Neurobiology of Pain最新文献

{"title":"Physiological actions of a humanized P2X4 scFv on peripheral and central neurons in male mice with neuropathic pain","authors":"Sachin Goyal ,&nbsp;Ian Adams ,&nbsp;Marena Montera ,&nbsp;Nesia A. Zurek ,&nbsp;Shivali Goyal ,&nbsp;Adinarayana Kunamneni ,&nbsp;Karin N. Westlund ,&nbsp;Sascha R.A. Alles","doi":"10.1016/j.ynpai.2025.100198","DOIUrl":"10.1016/j.ynpai.2025.100198","url":null,"abstract":"<div><div>Neuropathic pain remains a challenging clinical condition due to its resistance to conventional analgesics. The purinergic P2X4 receptor (P2X4R), an ATP-gated ion channel, is upregulated in sensory neurons and glial cells following nerve injury and is pivotal in chronic pain pathogenesis. This study evaluates the therapeutic potential of a novel humanized single-chain variable fragment antibody (hP2X4R scFv) targeting P2X4R in male mice models of neuropathic pain. Using spared nerve injury (SNI) and foramen rotundum inflammatory compression of the trigeminal infraorbital nerve (FRICT-ION) models, we demonstrate that a single intraperitoneal dose of hP2X4R scFv significantly reverses mechanical hypersensitivity for up to four weeks. Electrophysiological recordings from FosTRAP mice revealed that hP2X4R scFv reduced the excitability of Fos+ neurons in the spinal dorsal horn and ventrolateral periaqueductal gray (vlPAG), key regions involved in pain processing. <em>In vitro</em>, patch-clamp studies further showed that hP2X4R scFv selectively decreased action potential firing in larger diameter dorsal root ganglion (DRG) and trigeminal ganglion (TG) neurons from SNI and FRICT-ION mice, respectively, without affecting naïve neurons. These findings suggest that hP2X4R scFv modulates both central and peripheral neuronal excitability associated with chronic pain. The specificity and long-lasting efficacy of hP2X4R scFv highlights its promise as a non-opioid therapeutic candidate for neuropathic pain management.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100198"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145104592","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":"The impact of nerve injury on the immune system across the lifespan is sexually dimorphic","authors":"Wen Bo S. Zhou ,&nbsp;Xiang Q. Shi ,&nbsp;Alain P. Zhang ,&nbsp;Magali Millecamps ,&nbsp;Jeffrey S. Mogil ,&nbsp;Ji Zhang","doi":"10.1016/j.ynpai.2025.100195","DOIUrl":"10.1016/j.ynpai.2025.100195","url":null,"abstract":"<div><div>Although nerve injury-associated neuroinflammation contributes to neuropathic pain, the long-term impact of such injury on systemic homeostasis and its potential role in pain remains elusive. In this study, we aim to understand the systemic changes that are present alongside chronic pain in nerve-injured male and female mice across their lifespan. We monitored mechanical and cold sensitivity in male and female mice starting at the age of 3–4 months old when they received spared nerve injury (SNI), up to 20-month post-injury. Alongside, we collected blood samples to track changes in immune cells with flow cytometry, and to assess inflammation-related serum proteome using a 111-target Proteome Profiler. We also transferred serum from sham/SNI mice to naïve mice to determine the potential of systemic contribution to pain. While nerve injury did not affect immune cell composition in the blood, it triggered a long-lasting disturbance of molecular profile in the serum of sham/SNI mice, in a sex-dependent manner. Compared to sham surgery, nerve injury amplified regulation of inflammatory proteins in males, but slightly reduced it in females. These changes in the serum occurred in parallel with long-lasting mechanical and cold hypersensitivity in the nerve-injured mice. Both male and female SNI serum induced hypersensitivity when transferred to naïve mice, regardless of a sex-matched or sex-mismatched transfer. Our results highlight that a local nerve injury can have persistent systemic impact. Injury-associated systemic inflammation could contribute to neuropathic pain, but the underlying mechanisms may be sexually dimorphic.