Neuroscience最新文献

{"title":"The altered representation of interoceptive sensations in individuals with alexithymia: A mouse-tracking and EEG co-registration study","authors":"Xianrui Li ,&nbsp;Wenting Ye ,&nbsp;Yunhong Wang ,&nbsp;Chuyao Peng ,&nbsp;Rui Tao ,&nbsp;Junrong Ren ,&nbsp;Qian Luo ,&nbsp;Zhiting Ren ,&nbsp;Junlai Shan ,&nbsp;Dongtao Wei ,&nbsp;Jiang Qiu","doi":"10.1016/j.neuroscience.2026.01.013","DOIUrl":"10.1016/j.neuroscience.2026.01.013","url":null,"abstract":"<div><div>Humans primarily rely on bodily sensations to experience emotions. Alexithymia, however, alters individuals’ emotional experiences. Despite this, limited research has examined whether individuals with different levels of alexithymia experience the same emotions when exposed to identical bodily sensations. The present studies aimed to explore the altered representation of interoceptive sensations in individuals with alexithymia. In Study 1, we measured how participants associated interoceptive sensations with emotion categories using a computer mouse. In Study 2, event-related potentials (ERPs) were recorded simultaneously while participants performed the same task. Mouse trajectories and the N400 component were analyzed, and ANOVA was conducted to examine the differences in both mouse trajectories and N400 amplitudes. In Study 1, we found that individuals with high alexithymia (HA) exhibited less direct and more curved mouse trajectories compared to those with low alexithymia (LA). Study 2 confirmed these behavioral findings and further revealed that HA individuals exhibited greater N400 amplitudes than LA individuals. Our findings suggest that HA individuals experience deficits in the representation of interoceptive sensations, with the N400 serving as a potential index of these deficits in individuals with alexithymia.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"596 ","pages":"Pages 105-114"},"PeriodicalIF":2.8,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145985318","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":"Investigations on the effects of SH2B2 on Parkinson’s disease based on its in vivo and in vitro neurotoxic model","authors":"Lihui Zhao,&nbsp;Ke Han,&nbsp;Lifeng Sun","doi":"10.1016/j.neuroscience.2025.12.069","DOIUrl":"10.1016/j.neuroscience.2025.12.069","url":null,"abstract":"<div><div>Parkinson’s disease (PD) is characterized by dopaminergic neuron loss, motor dysfunction, and Lewy body formation. Src homology 2B adaptor protein 2 (SH2B2), a member of the SH2B family with known roles in neuroregulation, has not been fully explored in PD. This study aimed to investigate the neuroprotective effects and mechanisms of SH2B2 in PD. MPTP-induced mouse model and MPP⁺-treated SH-SY5Y cell model were established to simulate PD <em>in vivo</em> and <em>in vitro</em>. Mice were randomly divided into saline, MPTP, MPTP + OE-NC, and MPTP + OE-SH2B2 groups, while SH-SY5Y cells were randomly grouped into control, MPP⁺, MPP⁺ + OE-NC, and MPP⁺ + OE-SH2B2. Behavioral tests, Nissl staining, IHC, CCK-8, flow cytometry, qRT-PCR, and Western blot were used to assess outcomes. Our findings indicated that SH2B2 was downregulated in MPTP-induced mice and MPP⁺-treated SH-SY5Y cells (<em>P</em> &lt; 0.01). Overexpressing SH2B2 improved motor function in mice (evidenced by the prolonged rotarod and wire hang latencies and shortened pole climbing time (<em>P</em> &lt; 0.01)), upregulated TH expression (<em>P</em> &lt; 0.001), downregulated IBA1 levels (<em>P</em> &lt; 0.001), and alleviated dopaminergic neuron atrophy and Nissl body loss (<em>P</em> &lt; 0.001). In SH-SY5Y cells, overexpressing SH2B2 reversed MPP⁺-induced cell viability reduction and apoptosis (<em>P</em> &lt; 0.05). This study confirmed SH2B2 downregulation in PD models and demonstrated that overexpressing SH2B2 alleviates dopaminergic neuron injury and neuroinflammation, improving motor function. Therefore, SH2B2 emerges as a novel neuroprotective factor and potential therapeutic target for PD, warranting further research into its molecular mechanisms for clinical translation.