Neurobiology of Pain最新文献

{"title":"Brain aging among individuals with trigeminal neuralgia","authors":"Yenisel Cruz-Almeida ,&nbsp;Pedro A. Valdes-Hernandez ,&nbsp;Yun Liang ,&nbsp;Mingzhou Ding ,&nbsp;John K. Neubert","doi":"10.1016/j.ynpai.2025.100201","DOIUrl":"10.1016/j.ynpai.2025.100201","url":null,"abstract":"<div><div>Trigeminal neuralgia (TN) is a complex orofacial neuropathic pain condition with limited understanding of underlying mechanisms and therapeutic options. Emerging evidence suggests the involvement of the brain in persons with TN including widespread brain changes when employing a widely used brain aging biomarker that estimates a predicted brain age difference or brain age gap. The aim of the present cross-sectional study was to assess the predicted brain age difference (brain-PAD) or brain age gap across two TN subtypes (classical TN, and secondary/idiopathic TN) in comparison with age-and sex-matched pain-free controls and its association with several clinical and psychological characteristics. Thirty-four individuals diagnosed with Classical TN, 17 diagnosed with secondary/idiopathic TN were age- and sex-matched to pain-free controls (n = 54). All participants underwent a T1 brain MRI and completed clinical and psychological measures. There were significant differences in brain-PAD among TN subtypes (ANCOVA p = 0.0078, effect size f² = 0.28²), with individuals diagnosed with Classical TN having a brain-PAD significantly greater than the controls by 3.87 years (p = 0.01, Bonferroni-corrected). There were no significant brain-PAD differences between secondary/idiopathic TN and pain-free controls. Brain-PAD had a significant positive association with both pain catastrophizing (p &lt; 0.05) and pain-related anxiety (p &lt; 0.05), but no significant association with disease duration (p &lt; 0.05) or usual pain intensity (p &lt; 0.05) in persons with classical TN. The results were similar using a second brain aging biomarker. We report here accelerated brain aging processes in individuals with classical TN, but not in persons diagnosed with secondary/idiopathic TN. Our study replicates previous findings and adds to the literature that accelerated brain aging may not occur across all TN subtypes. Given the increased use of MRI for TN diagnostics, combined with our own recent work deriving brain aging biomarkers from clinical-grade scans, future studies within clinical settings are feasible and may help understand this debilitating condition.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100201"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145361115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuronal physiology of amygdala neurons in the context of injury and pain","authors":"Blesson K Paul,&nbsp;Maria Isabel Nunez-Ordaz,&nbsp;Joseph R. Samuel,&nbsp;Benedict J. Kolber","doi":"10.1016/j.ynpai.2025.100190","DOIUrl":"10.1016/j.ynpai.2025.100190","url":null,"abstract":"<div><div>The amygdala integrates polymodal information including nociceptive stimuli. It is implicated as a key node in regulating both sensory-discriminative and emotional-affective aspects of pain and central sensitization. While central sensitization mechanisms in persistent pain are not completely understood, studying the neuronal properties exhibited by the amygdala neurons within their functional context, in this case, nociception, is important. Such studies can shed light on the behavior-modulating potential of the amygdala. In the last twenty years, multiple laboratories have begun the process of dissecting the cell-type specific activity involved in amygdala function. This review surveys these electrophysiological properties of neurons from different amygdala nuclei, cell types and circuitry studied so far, in the context of nociception and injury. A population-level accounting of these cell types provides greater insight into identifying specific targets to develop interventions for pain-mediated affective conditions.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100190"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144563031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Individual differences in cognitive performance under pain linked to region-specific alpha power modulations","authors":"Francesca Storey ,&nbsp;Mariya Prokhorenko ,&nbsp;Michael L. Keaser ,&nbsp;Patrick Skippen ,&nbsp;Andrew J. Furman ,&nbsp;David A. Seminowicz ,&nbsp;Ali Mazaheri","doi":"10.1016/j.ynpai.2025.100196","DOIUrl":"10.1016/j.ynpai.2025.100196","url":null,"abstract":"<div><div>Chronic pain is associated with reduced cognitive function, potentially due to a diversion of cognitive resources to processing pain. However, reduced cognitive function during pain is not always consistently evidenced, perhaps due to individual differences in the attentional cost of pain processing. In the current electroencephalography investigation, we therefore examined differences in the top-down modulation of oscillatory activity in a cognitive task, between participants who performed better, and worse, during experimentally induced neuropathic-like pain. We employed a cross-modal attention task in which visual cues indicated whether participants needed to judge the visual orientation or discriminate the auditory pitch of