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Family support as a pain protective factor for African American older adults: latent class analyses across 2 national longitudinal data sets. 家庭支持作为非裔美国老年人疼痛保护因素:跨两个国家纵向数据集的潜在分类分析。
IF 5.5 1区 医学
PAIN® Pub Date : 2025-11-01 Epub Date: 2025-06-17 DOI: 10.1097/j.pain.0000000000003687
Patricia N E Roberson, Kendall P Brady, Bhaskar Thakur, Staja Booker, Zureyat Sola-Odeseye, Beatrice L Wood, Sarah Woods
{"title":"Family support as a pain protective factor for African American older adults: latent class analyses across 2 national longitudinal data sets.","authors":"Patricia N E Roberson, Kendall P Brady, Bhaskar Thakur, Staja Booker, Zureyat Sola-Odeseye, Beatrice L Wood, Sarah Woods","doi":"10.1097/j.pain.0000000000003687","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003687","url":null,"abstract":"<p><strong>Abstract: </strong>Family relationships dynamically affect pain outcomes. However, less is known about African American family relationships and chronic pain incidence and persistence. Using theoretically driven group characterizations of family emotional climate (FEC; Strained, Supportive, and Disengaged) across multiple relationship types, we conducted latent class analyses in 2 nationally representative data sets (Midlife in the United States [MIDUS]; Health Retirement Study [HRS]) aimed to identify a more ecologically valid model of family relationships and determine how the identified FEC groups, separately and concurrently, connect to chronic pain incidence and persistence for aging African Americans. For the family-only models in MIDUS and HRS, using logistic regression, Strained FEC compared with Supportive FEC increased the risk of pain incidence (odds ratio [OR] = 2.06) in MIDUS and the risk of pain persistence (OR = 2.14) in HRS. The next models extended to include parent-child relationships in HRS identified 4 FEC groups (eg, Strained Family and Parent-Child, Supportive and Strained Family and Parent-Child, Supportive Family and Parent-Child, and Disengaged Family and Parent-Child FEC). Again, using logistic regression, we identified a greater risk of pain incidence was linked to Strained Family and Parent-Child FEC (OR = 1.36) and Supportive and Strained Family and Parent-Child FEC (OR = 1.22), although not Disengaged Family and Parent-Child FEC (OR = 0.71). Strained Family and Parent-Child FEC also related to greater risk of pain persistence (OR = 1.89) compared with Supportive Family and Parent-Child FEC. These findings suggest utilization of a multidimensional modeling of family relationships to contextualize pain outcomes for aging African Americans.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"166 11","pages":"2588-2595"},"PeriodicalIF":5.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145293364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Advancing understanding of opioid mortality risks beyond initial findings in noncancer pain patients. 在非癌性疼痛患者的初步发现之外,推进对阿片类药物死亡风险的理解。
IF 5.5 1区 医学
PAIN® Pub Date : 2025-11-01 Epub Date: 2025-08-13 DOI: 10.1097/j.pain.0000000000003793
Hongjuan Jing
{"title":"Advancing understanding of opioid mortality risks beyond initial findings in noncancer pain patients.","authors":"Hongjuan Jing","doi":"10.1097/j.pain.0000000000003793","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003793","url":null,"abstract":"","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"166 11","pages":"e675-e676"},"PeriodicalIF":5.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145293398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The future of pain research: neuromodulation and surgery. 疼痛研究的未来:神经调节和外科。
IF 7.4 1区 医学
PAIN® Pub Date : 2025-11-01 DOI: 10.1097/j.pain.0000000000003662
Daniel Ciampi de Andrade,Prasad Shirvalkar
{"title":"The future of pain research: neuromodulation and surgery.","authors":"Daniel Ciampi de Andrade,Prasad Shirvalkar","doi":"10.1097/j.pain.0000000000003662","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003662","url":null,"abstract":"By 2075, neuromodulation and surgical treatments for pain will be heavily impacted by advances in artificial intelligence, regenerative medicine, and precision diagnostics. Digital brain twins will enable patient-specific simulations to optimize intervention selection, while adaptive neuromodulatory systems will provide real-time, responsive pain management. Personalized treatments will replace the current trial-and-error approach, using genetics, neurophysiology, and AI-driven decision tools. Minimally invasive, home-based neuromodulation will increase accessibility, and ethical data governance will enhance patient autonomy. These advances will transform pain from a chronic, partially relieved condition into a precisely treatable disorder, fundamentally improving patient outcomes and healthcare efficiency.By 2075, precision diagnostics will match each pain patient to the optimal neuromodulation or surgical strategy before treatment begins. Adaptive, minimally invasive, home-based devices will deliver real-time, closed-loop stimulation, shifting therapy from trial-and-error to responsive, individualized care. Big-data guidance on timing, modality, and duration will cut failure rates, while robotics and regenerative techniques expand access and shorten recovery. Adapted ethics and data-governance frameworks will safeguard autonomy, so chronic pain becomes a precisely treatable, and hopefully curable, condition.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"95 1","pages":"S116-S120"},"PeriodicalIF":7.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145288545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
