Neuroreport最新文献

{"title":"Multimodal characterization of cortical amplitude of low-frequency fluctuation alterations in chronic low back pain: integrating functional MRI, transcriptomics, and neurochemical mapping.","authors":"Yuan-Zhi He, Zhan-Xiang Hu, Xin Wan","doi":"10.1097/WNR.0000000000002279","DOIUrl":"10.1097/WNR.0000000000002279","url":null,"abstract":"<p><strong>Background: </strong>Chronic low back pain (CLBP) is associated with widespread disruptions in intrinsic brain activity; however, the underlying molecular and neurochemical mechanisms remain unclear. This study aimed to elucidate the multiscale biological substrates of alterations in spontaneous neural activity in CLBP using a multimodal framework.</p><p><strong>Methods: </strong>We enrolled 41 patients with CLBP and 41 matched healthy controls. Resting-state functional MRI was utilized to assess the amplitude of low-frequency fluctuations (ALFFs), a marker of spontaneous brain activity. Regional alterations in ALFF were mapped and correlated with spatial gene expression profiles from the Allen Human Brain Atlas and neurotransmitter receptor density maps derived from PET.</p><p><strong>Results: </strong>Compared with healthy controls, patients with CLBP exhibited increased ALFF in the left cerebellar lobule 10 and decreased ALFF in five cortical regions spanning the visual, default mode, sensorimotor, and frontoparietal networks. Transcriptomic analysis revealed that ALFF-related genes were enriched in pathways associated with synaptic transmission and immune response and were predominantly expressed in excitatory and inhibitory neurons. Spatial correlations further indicated significant alignment between ALFF alterations and the regional distributions of μ-opioid, 5-HT1a serotonin, and CB1 cannabinoid receptors.</p><p><strong>Conclusion: </strong>Our findings highlight a multiscale interplay among spontaneous brain activity, gene expression, and neuromodulatory systems in CLBP. Regionally specific alterations in ALFF reflect imbalances between neuronal excitation and neuroimmune regulation, constrained by the spatial architecture of neurotransmitter systems. These results enhance our understanding of the neurobiological basis of chronic pain and suggest potential targets for mechanism-informed interventions.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"37 12","pages":"443-458"},"PeriodicalIF":2.1,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"C-C motif chemokine ligand 3 mediates inflammatory response via NLRP3 inflammasome and neuron damage after traumatic brain injury.","authors":"Shaozhuang Xue, Zhangyi Wang, Wu Ji, Dong Tan, Yuxiang Sun, Shiyu Feng, Yan Wang, Yu Yuan","doi":"10.1097/WNR.0000000000002285","DOIUrl":"10.1097/WNR.0000000000002285","url":null,"abstract":"<p><strong>Objective: </strong>Traumatic brain injury (TBI) constitutes a major inducer of neuroinflammation within the initial 24 h, peak microglial reactivity by day 3 post-injury, and cytokine production through day 7. However, the precise underlying pathophysiology driving immune cell infiltration, inflammatory cascades, and subsequent neuronal damage remains incompletely defined. This study aims to investigate whether C-C motif chemokine ligand 3 (CCL3) plays a functional role in TBI-induced neuroinflammation and associated neuronal injury.</p><p><strong>Methods: </strong>Datasets of RNA-seq analysis used were: GSE58485 is mice neocortex at 3 days post-TBI, GSE92363 is rat hippocampus at day 1 post-TBI, and GSE59645 is rat hippocampus at day 14 post-TBI. GEO datasets, GSE92363 and GSE59645, sequencing analysis of the normal rat hippocampus were merged to provide a baseline to identify key differentially expressed genes (DEGs). DEGs were used to perform functional annotations through Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses, execute gene set enrichment analysis (GSEA), and construct protein-protein interaction (PPI) networks. Microglia HAPI cells and H19-7 cells co-culture system was used to functionally validate microglia-derived neuroinflammatory damage mechanisms on neuronal cells.