an upcoming target. The visual and auditory targets were presented either simultaneously or individually, enabling us to assess the “cost” of having a distractor present in each modality. Participants engaged in the task under two conditions: prolonged pain via the capsaicin-heat pain model, and pain-free. Participants less “costed” by visual distraction during pain demonstrated a greater increase in alpha power (8–12 Hz) over frontal/central electrodes during pain. This may reflect inhibition of regions related to the processing of painful stimuli (somatosensory cortex), which could increase availability of resources to meet task-demands – a possible task-favouring pattern. In conclusion, our results support the notion that better cognitive function during pain is associated with a behavioral strategy.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100196"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145332620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neutrophil dynamics in surgical wounds – A novel role of interleukin-7","authors":"Annika Biesold ,&nbsp;Philipp Burkard ,&nbsp;Ankita Rawat ,&nbsp;Laura Cyran ,&nbsp;Patrick Meybohm ,&nbsp;Heike Rittner ,&nbsp;Michael Briese ,&nbsp;Nana-Maria Wagner","doi":"10.1016/j.ynpai.2025.100199","DOIUrl":"10.1016/j.ynpai.2025.100199","url":null,"abstract":"<div><div>Postoperative pain and consequently chronic postsurgical pain remain a significant burden among patients. While neutrophilic granulocytes (neutrophils) are known to play a critical role in wound healing, their precise contribution to pain modulation is not fully understood. The neurotrophin nerve growth factor (NGF), released by fibroblasts and immune cells following injury, is an early mediator of pain development. A companion paper demonstrated that NGF administration to axons of cultured sensory neurons in microfluidic chambers induces upregulation of <em>Il7</em>, encoding interleukin-7 (IL-7). However, its role in neutrophil dynamics within surgical wounds remains broadly unclear. In a murine model of laparotomy, we observed that IL-7 was expressed at wound sites and co-localized with sensory nerve endings and infiltrating neutrophils within 24 h post-surgery. Laparotomy triggered neutrophil mobilization from the bone marrow, leading to an influx of both mature and immature neutrophils into the circulation. Flow cytometric analysis further revealed IL-7 receptor (IL-7R) surface expression on neutrophils, with IL-7 stimulation also enhancing the expression of activation and maturation markers on neutrophils in vitro. These findings suggest that NGF-induced IL-7 release from peripheral nerve terminals represents a novel neuroinflammatory mechanism modulating neutrophil dynamics in the surgical wound, potentially impairing wound healing and exacerbating pain. Therefore, targeting IL-7 signalling in peripheral nerves may offer a promising strategy for improving postoperative pain management.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100199"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145157314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial commitment to trust and integrity in science: Implications for pain and anesthesiology research","authors":"Tonya M. Palermo PhD,&nbsp;Didier Bouhassira MD, PhD,&nbsp;Karen D. Davis PhD, FCAHS, FRSC,&nbsp;Hugh C. Hemmings Jr MD, PhD, FRCA,&nbsp;Robert W. Hurley MD, PhD,&nbsp;Joel Katz PhD,&nbsp;Jaideep J. Pandit FRCA, DPhil, DM, MBA,&nbsp;Theodore J. Price PhD,&nbsp;Michael E. Schatman PhD,&nbsp;Stephan K.W. Schwarz MD, PhD, FESAIC,&nbsp;Dennis C. Turk PhD,&nbsp;Marc Van de Velde MD, PhD, EDRA, FESAIC,&nbsp;Matthew D. Wiles MRCP, FCRA, FFICM,&nbsp;Tony L. Yaksh PhD,&nbsp;David Yarnitsky MD","doi":"10.1016/j.ynpai.2025.100187","DOIUrl":"10.1016/j.ynpai.2025.100187","url":null,"abstract":"","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100187"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145692939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cerebral peak alpha frequency: Associations with chronic pain onset and pain modulation","authors":"Felicitas A. Huber ,&nbsp;Parker A. Kell ,&nbsp;Joanna O. Shadlow ,&nbsp;Jamie L. Rhudy","doi":"10.1016/j.ynpai.2025.100180","DOIUrl":"10.1016/j.ynpai.2025.100180","url":null,"abstract":"<div><div>Chronic pain is highly prevalent in the U.S. and leads to myriad negative sequalae and suffering. One way to address chronic pain is to identify who is at risk and intervene prior to symptom onset. Research suggests resting peak alpha frequency (PAF), the speed of alpha oscillations at rest, is slower in healthy individuals with greater pain sensitivity and in chronic pain patients. Thus, slower PAF may denote chronic pain vulnerability. Other research has shown that individuals at higher risk of chronic pain exhibit disrupted pain modulation, i.e., less efficient pain inhibition and increased pain facilitation. Currently, the ability of PAF to predict chronic pain and its relation to pain modulation is under-researched. This investigation aimed to address this gap by characterizing associations between PAF, onset of chronic pain, and pain modulation. Using archival data from three independent studies, this investigation assessed whether slower PAF is associated with