Neuroreport最新文献

{"title":"Biophysical characterization of Arc protein-RNA interactions.","authors":"Aya Al Othman, Tatiana Lupanova, Dmitry Bagrov, Mikhail Durymanov","doi":"10.1097/WNR.0000000000002306","DOIUrl":"10.1097/WNR.0000000000002306","url":null,"abstract":"<p><strong>Objectives: </strong>The activity-regulated cytoskeleton-associated protein (Arc) is essential for synaptic plasticity and memory formation. Arc binds RNA and self-assembles into capsid-like structures reminiscent of retroviral Gag proteins, but the molecular basis of this interaction remains poorly defined. This study sought to characterize the biophysical interactions between Arc protein and its mRNA, focusing on the specificity of mRNA binding and its role in regulating Arc self-assembly.</p><p><strong>Methods: </strong>Here, we combined biophysical approaches to characterize Arc's RNA binding, assembly behavior, and particle morphology. Transmission electron microscopy was employed to visualize complexes of recombinant human Arc and synthetic Arc mRNA at different mRNA molar ratios. Dynamic light scattering (DLS) quantified RNA-dependent changes in the hydrodynamic size of Arc assemblies, while biolayer interferometry (BLI) determined the binding affinity of Arc for cognate and non-cognate mRNA transcripts.</p><p><strong>Results: </strong>Using recombinant human Arc and synthetic Arc mRNA, we found that RNA binding markedly enlarges Arc complexes. At an optimal mRNA molar ratio of ~1 : 45, Arc forms ~50-nm capsid-like particles, compared with ~30-nm assemblies formed by Arc alone, whereas higher RNA levels promote oversized aggregates. DLS confirmed RNA-dependent particle size growth, and BLI showed that Arc binds its cognate mRNA ~1.5-fold more tightly than a non-cognate transcript.</p><p><strong>Conclusion: </strong>The results identify RNA as a crucial cofactor for Arc capsid assembly under physiologically relevant conditions and reveal measurable specificity of Arc for its own mRNA. These findings elucidate how Arc packages its own mRNA, providing insight into Arc-mediated neuronal RNA transfer and advancing the development of Arc-based therapeutic delivery systems.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"682-688"},"PeriodicalIF":2.1,"publicationDate":"2026-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148912018","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":"Maresin 1 delivered via a poly(lactic-co-glycolic acid) conduit enhances sciatic nerve regeneration in rats and is associated with glycogen synthase kinase-3β/β-catenin signaling.","authors":"Yuanhao Zhang, Wei Chen, Youxin Song","doi":"10.1097/WNR.0000000000002302","DOIUrl":"10.1097/WNR.0000000000002302","url":null,"abstract":"<p><strong>Objective: </strong>To fabricate Maresin 1 (MaR1)-loaded poly(lactic-co-glycolic acid) (PLGA) nerve conduits, evaluate their therapeutic effects on sciatic nerve defect repair in rats, and explore the association with glycogen synthase kinase-3β (GSK-3β)/β-catenin signaling.</p><p><strong>Methods: </strong>A 10-mm sciatic nerve defect model was established in Sprague-Dawley rats and randomly assigned to four groups: Sham, Injury, PLGA conduit, and MaR1-loaded PLGA conduit (PLGA/MaR1). Sciatic functional index (SFI) was assessed longitudinally after surgery. At 10 weeks postoperation, the wet weight ratio of the gastrocnemius muscle was measured, and regenerated nerve tissue was examined by hematoxylin-eosin (H&E) staining. Western blotting was performed to determine the expression of GSK-3β, β-catenin, and regeneration/myelination-related proteins (GAP-43, MBP, and S100). In vitro , oxidative stress injury was induced in PC12 cells using H 2 O 2 . Cells were treated with MaR1 with or without differentiation-inducing factor-3 (DIF-3), and changes in cell viability and regeneration-related phenotypes were evaluated.</p><p><strong>Results: </strong>Compared with the PLGA group, the PLGA/MaR1 group showed significantly improved SFI and an increased gastrocnemius wet weight ratio ( P  < 0.05). H&E staining indicated more compact regenerated nerve tissue and better-organized nerve fiber arrangement in the PLGA/MaR1 group. Western blot analysis showed upregulated β-catenin levels accompanied by increased expression of GAP-43, MBP, and S100. In PC12 cells, MaR1 alleviated oxidative stress-induced impairment and promoted regeneration-related phenotypes, whereas DIF-3 partially attenuated these effects.</p><p><strong>Conclusion: </strong>MaR1-loaded PLGA nerve conduits facilitate structural and functional recovery after sciatic nerve defects in rats. The beneficial effects may be associated with modulation of GSK-3β/β-catenin signaling and enhanced expression of axonal regeneration- and myelination-related proteins.