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"596 ","pages":"Pages 16-23"},"PeriodicalIF":2.8,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145892944","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":"Omega-3 supplementation prevents functional and neural respiratory damage present in an animal model of Parkinson’s disease","authors":"Taina O. Macedo ,&nbsp;Lais M. Cabral ,&nbsp;Nicole C. Miranda ,&nbsp;Fulvio A. Scorza ,&nbsp;Thiago S. Moreira ,&nbsp;Ana C. Takakura","doi":"10.1016/j.neuroscience.2026.01.016","DOIUrl":"10.1016/j.neuroscience.2026.01.016","url":null,"abstract":"<div><div>Parkinson’s Disease (PD) is a neurodegenerative disorder primarily characterized by the progressive loss of dopaminergic neurons in the substantia nigra, leading to classical motor symptoms such as tremors, rigidity, and bradykinesia. In later stages, patients frequently develop non-classical symptoms, including respiratory dysfunctions, which may result from neurodegeneration in brainstem regions involved in respiratory control, such as the pre-Bötzinger Complex (preBötC) and the retrotrapezoid nucleus (RTN). These changes are likely driven by oxidative stress and neuroinflammation.</div><div>Given the antioxidant and anti-inflammatory properties of omega-3 polyunsaturated fatty acids, this study investigated whether omega-3 supplementation could prevent respiratory-related neuroanatomical and respiratory dysfunctional alterations in a mouse model of PD induced by bilateral injection of 6-hydroxydopamine into the striatum. Omega-3 supplementation prevented respiratory dysfunction by preventing neuronal loss in the preBötC and RTN, reducing glial reactivity and oxidative stress, and maintaining respiratory frequency. These findings support the therapeutic potential of omega-3 in mitigating respiratory dysfunction in PD.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"596 ","pages":"Pages 115-127"},"PeriodicalIF":2.8,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145990215","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":"Cross-fostering affects microglia and cell death in the hippocampus of female and male degu pups","authors":"Gurprince Attlas ,&nbsp;Mallory Duprey ,&nbsp;Cassandra Carlson ,&nbsp;Kaja S. Arusha ,&nbsp;Krystle D. Boadi ,&nbsp;Sabrina S. Ellah ,&nbsp;Daniela Kim ,&nbsp;Charlis Raineki ,&nbsp;Carolyn M. Bauer ,&nbsp;Paula Duarte-Guterman","doi":"10.1016/j.neuroscience.2026.01.004","DOIUrl":"10.1016/j.neuroscience.2026.01.004","url":null,"abstract":"<div><div>Parental care is essential for social, behavioural, and neural development of offspring. Disruption of parental care, for example through parental separation, can negatively affect offspring development in rodents. While previous work has focused on maternal and paternal deprivation, the effects of cross-fostering, another form of parental-offspring instability, on brain development remain poorly understood. Such disruptions are thought to induce stress, which in turn can suppress neurogenesis and increases inflammation and apoptosis in the hippocampus, with effects that often differ between sexes. Given that degus (<em>Octodon degus</em>) are born precocial and form strong attachments with their parents early in life, this study investigated the effect of cross-fostering on hippocampal development in female and male degu pups. At postnatal day 8, degus were assigned to either control (remaining with parents and littermates), partial cross-foster (one pup exchanged per litter), or full cross-foster (entire litter exchanged) conditions. At weaning (5-weeks-old), brains were collected for immunohistochemistry to examine dentate gyrus volume, pyknotic cell density, immature neuron density, and microglia number and morphology. Both types of cross-fostering reduced hippocampal cell death in both sexes relative to controls, with no significant effects on dentate gyrus volume or density of immature neurons. Cross-fostering did not affect total microglia density in either sex, however full cross-fostered females had fewer amoeboid microglia compared to female controls. These findings indicate that cross-fostering affects hippocampal microglia and cell death during development, potentially disrupting circuit refinement and plasticity, with effects that vary by cross-fostering type, sex, and hippocampal region.