prospectively-determined chronic pain onset, decreased pain inhibition (i.e., impaired conditioned pain modulation, impaired erotica-induced pain inhibition), and increased pain facilitation (i.e., increased temporal summation of pain, augmented mutilation-induced pain facilitation). Results show that slower PAF was associated with greater facilitation of spinal (i.e., nociceptive flexion reflex) and supraspinal (i.e., N2 potential) nociception in response to unpleasant pictures (i.e., human injury images). This suggests that slower PAF is associated with threat-enhanced spinal and supraspinal nociception and may be relevant for chronic pain conditions with disrupted threat systems. Slower PAF was not associated with any other pain outcome, including prospectively determined chronic pain onset. However, chronic pain onset could only be assessed in one study with a mixed eyes open/eyes closed recording, limiting the significance of this finding.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100180"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143548952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Patient phenotyping for molecular profiling of neck and low back pain – Study protocol","authors":"Michele Curatolo ,&nbsp;Cathryn Payne ,&nbsp;Abby P. Chiu ,&nbsp;Nguyen T. Tran ,&nbsp;Natalie Yap ,&nbsp;Christoph P. Hofstetter ,&nbsp;Joseph B. Lesnak ,&nbsp;Asta Arendt-Tranholm ,&nbsp;Theodore J. Price ,&nbsp;Jeffrey G. Jarvik ,&nbsp;Judith A. Turner","doi":"10.1016/j.ynpai.2025.100186","DOIUrl":"10.1016/j.ynpai.2025.100186","url":null,"abstract":"<div><h3>Background</h3><div>Chronic neck and low back pain are highly prevalent, leading causes of disability, and associated with long-term opioid use. The development of effective therapeutics is hampered by the limited understanding of the molecular mechanisms underlying these conditions. The Human Nociceptor and Spinal Cord Molecular Signature Center is a consortium within the NIH PRECISION Human Pain Network. The Center aims to fundamentally advance the understanding of the molecular neurobiology and neuroimmunology underlying human neck and low back pain, thereby enabling the discovery of therapeutic targets. We are pursuing this aim by applying bulk, single cell and spatial transcriptomics to tissues recovered from patients with neck and low back pain undergoing C1-2 and lumbar arthrodesis. The C2 dorsal root ganglion, facet joints, muscles, fascia, and intervertebral discs are harvested; control tissues are obtained from organ donors. A critical advantage of human research is the study of molecular neurobiological mechanisms in the context of the phenotypic complexity of chronic pain. The aim of this article is to summarize the rationale and methods used in our project to phenotype patients.</div></div><div><h3>Methods</h3><div>Phenotyping domains include pain-related characteristics such as pain intensity, duration, and location; physical function; psychosocial function; neuropathic components assessed by self-report and quantitative sensory testing; somatosensory functions such as mechanical pain sensitivity and temporal summation; and radiological findings.</div></div><div><h3>Conclusion</h3><div>We anticipate that comprehensive phenotyping will greatly facilitate the identification of phenotype-specific transcriptional signatures associated with chronic neck and low back pain, revealing new neurobiological and/or neuro-immunological mechanisms of painful diseases.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100186"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144124077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling the peripheral nerve hallmarks of chemotherapy-induced neuropathy: insights from paclitaxel treatment in a murine model","authors":"Maria Maiarù ,&nbsp;Andrea Petrini ,&nbsp;Federica De Angelis ,&nbsp;Francesca Nazio ,&nbsp;Sara Marinelli","doi":"10.1016/j.ynpai.2025.100200","DOIUrl":"10.1016/j.ynpai.2025.100200","url":null,"abstract":"<div><div>Chemotherapy-induced peripheral neuropathy (CIPN) is a frequent and debilitating side effect of anticancer drugs like paclitaxel, significantly reducing the quality of life for cancer patients. Paclitaxel-induced peripheral neuropathy (PIPN) is primarily characterized by sensory disturbances such as mechanical allodynia and thermal hyperalgesia. Despite its prevalence, the mechanisms driving PIPN are not fully understood, and current treatment options remain limited. This study explores the impact of varying doses of paclitaxel on neuropathic pain, nerve structural changes, and metabolic alterations in a mouse model. Behavioural assessments demonstrated that paclitaxel induced dose-dependent mechanical allodynia and thermal hyperalgesia, with prolonged symptoms at higher doses. Furthermore, sciatic nerve dysfunction was observed, while metabolic tests revealed significant disruptions in glucose and triglyceride levels, suggesting a link between metabolic imbalances and neuropathy. Histological and molecular analyses identified increased TRPV1 and CGRP expression in skin nerve fibers, accompanied by Schwann cell dysfunction, characterized by myelin disorganization, decreased levels of myelin proteins (P0, MBP), and elevated LC3 levels, pointing to autophagy involvement. Moreover, infiltration of macrophages and mast cells into sciatic nerves indicated an innate immune response. These results emphasize the complex nature of PIPN, which involves sensory nerve sensitization, Schwann cell damage, and metabolic dysregulation. Elucidating these pathways could inform the development of more effective therapies aimed at preventing or alleviating the impact of CIPN.