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"673-681"},"PeriodicalIF":2.1,"publicationDate":"2026-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963505","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":"Gray matter plasticity associated with secondary trigeminal neuralgia in rats.","authors":"Yehan Li, Chen Zeng, Xiaodong Zhang, Xu Feng, Hao Deng, Xing Luo, Ruhui Xiao, Chuan Zhang, Hanfeng Yang","doi":"10.1097/WNR.0000000000002309","DOIUrl":"10.1097/WNR.0000000000002309","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to characterize brain regional structural alterations across distinct time points in a rat model of trigeminal neuralgia using MRI.</p><p><strong>Methods: </strong>A rat model of secondary trigeminal neuralgia was established by injecting a talc suspension into the infraorbital foramen. Sixty Sprague-Dawley rats were randomly assigned to six groups, including three experimental groups and three sham groups. This study employed a cross-sectional design. MRI scans were performed on one experimental group and one sham group at 4, 8, and 12 weeks postoperatively. Whole-brain voxel-based morphometry analysis was conducted using the SIGMA and Tohoku rat brain templates, and cross-template validation was performed using both templates. A two-sample t-test was used for intergroup comparisons, whereas analysis of variance was performed for intragroup analyses.</p><p><strong>Results: </strong>Our results demonstrated that, at 12 weeks after trigeminal neuralgia induction, the volumes of the right hippocampus, right primary visual cortex, right temporal association cortex, and left primary somatosensory cortex were significantly lower in experimental rats than those in the sham group. Cross-template validation consistently confirmed the involvement of the right hippocampus and left primary somatosensory cortex.</p><p><strong>Conclusion: </strong>Lower volumes in the ipsilateral hippocampus and contralateral primary somatosensory cortex were observed at 12 weeks following trigeminal neuralgia induction when compared with those in the sham group. Comparisons at the 4- and 8-week cross-sectional sampling time points revealed no significant intergroup differences.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"698-705"},"PeriodicalIF":2.1,"publicationDate":"2026-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148881183","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":"Olig2 downregulation mitigates early neurological deficits by modulating mitochondrial dynamics in neonatal hypoxic-ischemic brain injury.","authors":"Limin Yang, Jialin Wen, Lijun Yang","doi":"10.1097/WNR.0000000000002311","DOIUrl":"10.1097/WNR.0000000000002311","url":null,"abstract":"<p><strong>Objective: </strong>Mitochondrial dysfunction and apoptosis are key pathological events in neonatal hypoxic-ischemic brain damage (HIBD). Oligodendrocyte transcription factor 2 (Olig2) is upregulated during the early phase of hypoxic-ischemic brain injury. This study aimed to investigate whether Olig2 downregulation modulates mitochondrial dynamics, apoptosis-related signaling, and early neurobehavioral outcomes in neonatal HIBD.</p><p><strong>Methods: </strong>In vivo, postnatal day 3 (P3) rats were subjected to hypoxic-ischemic injury using the Rice-Vannucci model and were intracerebroventricularly injected with adenoviral vectors carrying Olig2-targeting RNAi or a matched control sequence. Olig2 knockdown and neurobehavioral performance were evaluated at P6/P10. In vitro, HT22 cells were subjected to 3-h oxygen-glucose deprivation, followed by 24 h of reoxygenation (OGD/R). Olig2 was silenced using small interfering RNA; then, mitochondrial morphology, ATP levels, and mitochondrial and apoptosis-related proteins were assessed.</p><p><strong>Results: </strong>In vivo, Olig2 expression was upregulated following hypoxic-ischemic injury, and its knockdown partially improved early neurological deficits, including righting reflex and forelimb grasp at P6, as well as righting reflex, forelimb grip, and cliff avoidance at P10. In vitro, OGD/R-induced Olig2 upregulation, while Olig2 knockdown increased mitochondrial aspect ratio and partially restored ATP levels. OGD/R also elevated dynamin-related protein 1 (Drp1) expression and reduced B-cell lymphoma 2 and optic atrophy 1 levels compared with controls. Olig2 knockdown reversed these changes while decreasing Drp1 and mitofusin 1 (Mfn1), with mitofusin 2 (Mfn2) remaining unchanged.