</p><p><strong>Results: </strong>For screening of DEGs related to TBI, we first performed an integrated analysis of the GSE92363 and GSE59645 datasets. Initial-phase TBI exhibited characteristic immune landscape alterations, marked by significant macrophage and neutrophil infiltration with concurrent M1 macrophage polarization. GSEA further revealed microglial phagocytic pathway dysregulation as the most profoundly perturbed signaling cascade in TBI pathogenesis. Subsequently, we identified CCL3 as a master regulatory hub orchestrating TBI progression with PPI analysis. In HAPI cells, short hairpin RNA-mediated CCL3 knockdown effectively attenuated lipopolysaccharide-induced pro-inflammatory cytokine elevation and suppressed nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain-containing 3 (NLRP3) inflammasome pathway activation. In the HAPI-H19-7 (neuron) co-culture system, CCL3 silencing demonstrated significant neuroprotection by mitigating H19-7 neuronal apoptosis.</p><p><strong>Conclusion: </strong>CCL3 functions as a key regulatory chemokine orchestrating NLRP3 inflammasome-mediated microglial activation in post-TBI neuroinflammation. Inhibition of CCL3 may be a promising therapeutic target for ameliorating secondary neuronal injury following TBI.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"477-489"},"PeriodicalIF":2.1,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148331629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture alleviates neuroinflammation and promotes recovery of neurological functions after intracerebral hemorrhage by modulating α7nAChR/JAK2/STAT3 signaling pathway.","authors":"Hongling Xu, Yun Wang, Liu Zi, Xubin Chang, Yangfan Gao, Xudong Cao, Chao You, Hao Li, Chengwei Wang, Meng Tian","doi":"10.1097/WNR.0000000000002283","DOIUrl":"10.1097/WNR.0000000000002283","url":null,"abstract":"<p><strong>Objectives: </strong>Electroacupuncture, a therapeutic modality integrating electrical stimulation with traditional acupuncture, has emerged as a promising intervention for intracerebral hemorrhage (ICH). This study aimed to elucidate the potential mechanisms underlying electroacupuncture's therapeutic effects in a mouse model of ICH.</p><p><strong>Methods: </strong>The mice were injected autologous blood into basal ganglia region of brain to establish an ICH model. The study comprised two parts. First, we evaluated the therapeutic efficacy of electroacupuncture at Baihui (GV20) and Dazhui (GV14) points using the ICH model by neurological deficit score, Fluoro-Jade C (FJC) staining, and ELISA. Subsequently, based on the observed therapeutic benefits, we further explored the underlying mechanisms via neurological deficit and adhesive removal score, immunofluorescence staining, immunohistochemical staining, ELISA, and Western blot assays.</p><p><strong>Results: </strong>The first part of the study showed that electroacupuncture treatment alleviated the expression of proinflammatory cytokines [tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β)], neuronal degeneration, and neurological deficits. The second part of the study showed that electroacupuncture treatment upregulated the expression of the α7 nicotinic acetylcholine receptor (α7nAChR), downregulated Janus kinase-2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) phosphorylation, promoted M2 microglia/macrophage polarization, and reduced IL-1β and TNF-α expression, contributing to improved neurobehavioral function.</p><p><strong>Conclusion: </strong>Electroacupuncture treatment can alleviate neuroinflammation and improve neurobehavioral function in ICH mice, which might be modulated by the α7nAChR/JAK2/STAT3 pathway, providing a new molecular mechanism of electroacupuncture treatment on ICH.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"466-476"},"PeriodicalIF":2.1,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148331576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-cell-autonomous regulation of Bhlhb5 expression in cortical projection neurons by GABAergic interneuron development and position.","authors":"Xiaolei Song, Fengzhu Zhang, Danyu Han, Jingzhe Yu, Xiaoming Xin, Rongliang Guo","doi":"10.1097/WNR.0000000000002284","DOIUrl":"10.1097/WNR.0000000000002284","url":null,"abstract":"<p><strong>Objective: </strong>The functional architecture of the cerebral cortex relies on the coordination between excitatory projection neurons and inhibitory GABAergic interneurons. While intrinsic programs governing their specification are well-characterized, it remains unclear whether the proper development of interneurons is required to maintain the molecular identity of projection neurons.</p><p><strong>Methods: </strong>We generated double conditional knockout (DCKO) mice lacking the transcription factors Sp8 and Sp9 specifically in the GABAergic lineage using the Dlx5/6-Cre driver. Cortical cytoarchitecture and neuronal identity were assessed via immunohistochemistry at postnatal days 4 (P4) and 11 (P11).