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 241-249"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145934087","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":"Alterations in auditory midbrain processing is observed in both female and male mouse model of Fragile X Syndrome","authors":"Abdullah Abdullah ,&nbsp;Xiuping Liu ,&nbsp;Kartikeya Murari ,&nbsp;Jun Yan ,&nbsp;Ning Cheng","doi":"10.1016/j.neuroscience.2025.12.062","DOIUrl":"10.1016/j.neuroscience.2025.12.062","url":null,"abstract":"<div><div>Auditory hypersensitivity is a common phenotype in Fragile X Syndrome. Electrophysiology studies at the inferior colliculus of male <em>FMR1-</em>knockout (KO) mice previously demonstrated increased neuronal firing, suggesting that the inferior colliculus is involved in auditory hypersensitivity. Here, we further explored whether the central nucleus of the inferior colliculus (ICc) is involved in auditory hypersensitivity in both female and male KO mice. Tone-evoked <em>in-vivo</em> electrophysiology recordings from ICc neurons of anesthetized (ketamine/xylazine) KO mice at both postnatal day 20 (P20) and 30 (P30) demonstrated increased spikes compared to age- and sex-matched wild-type (WT) mice. Within the KO group, increased spikes were observed in females compared with male mice. Both female and male KO mice also displayed decreased minimum threshold and enhanced response duration at both ages. Additionally, female P30 KO mice displayed weaker inverse relationship between response latency and spike number compared to their WT counterparts. Regarding developmental changes, spike number decreased with maturation in both female and male KO mice. Response duration reduced with age in both sexes of both genotypes, while minimum threshold decreased in the male mice. Finally, we observed an age-related strengthening of the inverse relationship between response latency and magnitude only in the WT mice. Our findings indicate that the ICc display auditory processing deficits particularly in the female KO mice and in young animals highlighting the importance of including female subjects in future studies, and studying early development, which could be an ideal stage for interventions.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 81-92"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145846726","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":"Misfolding protein pathology detected in a chronic mouse model of multiple sclerosis","authors":"Tatiana P. MacKeigan ,&nbsp;Megan L. Morgan ,&nbsp;Sierra Mitchell,&nbsp;Peter K. Stys","doi":"10.1016/j.neuroscience.2025.12.063","DOIUrl":"10.1016/j.neuroscience.2025.12.063","url":null,"abstract":"<div><div>Multiple sclerosis (MS) is one of the most common causes of neurological disability in young adults. The pathobiology of MS includes both autoimmune inflammation and underlying degeneration, with the current challenge being to better understand and treat MS progression. The cuprizone (CPZ) mouse model is commonly used to study de- and remyelination. Despite initial robust myelin repair after toxin withdrawal, mice display progressive callosal atrophy, myelin loss, and gliosis. We tested the hypothesis that this delayed demyelination is due to a progressive degenerative proteopathy. Male C57BL/6 mouse brain sections harvested 8 months after a demyelinating CPZ insult followed by repair were positive for anti-oligomer and anti-fibril epitopes using the antibodies A11 and LOC (p &lt; 0.05 and p &lt; 0.001, respectively). Tissues were also stained with the fluorescent amyloid probes Thioflavin-S (ThS) or pFTAA. Quantitative spectral analysis of the corpus callosum (CC) indicated a subtle but widespread accumulation of ß-sheet-rich material (p &lt; 0.001 and p &lt; 0.0001, respectively). Taken together, our results are consistent with deposition of misfolded proteins facilitating chronic degeneration of axons and myelin in the post-CPZ CC leading to a progressive MS-like pathology. This “late post-CPZ” model could shed light on mechanisms of progressive late degeneration in the MS brain and represents a new animal model of progressive MS, allowing development of novel therapies for this phase of the disease. Our data also raise the possibility that the underlying cytodegenerative component of MS may be driven by subtle toxic amyloid accumulation as in many other traditional neurodegenerative disorders.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 28-36"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145846789","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":"Reduced EEG complexity in stable coronary artery disease: an evidence of covert brain dysfunction","authors":"Bixiu Huo ,&nbsp;Bin Wang ,&nbsp;Hongxiao Jia","doi":"10.1016/j.neuroscience.2025.12.061","DOIUrl":"10.1016/j.neuroscience.2025.12.061","url":null,"abstract":"<div><h3>Background</h3><div>Accumulating evidence indicates that coronary heart disease (CHD) is frequently accompanied by cerebral injury. Non-linear electroencephalogram (EEG) analysis is an effective method for capturing abnormal EEG signal dynamics. This study characterized the complexity of EEG in CHD patients based on non-linear indices.