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100200"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145332498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Left nucleus accumbens volume is associated with poor sleep in hip osteoarthritis","authors":"Natalia Egorova-Brumley ,&nbsp;Luiza Bonfim Pacheco ,&nbsp;Gabby Knox ,&nbsp;Leila Nategh ,&nbsp;Fiona Dobson ,&nbsp;Michelle Hall","doi":"10.1016/j.ynpai.2025.100203","DOIUrl":"10.1016/j.ynpai.2025.100203","url":null,"abstract":"<div><h3>Objective</h3><div>Reduction in the volume of the nucleus accumbens (NAc) has emerged as a promising signature of chronic pain transition, including in osteoarthritis (OA). Yet, less is known about the factors that could influence these changes in the mesolimbic system. Given that poor sleep is common in OA, and recent studies of sleep disturbance on pain perception in animals and healthy populations have specifically implicated the NAc, we hypothesised that the left NAc volume in hip OA would be associated with sleep quality and quantity. Furthermore, we explored how sex interacts with this relationship.</div></div><div><h3>Methods</h3><div>Cross-sectional study in participants with hip OA (n = 34; aged 60+/-12 years, 67 % females) who reported moderate pain were recruited.</div></div><div><h3>Results</h3><div>A one-sample <em>t</em>-test showed that the left NAc volumes were significantly lower than normative values (t = -2.7368, df = 33, p-value = 0.009). In a model (F(4, 29) = 6.642, p &lt; 0.001, R2 = 0.4781) including the total intracranial volume (TIV), sex and age, the left NAc volume was significantly predicted by sleep quality (t = -3.416, p = 0.002) assessed with Pittsburgh Sleep Quality Index (PSQI). Sleep efficiency (t = 2.362, p = 0.025) but not hours spent in bed (p &gt; 0.05) was also a significant predictor. With models exploring sleep*sex interactions, only sleep efficiency demonstrated an interaction, suggesting that the left NAc volume is lower in females with worse sleep efficiency (t = -2.086, p = 0.046, albeit not significant when corrected for multiple comparisons, pFDR = 0.138.)</div></div><div><h3>Conclusions</h3><div>Our results suggest that the reduction of the NAc volumes as a candidate biomarker of pain might be influenced by sleep. This exploratory finding in a chronic hip OA population is consistent with the results previously only reported in animal and experimental pain/sleep studies in healthy participants.</div></div><div><h3>Significance</h3><div>The left NAc as a candidate biomarker of chronic pain is sensitive to the effects of sleep quality, especially in females with OA.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100203"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145571069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhanced trafficking of an inherited erythromelalgia NaV1.7 mutant channel at a physiological temperature","authors":"Malgorzata A. Mis ,&nbsp;Sidharth Tyagi ,&nbsp;Elizabeth J. Akin ,&nbsp;Mohammad-Reza Ghovanloo ,&nbsp;Peng Zhao ,&nbsp;Fadia Dib-Hajj ,&nbsp;Andrew D. Randall ,&nbsp;Stephen G. Waxman ,&nbsp;Sulayman D. Dib-Hajj","doi":"10.1016/j.ynpai.2025.100188","DOIUrl":"10.1016/j.ynpai.2025.100188","url":null,"abstract":"<div><div>Gain-of-function mutations which enhance activation of Na_V1.7, a widely expressed sodium channel in nociceptors, cause human pain disorders including inherited erythromelalgia (IEM). IEM is characterized by attacks of burning pain in distal extremities triggered by warmth, with cooling of affected limbs providing temporary relief. We investigated the behaviour of the IEM-linked L858F mutant Na_V1.7 channel at physiological normal skin temperature (NST, 33–35 °C) in IB4-negative DRG sensory neurons known to include thermosensors. Using voltage-clamp recordings at NST we found that the Na_V1.7-L858F mutant channel shows the characteristic hyperpolarizing shift in activation as has been previously found in recordings at room temperature, and that the current density of the L858F channels is significantly larger than that of WT channels. Using a live-cell optical pulse-chase imaging methodology at NST we observed that accelerated forward-trafficking significantly increases membrane insertion of mutant channels in IB4^- neurons. Current-clamp recordings at NST show increased firing of IB4^- neurons that express the L858F mutant channel, consistent with increased trafficking of the channel at this physiological temperature. Our findings identify enhanced trafficking and membrane insertion of the L858F mutant channels at normal skin temperature in IB4^- neurons as an additional mechanism underlying IEM-related neuronal hyperexcitability.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100188"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144322280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}