</p><p><strong>Conclusion: </strong>Downregulation of Olig2 was associated with improvements in early neurobehavioral outcomes and mitochondrial function, potentially mediated through suppression of apoptosis and modulation of mitochondrial dynamics.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"706-713"},"PeriodicalIF":2.1,"publicationDate":"2026-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148912399","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":"Low-dose N-methyl-D-aspartate protects against amyloid-β-induced neurotoxicity by suppressing the MLK3-MKK7-JNK3 pathway and activating the PI3K-PDK1-Akt pathway.","authors":"Yi Liu, Jian Wu","doi":"10.1097/WNR.0000000000002310","DOIUrl":"10.1097/WNR.0000000000002310","url":null,"abstract":"<p><strong>Objective: </strong>Oligomeric amyloid-β (Aβ) peptide-induced neuronal apoptosis is a key process in Alzheimer's disease pathogenesis. Low-dose N-methyl-D-aspartate (NMDA) has been shown to promote cell survival both in vitro and in vivo , but its effect on Aβ neurotoxicity remains largely unknown. This study aimed to investigate whether low-dose NMDA protects against Aβ-induced neurotoxicity and to elucidate the underlying molecular mechanisms.</p><p><strong>Methods: </strong>Primary rat cortical neurons were exposed to 10 μM Aβ25-35 to establish a neurotoxicity model. Neuronal apoptosis was assessed by 4',6-diamidino-2-phenylindole staining. The effects of low-dose NMDA (10 μM) on the PI3K-Akt and MLK3-MKK7-JNK3 signaling pathways were examined by immunoprecipitation and Western blotting. The PI3K inhibitor LY294002 was used to verify the role of PI3K signaling in NMDA-mediated regulation of the JNK3 pathway.</p><p><strong>Results: </strong>Low-dose NMDA (10 μM) significantly reduced 10 μM Aβ25-35-induced neuronal apoptosis. Mechanistically, NMDA reversed the Aβ-induced decrease in p-PDK1 and p-Akt levels and concurrently suppressed the activation of the MLK3-MKK7-JNK3 cascade. Moreover, treatment with LY294002 attenuated the inhibitory effect of NMDA on the MLK3-MKK7-JNK3 pathway.</p><p><strong>Conclusion: </strong>Low-dose NMDA exerts neuroprotective effects against Aβ-induced neurotoxicity. These effects are mediated by the dual modulation of the pro-survival PI3K-PDK1-Akt pathway and the pro-apoptotic MLK3-MKK7-JNK3 pathway.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"689-697"},"PeriodicalIF":2.1,"publicationDate":"2026-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148881298","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":"Melatonin attenuates ferroptosis-associated injury through modulation of the thioredoxin-interacting protein/thioredoxin-1/glutathione peroxidase 4 pathway after neonatal hypoxic ischemic brain damage.","authors":"Youcheng Qin, Peilun Xiao, Xinyue Zhang, Zhigang Yang, Wenjie Xiang, Xiaozu Zhang, Haimo Zhang, Yanyu Zeng, Miao Yu, Yan Li, Jing Sui, Xiaoli Wang","doi":"10.1097/WNR.0000000000002305","DOIUrl":"10.1097/WNR.0000000000002305","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to elucidate the neuroprotective mechanism of melatonin (Mel) against hypoxic-ischemic brain damage (HIBD) in neonatal rats, specifically through the thioredoxin-interacting protein (TXNIP)/thioredoxin-1 (Trx-1)/glutathione peroxidase 4 (GPX4) pathway in neuronal ferroptosis, and to concurrently evaluate its therapeutic efficacy using multimodal MRI.</p><p><strong>Methods: </strong>A neonatal rat HIBD model was established with pre- and postmodeling Mel administration. Neuroprotective effects were dynamically assessed in vivo via multimodal MRI. Hippocampal tissues were analyzed for ferroptosis markers and pathway components. In vitro , PC12 cells underwent oxygen-glucose deprivation (OGD) with or without Mel. TXNIP-overexpressing cells were used to verify the axis's specific role.</p><p><strong>Results: </strong>MRI confirmed that Mel significantly reduced infarct volume and improved cerebral blood flow (all P  < 0.05). It preserved neuronal and mitochondrial integrity. Molecularly, Mel restored GPX4/Trx-1 and suppressed acyl-CoA synthetase long-chain family member 4/TXNIP (all P  < 0.05). These effects were replicated in OGD-PC12 cells and persisted in TXNIP-overexpressing cells, supporting the involvement of this pathway.</p><p><strong>Conclusion: </strong>Mel attenuates acute neonatal HIBD and reduces ferroptosis-associated neuronal injury, potentially involving modulation of the TXNIP/Trx-1/GPX4 pathway. Multimodal MRI may serve as a useful in-vivo tool for evaluating therapeutic responses after neonatal HIBD.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"638-650"},"PeriodicalIF":2.