How people resolve pain: insights from human transcriptomics into immune activation and therapeutic innovations. 人们如何解决疼痛:从人类转录组学到免疫激活和治疗创新的见解。
IF 7.4 1区 医学
PAIN® Pub Date : 2025-11-01 DOI: 10.1097/j.pain.0000000000003671
Andrey Bortsov,Sahel Jahangiri Esfahani,Lucas V Lima,Ru-Rong Ji,Jeffrey S Mogil,Luda Diatchenko
{"title":"How people resolve pain: insights from human transcriptomics into immune activation and therapeutic innovations.","authors":"Andrey Bortsov,Sahel Jahangiri Esfahani,Lucas V Lima,Ru-Rong Ji,Jeffrey S Mogil,Luda Diatchenko","doi":"10.1097/j.pain.0000000000003671","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003671","url":null,"abstract":"Patients with chronic pain commonly exhibit elevated inflammatory markers in the blood that correlate with reported pain and pain-related disability. Although inflammation is traditionally seen as a driver of chronic pain, recent transcriptomic data challenge this view, highlighting the beneficial role of acute inflammation in pain resolution. Here, we present evidence pointing to the overall dynamics of the inflammatory response being critical for pain resolution with the initial acute inflammatory response necessary to trigger pain resolution processes. We posit that chronic pain reflects an inability to resolve inflammation rather than its mere presence. Pharmacological or nonpharmacological reactivation of acute inflammatory pathways may thus provide novel therapeutic strategies targeting pain resolution instead of merely mitigating pain perception. This novel hypothesis regarding the effect of inflammation on pain is an example of what can be learned using unbiased approaches such as human transcriptomics. We believe that the near future will feature more examples of hypothesis generation using human genetics followed up by mechanistic experimentation in animal models.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"4 1","pages":"S60-S64"},"PeriodicalIF":7.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145288554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
SARS-CoV-2 N protein interacts with Na v 1.7 to promote pathological pain. sars - cov - 2n蛋白与Nav1.7相互作用促进病理性疼痛
IF 5.5 1区 医学
PAIN® Pub Date : 2025-11-01 Epub Date: 2025-06-04 DOI: 10.1097/j.pain.0000000000003675
Jin-Kun Liu, Zi-Su Zhou, Shu-Hang Wang, Shi-Yu Zuo, Xiao-Fan Lu, Ying He, Hao Tang, Yan Xie, Man-Xiu Xie, Xiao-Long Zhang
{"title":"SARS-CoV-2 N protein interacts with Na v 1.7 to promote pathological pain.","authors":"Jin-Kun Liu, Zi-Su Zhou, Shu-Hang Wang, Shi-Yu Zuo, Xiao-Fan Lu, Ying He, Hao Tang, Yan Xie, Man-Xiu Xie, Xiao-Long Zhang","doi":"10.1097/j.pain.0000000000003675","DOIUrl":"10.1097/j.pain.0000000000003675","url":null,"abstract":"<p><strong>Abstract: </strong>Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to a global health crisis, with many patients experiencing not only acute neurological and sensory symptoms but also persistent sensory abnormalities, commonly referred to as long COVID sequelae. The mechanisms underlying somatosensory abnormalities induced by SARS-CoV-2 remain largely unclear. In this study, we investigate the role of the SARS-CoV-2 nucleocapsid (N) protein in pain regulation. Our data show that SARS-CoV-2 N protein exacerbates pathological pain in mouse models of bone cancer, chemotherapy, neuropathic, and inflammatory, and promotes the chronification of acute inflammatory pain. We also identify a potential interaction between the N protein and Na v 1.7 in dorsal root ganglion neurons from mice, monkeys, and humans. Furthermore, the N protein significantly increases Na v 1.7 currents in dorsal root ganglion neurons from both mice and monkeys by delaying Na v 1.7 inactivation without altering its expression or membrane trafficking. This modulation of Na v 1.7 function by the N protein not only intensifies pain hypersensitivity but also prolongs the duration of pain, potentially facilitating the transition from acute to chronic pain. Our findings underscore the importance of vigilant management of SARS-CoV-2 infection in patients with pathological pain and suggest potential therapeutic targets for mitigating COVID-19-related pain.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":"e635-e651"},"PeriodicalIF":5.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Impact of different acute low back pain definitions on the predictors and on the risk of transition to chronic low back pain: a prospective longitudinal cohort study. 不同急性腰痛定义对预测因子和向慢性腰痛过渡风险的影响:一项前瞻性纵向队列研究。