</div></div><div><h3>Methods</h3><div>Twenty-seven patients with CHD were enrolled, as well as an equal number of non-coronary controls. Five-minute, resting-state EEG recordings were obtained under standardized conditions. Non-linear dynamics were quantified using Lempel–Ziv complexity (LZC), permutation Lempel–Ziv complexity (PLZC), sample entropy (SampEn), and permutation entropy (PE). Between-group differences were assessed by independent-samples t-tests. Within the CHD cohort, Pearson correlations were calculated between each non-linear index and clinical variables—age, disease duration, left-ventricular ejection fraction (LVEF %), and number of affected coronary arteries.</div></div><div><h3>Results</h3><div>Compared with controls, the CHD cohort exhibited significantly reduced LZC_mean, LZC_midp, SampEn, PLZC, and PE at multiple electrodes distributed across the entire scalp. A representative finding showed that: at electrode T8, LZC_mean was lower in CHD patients than in controls (0.73 ± 0.09 vs 0.79 ± 0.08; t = −2.683, p = 0.010). Age and disease duration were negatively correlated with several non-linear indices; for example, disease duration inversely predicted LZC_midp at FPz (r = −0.573, adjusted p = 0.004). LVEF% was positively associated with selected measures. No significant correlations were found between the number of affected coronary arteries and any EEG complexity metrics.</div></div><div><h3>Conclusion</h3><div>CHD patients demonstrated significantly lower total spectrum EEG complexity compared to non-CHD controls, offering novel electrophysiological evidence of central nervous system impairment in cardiovascular disease and suggesting potential functional brain alterations.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 229-240"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145850511","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":"Comprehensive analysis of spinal cord inflammatory factors in HIV Tat-induced neuropathy in mice","authors":"Ahmad Kohsar ,&nbsp;Peter Wilson-Braun ,&nbsp;Elizabeth N. Bean ,&nbsp;Madison Philhower ,&nbsp;Benjamin J. Harrison ,&nbsp;Ling Cao","doi":"10.1016/j.neuroscience.2026.01.005","DOIUrl":"10.1016/j.neuroscience.2026.01.005","url":null,"abstract":"<div><div>Despite advancements in HIV treatment, HIV neuropathy, caused by nerve damage following HIV infection, continues to be a major cause of morbidity. Inflammatory responses both in the central and peripheral nervous systems have been implicated as contributing mechanisms, but the role of the HIV protein Trans-Activator of Transcription (Tat) in HIV neuropathy is not well understood. In this study, we report the development of neuropathy-like behavioral changes in doxycycline-inducible HIV Tat transgenic (iTat) mice using comprehensive behavioral assessments. These changes include increased hind paw mechanical sensory sensitivities in both sexes, and increased cold sensitivity and reduced hind paw grip strength predominantly in females. Hind paw skin intra-epidermal nerve fiber (IENF) density showed a small but significant transient increase in the density of CGRP+ fibers at day 21 post-Tat induction in both sexes, while the recovery was faster in females. As Tat is induced primarily in the central nervous system in iTat mice, we therefore focused on elucidating central mechanisms by performing inflammation-targeted RNA profiling in lumbar spinal cord via NanoString assay followed by bioinformatic analysis to identify signaling pathways that may be responsible for the observed symptomatic changes. Three key signaling pathways − apoptosis, inflammation mediated by chemokine and cytokine, and Toll-like receptor signaling pathways − were identified. Subsequent qRT-PCR assays confirmed Tat-induced changes of selected genes. Altogether, we demonstrated that Tat induction is associated with sex-dependent neuropathy-like changes. The concurrent changes in selected inflammation-related signaling pathways within lumbar spinal cord shed light on potential underlying central mechanisms.