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148881276","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":"sAPPα acts as an endogenous ligand for TREM2 to regulate microglial survival and inflammatory responses in Alzheimer's disease.","authors":"Zongqi Wang, MiHua Liu, Jing Xu, Yihong Liu, Ting Liu","doi":"10.1097/WNR.0000000000002307","DOIUrl":"10.1097/WNR.0000000000002307","url":null,"abstract":"<p><strong>Background: </strong>Triggering receptor expressed on myeloid cells 2 (TREM2) regulates microglial functions in Alzheimer's disease, whereas soluble amyloid precursor protein alpha (sAPPα) has neuroprotective effects. Whether sAPPα directly interacts with TREM2 remains unclear.</p><p><strong>Methods: </strong>Single-cell RNA sequencing data from wild-type and APP/PS1 mouse cortices and bulk RNA-seq data (GSE18309) were analyzed. Solid-phase binding, pull-down, and co-immunoprecipitation assays were used to examine TREM2-sAPPα binding and map the interacting regions. LPS-stimulated BV-2 cells were used to assess the effects of TREM2 knockdown and sAPPα supplementation on viability, apoptosis, invasion, phagocytosis, cytokine production, and polarization.</p><p><strong>Results: </strong>A TREM2-positive microglial subpopulation was more abundant in the APP/PS1 dataset and showed relatively restrained inflammatory signaling. Cell-cell communication analysis predicted enhanced APP-(TREM2+TYROBP) signaling. Biochemical assays confirmed direct binding between TREM2 and sAPPα. The TREM2 51-71 amino acid region and the APP E1+Ac fragment contributed to this interaction, whereas TREM2 variants Y38C, R47H, R62H, and T66M reduced binding affinity. TREM2 knockdown aggravated LPS-induced loss of viability, apoptosis, inflammatory cytokine production, and M1-like polarization in BV-2 cells. Exogenous sAPPα reversed these changes.</p><p><strong>Conclusion: </strong>sAPPα directly binds TREM2 and may limit excessive inflammatory activation of microglia under LPS stimulation. The TREM2-sAPPα interaction may represent a regulatory pathway relevant to Alzheimer's disease.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"651-671"},"PeriodicalIF":2.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148880294","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":"Treadmill exercise rescues cognitive deficits in Alzheimer's mice by repairing axonal mitochondrial transport and synaptic function.","authors":"Baixia Li, Zhiling Zhang, Hegui Bao, Yiran Wang, Xinming Ye, Haixia Tu, Wen Fang","doi":"10.1097/WNR.0000000000002300","DOIUrl":"10.1097/WNR.0000000000002300","url":null,"abstract":"<p><strong>Objective: </strong>Alzheimer's disease is a progressive neurological disorder characterized by synaptic injury and loss in its early stage. This study aimed to investigate the effects of treadmill exercise on Alzheimer's disease mice, focusing on the related molecular mechanism of axonal transport.</p><p><strong>Method: </strong>In this study, 3-month-old male APP/PS1 mice and C57BL/6J mice were used and divided into four groups ( n  = 9). Behavioral performance was evaluated using the Morris water maze, open field test, and tail suspension test. Transmission electron microscopy and ELISA were used to assess the morphology and function of mitochondria and synapses, individually. The colocalization of mitochondria and synapses was analyzed by double-labeling immunofluorescence. Finally, the underlying mechanism of treadmill exercise on Alzheimer's disease mice was evaluated by Western blotting.</p><p><strong>Results: </strong>APP/PS1 mice exhibited significant deficits in spatial learning and memory, accompanied by abnormal ultrastructure and dysfunction in hippocampal mitochondria and synapses. Treadmill exercise could ameliorate cognitive impairments and affective disorders in Alzheimer's disease mice, reduce amyloid-beta levels, improve the morphology and function of mitochondria and synapses, and enhance mitochondrial axonal transport, which might be regulated by the related proteins of kinesins, syntabulin, and dyneins.</p><p><strong>Conclusion: </strong>These results suggest that exercise-induced modulation of mitochondrial dynamics can provide neuroprotection and support the development of novel therapeutic strategies for Alzheimer's disease (Video Abstract, SDC 1).</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"625-637"},"PeriodicalIF":2.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148880571","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":"Involvement of phosphorylated caveolin-1 in the dorsal root ganglion in diabetic neuropathic pain and the interventional effect of electroacupuncture.","authors":"Jingqi Liang, Jingjing Zhang, Zhouqi Liu, Zhou-Yuan Wei, Yurong Kang, Xiaofen He, Xiaomei Shao, Jianqiao Fang, Yongliang Jiang, Zhenzhong Lu","doi":"10.1097/WNR.0000000000002303","DOIUrl":"https://doi.org/10.1097/WNR.0000000000002303","url":null,"abstract":"<p><strong>Objective: </strong>The aim of the study was to observe the changes in phosphorylated caveolin-1 (p-Cav-1) expression in the dorsal root ganglion (DRG) of rats with diabetic neuropathic pain (DNP) and to explore the interventional effect of electroacupuncture on Cav-1.