IF 5.5 1区 医学
PAIN® Pub Date : 2025-11-01 Epub Date: 2025-06-11 DOI: 10.1097/j.pain.0000000000003669
Rachael O Osagie, Iulia Tufa, Adriana Angarita-Fonseca, M Gabrielle Pagé, Anaïs Lacasse, Laura S Stone, Pierre Rainville, Mathieu Roy, Pascal Tétreault, Maryse Fortin, Guillaume Léonard, Hugo Massé-Alarie, Jean-Sébastien Roy, Audrey V Grant, Carolina B Meloto
{"title":"Impact of different acute low back pain definitions on the predictors and on the risk of transition to chronic low back pain: a prospective longitudinal cohort study.","authors":"Rachael O Osagie, Iulia Tufa, Adriana Angarita-Fonseca, M Gabrielle Pagé, Anaïs Lacasse, Laura S Stone, Pierre Rainville, Mathieu Roy, Pascal Tétreault, Maryse Fortin, Guillaume Léonard, Hugo Massé-Alarie, Jean-Sébastien Roy, Audrey V Grant, Carolina B Meloto","doi":"10.1097/j.pain.0000000000003669","DOIUrl":"10.1097/j.pain.0000000000003669","url":null,"abstract":"<p><strong>Abstract: </strong>Inconsistencies in the identification of predictors for the transition from acute low back pain (aLBP) to chronic LBP (cLBP) may be attributed to the varying definitions of aLBP used in different studies. We investigated how adopting different aLBP definitions affects the set of predictors and the risk of transition to cLBP (LBP > 3 months that caused a problem for at least half the days in the past 6 months). We leveraged data from the ongoing prospective Quebec Low Back Pain Study to compose 3 aLBP groups at baseline: nonchronic (individuals not meeting the cLBP criteria, n = 788), acute (LBP < 3 months, n = 230), and new episode (LBP < 3 months preceded by ≥3 pain-free months, n = 182). The primary outcome was the transition to cLBP at 6 months. We built predictive models within groups using the minimum redundancy maximum relevance algorithm to identify key predictors, focusing on models discrimination and calibration. Risks of transition were 35.8%, 44.3%, and 45.6%, for the nonchronic, acute, and new episode groups, respectively. Pain intensity, disability, and depression emerged as consistent predictors across definitions. The acute and new episode models, but not the nonchronic , were considered clinically useful (area under the receiver operating characteristic curve > 0.7), with the latter displaying better calibration and increased performance after adjustment to pain duration. These findings highlight the importance of standardizing aLBP definitions to improve risk stratification and targeted early interventions. Clearer definitions can enhance predictive accuracy, ensuring more effective resource allocation and preventive strategies for individuals at risk of developing chronic pain.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":"e577-e589"},"PeriodicalIF":5.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A special supplement to celebrate the 50th anniversary of PAIN: advancing pain research and management for the next 50 years. 一个特别的补充,以庆祝疼痛50周年:推进疼痛的研究和管理,为未来50年。
IF 5.5 1区 医学
PAIN® Pub Date : 2025-11-01 Epub Date: 2025-07-23 DOI: 10.1097/j.pain.0000000000003752
Karen Deborah Davis
{"title":"A special supplement to celebrate the 50th anniversary of PAIN: advancing pain research and management for the next 50 years.","authors":"Karen Deborah Davis","doi":"10.1097/j.pain.0000000000003752","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003752","url":null,"abstract":"","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"166 11S","pages":"S1"},"PeriodicalIF":5.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145293361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Accelerating discovery in pain science: the Acute to Chronic Pain Signatures program. 加速疼痛科学的发现:急性到慢性疼痛特征项目。
IF 7.4 1区 医学
PAIN® Pub Date : 2025-11-01 DOI: 10.1097/j.pain.0000000000003674
Tor D Wager,Stephani P Sutherland,Martin A Lindquist,Kathleen A Sluka,
{"title":"Accelerating discovery in pain science: the Acute to Chronic Pain Signatures program.","authors":"Tor D Wager,Stephani P Sutherland,Martin A Lindquist,Kathleen A Sluka, ","doi":"10.1097/j.pain.0000000000003674","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003674","url":null,"abstract":"Chronic pain is a complex and multifaceted disease, with biological causes distributed across tissues and bodily systems and influenced by psychological and social factors. A major aim of pain research is to find better ways to measure signals associated with chronic pain and thus predict, track, and treat pain conditions. Emerging biological measures related to the metabolic, immune, and nervous systems hold promise for identifying the physiology underlying pain and developing new treatments. Developing such measures will require multimodal datasets from large samples in combination with methodological advances. The Acute to Chronic Pain Signatures (A2CPS) Program serves as a model for such an effort, and its data will provide investigational opportunities for years to come. Acute to Chronic Pain Signatures is collecting multiomics, psychosocial, functional, and neuroimaging data from 2800 individuals before and after thoracic or knee replacement surgery. In addition to evaluating the prognostic value of previously identified biomarkers for predicting the transition to chronic pain, A2CPS will use machine learning and artificial intelligence to link these multiple data types and identify multimodal biosignatures of future pain. Open sharing of large datasets like that of the A2CPS, and models derived from them, will accelerate discovery and allow researchers to model brain, metabolic, and immune relationships relevant for multiple facets of health.