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 205-219"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145934142","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":"Persons with cerebral palsy display improved occipital cortical entrainment after gait training","authors":"Max J. Kurz ,&nbsp;Elizabeth Dao ,&nbsp;Morgan T. Busboom ,&nbsp;Elizabeth Heinrichs-Graham ,&nbsp;Brad Corr ,&nbsp;Katie L. Bemis ,&nbsp;Logan White ,&nbsp;Kimberley S. Scott ,&nbsp;Tony W. Wilson","doi":"10.1016/j.neuroscience.2025.12.043","DOIUrl":"10.1016/j.neuroscience.2025.12.043","url":null,"abstract":"<div><div>Prior neuroimaging work has shown that people with cerebral palsy (CP) often have visual processing impairments that impact their motor actions. We evaluated if a physical therapy gait training paradigm that incorporated visuomotor tasks has the potential to improve mobility and result in training-related changes in the entrainment of the occipital cortices of people with CP. People with CP (N = 29; Age = 19.9 ± 7.3 years; Gross Motor Classification Score Levels I-III) underwent 24 gait training sessions and completed a comprehensive battery of clinical assessments to quantify their mobility improvements. Magnetoencephalography (MEG) was used to image the cortical activity induced by viewing a 15 Hz flashing stimulus before and after therapy. Neurotypical controls (N = 34; Age = 23.1 ± 3.7 years) were used to gauge the extent of the cortical aberrations and the direction of treatment effects. The group with CP exhibited significantly weaker neural activity in the occipital cortices relative to the neurotypical controls prior to therapy. However, the strength of this event-related synchronization (ERS) increased following therapy. Furthermore, those with a larger change in the strength of the ERS tended to have the greatest improvements in preferred walking speed after therapy. Gait training paradigms that incorporate visuomotor tasks might have the potential to improve mobility, as well as occipital cortical activity in people with CP.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 73-80"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145794318","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":"Spinal dorsal horn GABAergic neuron activation underlies electroacupuncture analgesia in inflammatory pain","authors":"Hao Zheng,&nbsp;Xiaoyue Sun,&nbsp;Junkang Chen,&nbsp;Liaoyuxian Deng,&nbsp;Yani Li,&nbsp;Xiaoyu Wang,&nbsp;Yangshuai Su,&nbsp;Xianghong Jing,&nbsp;Zhiyun Zhang","doi":"10.1016/j.neuroscience.2025.12.060","DOIUrl":"10.1016/j.neuroscience.2025.12.060","url":null,"abstract":"<div><div>While acupuncture is known to alleviate pain by activating local low-threshold afferents and engaging gate control mechanisms in the spinal cord dorsal horn, the specific role of spinal inhibitory neurons in this process remains unclear. The present study aimed to identify whether A-fiber intensity electroacupuncture (EA) enhances spinal inhibitory tone by recruiting gamma-aminobutyric acidergic (GABAergic) neurons to suppress spinal nociceptive transmission in inflammatory pain. We employed single-fiber recordings on sciatic nerve to determine the A-fiber activation threshold for EA intervention. Behavioral tests confirmed that EA at A-fiber intensity significantly alleviated mechanical hyperalgesia, weight-bearing imbalance, and gait abnormalities in mice with complete Freund’s adjuvant (CFA)-induced inflammatory pain. Transgenic mice with Cre recombinase expression driven by the vesicular GABA transporter promoter (VGAT-Cre) combined with <em>in vivo</em> fiber photometry revealed that this analgesia was associated with enhanced activity of dorsal horn GABAergic neurons. Crucially, chemogenetic activation of GABAergic dorsal horn neurons produced robust analgesic effects, whereas their inhibition increased mechanical sensitivity and enhanced neuronal activation in the superficial laminae of dorsal horn. Furthermore, EA at A-fiber intensity significantly attenuated noxious stimulus-induced neuronal c-Fos expression in the superficial dorsal horn. Notably, optogenetic inhibition of GABAergic neurons reversed EA-induced analgesia. Our results demonstrate that EA at A-fiber intensity alleviates inflammatory pain by recruiting GABAergic neurons in the spinal dorsal horn, thereby enhancing inhibitory tone on spinal nociceptive transmission.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 37-49"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145843932","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}