</p><p><strong>Methods: </strong>In experiment 1, DNP was induced by intraperitoneal streptozotocin (STZ). Fasting blood glucose (FBG), body weight, and paw withdrawal latency (PWL) to thermal stimuli were measured at baseline and on days 7, 14, and 21 post-STZ. p-Cav-1-positive cells in L4-L6 DRG were detected by immunofluorescence. In experiment 2, rats were divided into normal, STZ, and STZ+siRNA groups. From days 15-21, cav-1-siRNA or blank liposomes were administered intrathecally. FBG, body weight, and PWL were measured. In experiment 3, rats were divided into normal, STZ, and STZ+electroacupuncture groups. From days 15-21, electroacupuncture (2 Hz, 30 min daily) was applied at ST36 and BL60. The above indicators and p-Cav-1 expression were detected.</p><p><strong>Results: </strong>In experiment 1, compared with the normal group, the DNP group showed increased FBG, decreased body weight (D7-D21), and shortened PWL (D14, D21). The number of p-Cav-1-positive neurons in DRG significantly increased in L4-L5 (D7) and L4-L6 (D14, D21). In experiment 2, after siRNA intervention, the PWL of the STZ + siRNA group was significantly prolonged compared with the DNP group. In experiment 3, after electroacupuncture intervention, the PWL of the STZ + electroacupuncture group was significantly prolonged compared with the DNP group (D21), and the expression of p-Cav-1-positive cells in DRG was significantly decreased compared with the STZ group.</p><p><strong>Conclusion: </strong>Upregulation of p-Cav-1 expression in DRG is involved in the development of DNP. Electroacupuncture can effectively alleviate hyperalgesia in DNP rats, and its mechanism may be related to the inhibition of p-Cav-1 expression in DRG.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"37 15","pages":"615-624"},"PeriodicalIF":2.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148912439","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":"Encouraging attention to inclusion cues enhances P3b responses and subjective amelioration after social exclusion.","authors":"Tsubasa Izaki","doi":"10.1097/WNR.0000000000002304","DOIUrl":"10.1097/WNR.0000000000002304","url":null,"abstract":"<p><strong>Objective: </strong>Previous research suggests that attentional allocation to inclusion cues is associated with subjective amelioration from social exclusion. However, individuals high in avoidant attachment show reduced attention to inclusion cues while still exhibiting subjective amelioration comparable with those low in avoidance. This study examined whether experimentally encouraging attention to inclusion cues enhances attentional processing and subjective amelioration following social exclusion, and whether these effects differ as a function of avoidant attachment.</p><p><strong>Methods: </strong>Thirty-six undergraduate students completed a Cyberball task consisting of exclusion and subsequent inclusion sessions under two conditions: an attention-manipulation condition, in which they counted ball receptions, and a natural condition without additional attention instructions. P3b amplitudes elicited by inclusion cues during the inclusion session indexed attentional processing. Subjective amelioration was defined as the reduction in Need-Threat scores from exclusion to inclusion.</p><p><strong>Results: </strong>Preregistered analyses of covariance showed that encouraging attention to inclusion cues increased P3b amplitudes ( P = 0.02) and subjective amelioration ( P = 0.04), with no significant moderation by avoidant attachment ( P s > 0.39). However, additional group-based analyses of variance showed that the attention manipulation significantly increased P3b amplitudes in the high-avoidance group ( P = 0.004), but not in the low-avoidance group ( P = 0.55), whereas no corresponding Group × Condition interaction was observed for subjective amelioration ( P = 0.94).</p><p><strong>Conclusion: </strong>The present study suggests that encouraging attention to inclusion cues facilitates amelioration from social exclusion without disrupting this process among individuals high in avoidance.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"607-613"},"PeriodicalIF":2.1,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148760906","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}