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"42 1","pages":"S95-S98"},"PeriodicalIF":7.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145288546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Optimising physical rehabilitation for people with musculoskeletal pain. 优化肌肉骨骼疼痛患者的身体康复。
IF 7.4 1区 医学
PAIN® Pub Date : 2025-11-01 DOI: 10.1097/j.pain.0000000000003719
Aidan G Cashin,Michele Sterling
{"title":"Optimising physical rehabilitation for people with musculoskeletal pain.","authors":"Aidan G Cashin,Michele Sterling","doi":"10.1097/j.pain.0000000000003719","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003719","url":null,"abstract":"The World Health Organisation has recognised the importance of accessible and effective rehabilitation for people with musculoskeletal pain disorders. However, most current rehabilitation interventions provide only modest short-term benefits. In this article, we discuss opportunities for optimisation of rehabilitation to improve health outcomes for people with musculoskeletal pain. We argue that greater consideration for the mechanisms explaining how rehabilitation interventions work has the potential to improve intervention effectiveness, efficiency, and implementation. We also discuss improvements that could be made to identifying whom interventions are most beneficial for and the stratification of patients based on outcome risk, particularly regarding the management of patients deemed at high risk of poor recovery.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"8 1","pages":"S131-S135"},"PeriodicalIF":7.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145288547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Endophilin A1 and synaptojanin 1-dependent endocytosis of synaptic vesicles in nociceptive spinal circuits maintains postoperative and cancer pain. 痛觉性脊髓回路中突触囊泡的嗜内蛋白A1和突触蛋白1依赖性内吞维持术后和癌性疼痛。
IF 5.5 1区 医学
PAIN® Pub Date : 2025-11-01 Epub Date: 2025-05-27 DOI: 10.1097/j.pain.0000000000003657
Maria Fernanda Pessano Fialho, Gokul Sriman Thanigai Arasu, Shen Chen, Wendy L Imlach, Nigel W Bunnett, Raquel Tonello
{"title":"Endophilin A1 and synaptojanin 1-dependent endocytosis of synaptic vesicles in nociceptive spinal circuits maintains postoperative and cancer pain.","authors":"Maria Fernanda Pessano Fialho, Gokul Sriman Thanigai Arasu, Shen Chen, Wendy L Imlach, Nigel W Bunnett, Raquel Tonello","doi":"10.1097/j.pain.0000000000003657","DOIUrl":"10.1097/j.pain.0000000000003657","url":null,"abstract":"<p><strong>Abstract: </strong>The continued release of neurotransmitters from central projections of nociceptors during chronic pain requires synaptic vesicle (SV) recycling. Mediators of SV endocytosis and recycling are thus pivotal for sustained pain transmission in nociceptive spinal circuits. We hypothesized that disruption of SV endocytosis in dorsal root ganglia (DRG) nociceptors would impede synaptic transmission and thereby provide sustained relief from multimodalities of pain. Synaptojanin 1 (Synj1) and endophilin A1 (EndoA1), which mediate the neck formation of the endocytic pit and subsequent endocytosis, were detected in primary sensory neurons of mouse DRG by immunofluorescence and RNAScope in situ hybridization. Intrathecal injection of Synj1 and EndoA1 siRNA or shRNA successfully knocked down Synj1 and Sh3gl2 (EndoA1) mRNA in DRG neurons and suppressed acute nociception induced by agonists of pronociceptive receptors and ion channels in male mice, without affecting normal motor functions. Synj1 and EndoA1 knockdown inhibited synaptic transmission between primary sensory neurons and neurons in lamina I/II of the spinal cord dorsal horn by suppressing SV release from presynaptic primary afferent neurons. Synj1 and EndoA1 silencing reversed mechanical allodynia and thermal hyperalgesia in preclinical models of postoperative and cancer pain. Knockdown of dynamin 1 (Dnm1) and adaptor-associated protein kinase 1 (AAK1), previously characterized mediators of SV endocytosis in nociceptive spinal circuits, also alleviated pain-like behavior in these models. Thus, Synj1, EndoA1, Dnm1, and AAK1 mediate SV recycling and are thus required for sustained synaptic transmission in nociceptive spinal circuits. Disruption of SV recycling effectively reduces nociceptive transmission, providing a novel strategy for pain relief.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":"e563-e576"},"PeriodicalIF":5.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12353041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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