches and key targets of VaD, respectively. Transmission electron microscopy (TEM), ELISA, quantitative PCR, and Western blotting were performed to validate the involvement of the TLR4/NF-κB signaling pathway in leech treatment against VaD.</div></div><div><h3>Results</h3><div>Medicinal leeches alleviated the cognitive deficits and neuronal injuries in VaD rats. Seven key targets were predicted as the leading contributors to the neuroprotective potential of medicinal leeches against VaD. Enrichment analyses further showed that the Toll-like receptor and NF-κB signaling pathways were enriched in the key targets of medicinal leeches. Experimental assays showed that expression levels of TLR4, MyD88, p-p65, and pro-inflammatory mediators were significantly elevated in VaD rats, which were further enhanced by LPS induction. Encouragingly, leech treatment significantly downregulated their levels.</div></div><div><h3>Conclusion</h3><div>Medicinal leeches can effectively alleviate the learning and cognitive impairments, neurological pathology in the hippocampal CA1 region, and the loss of BBB integrity in VaD rats. Moreover, medicinal leeches can suppress the neuroinflammation in VaD rats through inhibiting the TLR4/NF-κB signaling pathway.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"245 ","pages":"Article 112131"},"PeriodicalIF":4.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Napping during night shift preserves normal neural activity in nurses with sleep deprivation: Evidence from functional magnetic resonance imaging study","authors":"Zhu-Ling Gao,&nbsp;Zhe-Yi Huang,&nbsp;Hong-Yu Lin,&nbsp;Hua-Jun Chen,&nbsp;Jia-Hui Lin","doi":"10.1016/j.brainresbull.2026.112141","DOIUrl":"10.1016/j.brainresbull.2026.112141","url":null,"abstract":"<div><h3>Background and purpose</h3><div>Neuropsychological studies suggest that napping during night shifts may benefit nurses’ brain functions and clinical performance. However, in vivo neuroimaging evidence remains scarce. This study aims to use resting-state functional magnetic resonance imaging (rs-fMRI) to investigate how night-shift napping modulates neural activity in nurses experiencing sleep deprivation (SD), addressing a critical gap in understanding the neurophysiological mechanisms underlying nap-induced recovery.</div></div><div><h3>Methods</h3><div>rs-fMRI was administered to 24 nurses during three sessions: rested wakefulness (RW), SD, and napping (NAP). Within a biological day, RW represented normal sleep duration, SD indicated an absence of sleep, and NAP referred to naps lasting less than two hours during the night. Amplitude of low-frequency fluctuations (ALFF) analysis was performed to assess spontaneous neural activity and reflect brain function. One-way repeated measures analysis of variance, followed by post hoc paired t-tests, was used to examine ALFF differences.</div></div><div><h3>Results</h3><div>A comparison between RW and SD revealed a significant SD-related reduction in ALFF, predominantly affecting the bilateral frontal and temporal cortices, insula, subcortical structures, and cerebellum, and a notable ALFF increase predominantly involving the bilateral occipital cortex, motor and sensory-related areas, parietal lobe, and several temporal regions (FWE-corrected P &lt; 0.05). When comparing RW with NAP sessions, the spatial extent of ALFF alterations was significantly reduced (FWE-corrected P &lt; 0.05). Additionally, comparison between SD and NAP sessions showed that NAP effectively mitigated the ALFF disturbances induced by SD.</div></div><div><h3>Conclusion</h3><div>Night-shift napping may serve as an effective strategy for restoring disturbed neural activity and thereby preserving cognitive and perceptual brain functions. These findings provide novel neuroimaging evidence supporting napping as a neuroprotective strategy for sleep-deprived nurses.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"245 ","pages":"Article 112141"},"PeriodicalIF":4.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149036254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suppression of microglial MEF2C by α-Synuclein is associated with neuroinflammation in a mouse model of Parkinson's disease and promotes degeneration In Vitro","authors":"Xiaohuan Liu,&nbsp;Rong Zhou,&nbsp;Cheng Wen,&nbsp;Rulin Geng,&nbsp;Jiehua Su,&nbsp;Zhuoying Lai,&nbsp;Kaixun Huang,&nbsp;Yiqiang Zhan,&nbsp;Danyu Lin,&nbsp;Enxiang Tao","doi":"10.1016/j.brainresbull.2026.112145","DOIUrl":"10.1016/j.brainresbull.2026.112145","url":null,"abstract":"<div><ul><li><span>•</span><span><div>α-Synuclein downregulates the expression of microglial MEF2C in Parkinson’ disease.</div></span></li><li><span>•</span><span><div>MEF2C suppression promotes HMC3 and SH-SY5Y cells’ apoptosis through activating Bax/Bcl-2 pathway.</div></span></li><li><span>•</span><span><div>Decreased MEF2C drives microglia proinflammatory polarization, with elevated cytokines secretion.</div></span></li><li><span>•</span><span><div>Nucleolin and nucleophosmin are identified as upstream regulators of α-syn-induced MEF2C suppression.</div></span></li></ul></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"245 ","pages":"Article 112145"},"PeriodicalIF":4.