</p><p><strong>Results: </strong>Sp8&Sp9-DCKO mice exhibited severe defects in the development and laminar positioning of cortical interneurons, resulting in their abnormal distribution and reduced abundance in the cortex. Despite these inhibitory defects, the general laminar organization, checked by the expression of TBR1, CTIP2, FOXP2, FOXP1, CUX1, and NeuN, remained intact. Strikingly, the expression of BHLHB5, a key regulator of sensory area identity, was specifically downregulated in projection neurons at P11. Crucially, BHLHB5 expression was indistinguishable from controls at P4, indicating that the proper development of cortical interneurons is essential for stabilizing the molecular identity of projection neurons.</p><p><strong>Conclusion: </strong>These findings reveal a novel non-cell-autonomous mechanism where proper GABAergic interneuron positioning and development are essential for the maintenance, but not the acquisition, of specific projection neuron molecular identities.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"459-465"},"PeriodicalIF":2.1,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148331569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Surviving microglia and nonmicroglial progenitors contribute to microglial repopulation following colony-stimulating factor 1 receptor inhibition.","authors":"Eric Yuhsiang Wang, Hank Szuhan Chen, Ya Lan Yang, Ching Mei Wu, Yi-Wen Chang, Ted Weita Lai","doi":"10.1097/WNR.0000000000002286","DOIUrl":"10.1097/WNR.0000000000002286","url":null,"abstract":"<p><strong>Background: </strong>Microglial repopulation after depletion via colony-stimulating factor 1 receptor (CSF1R) inhibition holds therapeutic potential for neurological disorders, but the cellular sources remain debated. We investigated whether repopulation arises solely from surviving microglia or also from nonmicroglial progenitors.</p><p><strong>Methods: </strong>Using Cx3cr1 CreER :Ai14 (tdTomato) reporter mice, we labeled microglia before PLX3397-induced depletion and assessed repopulation. Next, in Cx3cr1 CreER+/- :Csf1r fl/fl mice, we combined tamoxifen-induced genetic CSF1R deletion with PLX3397 to ablate microglia completely and evaluated recovery.</p><p><strong>Results: </strong>We found that repopulated microglia were predominantly tdTomato + , indicating derivation from surviving Cx3cr1 + microglia. Combined tamoxifen and PLX3397 achieved near-complete ablation, yet microglia repopulated and were re-depletable by PLX3397, confirming potential nonmicroglial origins.</p><p><strong>Conclusion: </strong>Microglial repopulation primarily involves proliferation of surviving microglia but can recruit nonmicroglial progenitors when depletion is exhaustive. These insights resolve prior inconsistencies and guide therapeutic strategies for microglial replacement treatment.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"497-503"},"PeriodicalIF":2.1,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148283791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fear prioritizes feedforward sensory coding at the expense of contextual processing in monkey V1.","authors":"An Yan, Zhengxuan Li, Xiangmeng Fu, Zhihan Li, Yin Yan, Kun Guo, Wu Li","doi":"10.1097/WNR.0000000000002287","DOIUrl":"10.1097/WNR.0000000000002287","url":null,"abstract":"<p><strong>Objective: </strong>The primary visual cortex (V1) supports both rapid feedforward coding of local features and contextual processing shaped by recurrent and top-down feedback. While fear learning is known to prioritize threat-predictive signals in V1, it remains unclear whether this prioritization uniformly enhances all stages of cortical processing or selectively biases certain computations. We investigated how fear conditioning modulates V1 population coding for simple gratings versus global contours, which rely on distinct temporal stages of integration.</p><p><strong>Methods: </strong>Monkeys were trained in a visual fear-conditioning paradigm. We utilized chronic microelectrodes to record V1 population activity while monkeys viewed conditioned and nonconditioned stimuli. Using a Fisher linear discriminant classifier, we quantified stimulus discriminability ( d ') during early and late response epochs to distinguish between feedforward and feedback-driven coding.</p><p><strong>Results: </strong>Fear conditioning produced a striking temporal and stimulus-specific dissociation. For gratings, conditioning significantly enhanced orientation decoding during the early response epoch, consistent with a rapid retuning of feedforward encoding. This early facilitation was also present for contour stimuli involving contextual integration. By contrast, during the late response epoch, fear conditioning significantly reduced decoding performance for contours, while leaving grating discrimination largely unaffected.</p><p><strong>Conclusion: </strong>Fear conditioning does not act as a global gain control. Instead, it reconfigures V1 dynamics to prioritize rapid, feedforward threat detection at the functional cost of later, recurrent- and feedback-dependent contextual processing. This shift suggests an adaptive trade-off: emotional learning sharpens the detection of isolated predictive cues but reduces the fidelity of the complex spatial integration required for scene analysis.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"490-496"},"PeriodicalIF":2.1,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148265522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional exploration of metabotropic glycine receptors in cultured rat hippocampal slices.","authors":"Kirika Takenaka, Masahiro Mori","doi":"10.1097/WNR.0000000000002281","DOIUrl":"10.1097/WNR.0000000000002281","url":null,"abstract":"<p><strong>Objective: </strong>Metabotropic glycine receptors (mGlyRs) have been identified in the prefrontal cortex and nucleus accumbens, but their function in the hippocampus remains unreported. This study aimed to probe functional mGlyR signaling in the hippocampus.</p><p><strong>Methods: </strong>We pharmacologically isolated conditions favoring mGlyR activation and performed gramicidin-perforated whole-cell recordings from CA3 pyramidal cells in rat organotypic hippocampal slice cultures. Intrinsic electrophysiological properties were compared before and after bath application of glycine. To assess G protein dependence, we examined responses after pretreatments with N-ethylmaleimide (NEM), a broad G protein blocker, and pertussis toxin (PTX), a Gi/o-selective inhibitor.</p><p><strong>Results: </strong>Under control conditions, we observed changes indicating enhanced neuronal excitability, including an increase in the number of action potentials fired and a reduction in the amplitude of the medium after hyperpolarization. Moreover, in the presence of either NEM or PTX, the changes observed in the control group were abolished.</p><p><strong>Conclusion: </strong>These results indicate that there are functional mGlyRs in the hippocampus and that they mediate their effects via Gi/o signaling.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"37 11","pages":"415-419"},"PeriodicalIF":2.1,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial frequency processing preferentially recruits distributed cortical interactions in V1.","authors":"Yahia Yassine Belkacemi, Ekta Jain, Jade Vanderpool, Jessica Singh, Oliver Flouty, Stéphane Molotchnikoff, Vishal Bharmauria","doi":"10.1097/WNR.0000000000002278","DOIUrl":"https://doi.org/10.1097/WNR.0000000000002278","url":null,"abstract":"<p><strong>Objectives: </strong>The primary visual cortex (V1) is tuned to several visual features, including orientation and spatial frequency, that are organized into overlapping functional maps. Local neurons sharing tuning properties tend to connect more strongly, but how these features lead to distal functional connectivity in V1 remains unclear.</p><p><strong>Methods: </strong>We recorded multiunit activity from layers II/III of cat V1 using electrode pairs separated by 410 µm and assessed functional connectivity using shift-corrected cross-correlograms. Visual stimuli were positioned to largely overlap the receptive fields of neurons at both recording sites. Functional connectivity was compared during orientation-constant and spatial frequency-constant stimulus conditions.</p><p><strong>Results: </strong>Neurons in the same ensemble exhibited significantly more and stronger distal functional connections during the spatial frequency-constant condition than during the orientation-constant condition. This effect persisted at the population level, indicating that distal connectivity is selectively recruited depending on the stimulus feature rather than anatomical proximity or differential stimulus drive.