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiscale white- and gray-matter diffusion abnormalities and their associations with serum ammonia in hepatic encephalopathy: A free-water elimination diffusion MRI study","authors":"Taipeng Zeng,&nbsp;Chaoshang Lin,&nbsp;Li Chen,&nbsp;Xiaoyang Wang,&nbsp;Chengkun Hong,&nbsp;Minghui Mao,&nbsp;Hao Huang,&nbsp;Aling Shen,&nbsp;Liyuan Fu","doi":"10.1016/j.brainresbull.2026.112126","DOIUrl":"10.1016/j.brainresbull.2026.112126","url":null,"abstract":"<div><h3>Background</h3><div>Hepatic encephalopathy (HE) involves complex brain edema, but conventional diffusion models may be confounded by extracellular water and cannot readily distinguish tissue-specific abnormalities from fluid-related effects. This study used a free-water elimination (FWE) diffusion tensor imaging framework to characterize multiscale white- and gray-matter (GM) diffusion abnormalities in HE and to examine their associations with serum ammonia and clinical measures.</div></div><div><h3>Methods</h3><div>Patients with HE and healthy controls (HCs) were prospectively enrolled in a cross-sectional observational case-control study. FWE-DTI was used to derive conventional diffusion metrics (FA, MD, AD, and RD), tissue-specific metrics (FAt, MDt, ADt, and RDt), and the fractional volume of free water (FW). White-matter (WM) and cortical GM alterations were evaluated using tract-based spatial statistics (TBSS) and GM-based spatial statistics (GBSS), respectively. Conventional peak width of skeletonized mean diffusivity (PSMD) quantified global WM diffusivity heterogeneity. Within the HE group, voxel-wise multiple linear regression models assessed associations of diffusion metrics with serum ammonia, MELD, PHES, and MMSE, adjusting for age, sex, and TIV. TFCE with 5000 permutations and FWER correction within each statistical map was applied.</div></div><div><h3>Results</h3><div>Compared with HCs, patients with HE showed elevated PSMD and widespread diffusion abnormalities across the WM and cortical GM skeletons. Increased FW was observed in the WM skeleton. Within the HE group, higher serum ammonia was associated with lower AD, ADt, and FW in WM and with lower AD, MD, RD, ADt, MDt, and RDt in cortical GM. Exploratory analyses identified positive associations between PHES and selected white- and GM diffusion metrics and between MMSE and selected WM diffusion metrics; no significant MELD-related associations were detected. All reported voxel-wise associations survived TFCE-based FWER correction.</div></div><div><h3>Conclusions</h3><div>The findings indicate coexisting white- and GM diffusion abnormalities in HE and distinct within-HE associations between serum ammonia and selected diffusion metrics. FWE-derived metrics provide complementary estimates of free-water fraction and tissue-specific diffusion, but their cellular basis, temporal evolution, and causal interpretation remain uncertain. These findings require validation in larger longitudinal cohorts using multi-shell diffusion MRI and complementary biological assessments.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"245 ","pages":"Article 112126"},"PeriodicalIF":4.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149011910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances in research on the amygdala complex in sleep and anesthesia awakening: A hub for the integration of emotion and arousal","authors":"Kaixin Wang,&nbsp;Xiaojin Li,&nbsp;Rui Yu,&nbsp;Shujun Sun,&nbsp;Daling Deng,&nbsp;Qiaofeng Zhang,&nbsp;Tianhao Zhang,&nbsp;Yanyan Zhang,&nbsp;Ruili Ding,&nbsp;Jiwei Shen,&nbsp;Xu Ku,&nbsp;Zhipeng Wang,&nbsp;Shiwen Fan,&nbsp;Xiangdong Chen","doi":"10.1016/j.brainresbull.2026.112134","DOIUrl":"10.1016/j.brainresbull.2026.112134","url":null,"abstract":"<div><div>The amygdala complex (comprising the lateral, central, and medial amygdala) has traditionally been regarded as playing a central role in emotional learning and fear memory. However, recent studies have revealed its critical functions in the regulation of sleep cycles and recovery from anesthesia. This review proposes a new theoretical framework that views the amygdala complex as an “emotion-arousal integration network” that integrates internal emotional states with external environmental demands to dynamically regulate overall arousal levels and states of consciousness. This review first outlines the neuroanatomy and cellular composition of the various subnuclei of the amygdala, then systematically elaborates on the role of the basolateral amygdala in the regulation of the physiological sleep-wake cycle, and explores its new role in promoting the recovery of consciousness during general anesthesia. Building on this foundation, the review further analyzes the complementary roles of the central and medial amygdala in sleep regulation, as well as how functional imbalances in the amygdala lead to sleep and emotional symptoms in conditions such as post-traumatic stress disorder. Finally, the review outlines potential clinical translation strategies based on amygdala circuits and neurochemical mechanisms, and discusses current research challenges and future directions.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"245 ","pages":"Article 112134"},"PeriodicalIF":4.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149023931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}