</p><p><strong>Conclusion: </strong>These findings demonstrate that functional connectivity in V1 is stimulus-dependent, with spatial frequency processing preferentially engaging distributed cortical interactions. Such feature-dependent distal connectivity may support integration across spatial scales and reflect the flexible organization of early visual cortical networks.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"37 11","pages":"402-408"},"PeriodicalIF":2.1,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered development in auditory white matter and cortical response latency in youth with neurofibromatosis type I.","authors":"Matthew C Hocking, Jeffrey I Berman, May V Albee, Lisa Blaskey, Michael J Fisher, Timothy P L Roberts","doi":"10.1097/WNR.0000000000002277","DOIUrl":"10.1097/WNR.0000000000002277","url":null,"abstract":"<p><strong>Objectives: </strong>Neurofibromatosis type 1 (NF1) is a genetic disorder that affects brain development and increases the risk for neurodevelopmental conditions, including autism spectrum disorder. Given similar behavioral phenotypes and potential shared neurobiological processes in NF1 and autism spectrum disorder, this study evaluates two markers of brain maturation in youth with NF1 and typically developing youth, including auditory white matter and cortical response latency.</p><p><strong>Basic methods: </strong>Participants, aged 8-12 years, completed a multimodal neuroimaging protocol that included MRI with diffusion tensor imaging of the auditory radiation and magnetoencephalography. Analyses included group comparisons on fractional anisotropy measures of white matter and M50 latency responses from magnetoencephalography and the coupling between fractional anisotropy and M50.</p><p><strong>Main results: </strong>Compared to typically developing youth, youth with NF1 did not show maturation in fractional anisotropy or M50 with age and demonstrated shorter M50 auditory response latency. The association between auditory radiation fractional anisotropy and M50 was different in youth with NF1 compared to typically developing youth with youth with NF1 not showing a significant association between fractional anisotropy and M50.</p><p><strong>Conclusion: </strong>Maturation of auditory white matter and auditory cortical response latency is disrupted in NF1 and there is a lack of coupling between structure and function. Longitudinal imaging research is needed to further evaluate neurodevelopment and associations between these immaturities and behavior.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"37 11","pages":"409-414"},"PeriodicalIF":2.1,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367524/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hand mental rotation reaction time reflects motor imagery strategy and predicts changes in finger dexterity after motor imagery.","authors":"Yuki Fukumoto, Keisuke Fujii, Marina Todo, Toshiaki Suzuki","doi":"10.1097/WNR.0000000000002280","DOIUrl":"10.1097/WNR.0000000000002280","url":null,"abstract":"<p><strong>Background: </strong>Motor imagery can improve motor performance, but its effects vary among individuals. Hand mental rotation may reflect individual characteristics related to motor imagery processing, including imagery strategies. This study examined whether the reaction time in a hand mental rotation task could explain interindividual differences in motor imagery-induced changes in finger dexterity and spinal motor neuron excitability.</p><p><strong>Methods: </strong>Participants were classified into 'good' and 'poor' groups according to the reaction times for right- and left-hand mental rotation judgments. Finger dexterity was assessed using the Purdue Pegboard task, and spinal motor neuron excitability during motor imagery was evaluated using F-waves.</p><p><strong>Results: </strong>Grouping based on hand mental rotation reaction time showed no interaction effect on the F/M amplitude ratio. In contrast, grouping based on left-hand mental rotation reaction time revealed greater improvement in finger dexterity in the poor group. Left-hand mental rotation reaction time showed a weak association with backward digit span performance but not with other measures of working memory.</p><p><strong>Conclusion: </strong>The hand mental rotation reaction time may reflect differences in motor imagery strategy rather than motor imagery ability and may explain interindividual differences in motor imagery-related improvements in finger dexterity.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"37 11","pages":"420-429"},"PeriodicalIF":2.1,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}