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100195"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144890930","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":"Nrxn3 reduces myofascial nociceptive pain","authors":"Lauren Nguyen,&nbsp;Mikhail Umorin,&nbsp;Phillip R. Kramer","doi":"10.1016/j.ynpai.2025.100197","DOIUrl":"10.1016/j.ynpai.2025.100197","url":null,"abstract":"<div><div>Neurexin 3 (Nrxn3) has a role in neuronal signaling. Previous reports indicated that reducing Nrxn3 expression in the central amygdala increased orofacial neuropathic pain. A common temporomandibular disorder is myofascial pain. Thus, we hypothesized that Nrxn3 would reduce myofascial hypersensitivity. To test this hypothesis Nrxn3 shRNA was infused into the central amygdala of male rats. Then a ligature of the tendon attachment of the anterior superficial portion of the masseter muscle was performed to induce inflammatory orofacial pain. Dark phase meal duration was measured continuously, and von Frey filament testing was completed every 7 days for 21 days to measure the nociceptive response. After testing tissues were collected and the amount of Nrxn3 was measured. Neuronal activity in the orofacial pain pathway was quantitated by c-Fos staining of the central amygdala, lateral parabrachial nucleus, trigeminal ganglia and trigeminal nucleus caudalis. Knockdown of Nrxn3 in the central amygdala significantly increased the pain response and increased the levels of c-Fos. This increased response was observed for greater than two weeks. The data suggests Nrxn3 expression within the central amygdala attenuates nociceptive orofacial pain by reducing neuronal activity.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100197"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145048131","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":"Humanized NaV1.8 rats overcome cross-species potency shifts in developing novel NaV1.8 inhibitors","authors":"Dillon S. McDevitt ,&nbsp;Joshua D. Vardigan ,&nbsp;Xiaoping Zhou ,&nbsp;Thomas W. Rosahl ,&nbsp;Heather Zhou ,&nbsp;Eric A. Price ,&nbsp;Michelle K. Clements ,&nbsp;Yuxing Li ,&nbsp;Nissi Varghese ,&nbsp;Alicja Krasowska-Zoladek ,&nbsp;Shawn J. Stachel ,&nbsp;Michael J. Breslin ,&nbsp;Christopher S. Burgey ,&nbsp;Richard L. Kraus ,&nbsp;Parul S. Pall ,&nbsp;Darrell A. Henze ,&nbsp;Vincent P. Santarelli","doi":"10.1016/j.ynpai.2025.100182","DOIUrl":"10.1016/j.ynpai.2025.100182","url":null,"abstract":"<div><div>Voltage-gated sodium channel isoform 1.8 (Na_V1.8) has emerged as a promising pharmaceutical target for the treatment of acute and chronic pain. However, highly selective and potent inhibitors for this channel have been difficult to develop and only recently have advanced to clinical testing. Our efforts to develop Na_V1.8 small molecule inhibitors yielded a series of molecules with favorable <em>in vitro</em> potency and selectivity against the human Na_V1.8 channel but exhibited dramatic rightward potency shifts against the rodent channel, severely limiting <em>in vivo</em> screening and candidate selection. In anticipation of supporting drug discovery efforts, a transgenic rat line expressing the human Na_V1.8 channel in lieu of the rodent channel was developed. Utilizing these humanized animals, the <em>in vitro</em> potency of our chemical matter in freshly isolated humanized rat DRG neurons was consistent with <em>in vitro</em> human potency values, enabling <em>in vivo</em> work to progress. We demonstrate capsaicin-induced nocifensive behaviors (CNB) as a moderate throughput <em>in vivo</em> screening assay, from which we demonstrate pharmacokinetic-pharmacodynamic (PK-PD) and <em>in vitro</em>-<em>in vivo</em> correlation (IVIVC) relationships. We identified MSD199 as a potent Na_V1.8 inhibitor with acute pain efficacy and assessed it in traditional inflammatory (Complete Freund’s Adjuvant) and neuropathic (spinal nerve ligation) behavioral chronic pain assays where it was shown to significantly reduce pain-related behaviors. Overall, we demonstrate the utility of humanized transgenic animals when cross-species potency shifts are observed within an otherwise promising chemical series.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100182"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143682473","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":"Voluntary exercise prevents and eradicates anxiety-like behavior by influencing parvalbumin-positive neurons, perineuronal nets, and microglia activation in corticolimbic regions of neuropathic pain rats","authors":"Thu Nguyen Dang ,&nbsp;Cuong Nguyen Van ,&nbsp;Ryosuke Ochi ,&nbsp;Hiroki Kuwamura ,&nbsp;Tomoyuki Kurose ,&nbsp;Yoki Nakamura ,&nbsp;Kazue Hisaoka-Nakashima ,&nbsp;Norimitsu Morioka ,&nbsp;Hisao Nishijo ,&nbsp;Naoto Fujita ,&nbsp;Susumu Urakawa","doi":"10.1016/j.ynpai.2025.100181","DOIUrl":"10.1016/j.ynpai.2025.100181","url":null,"abstract":"<div><div>Anxiety-like behavior often emerges in the later stages of neuropathic pain, exacerbating the pain condition and potentially involving parvalbumin-positive (PV⁺) neurons. This study aimed to investigate the effects of voluntary exercise on neuropathic pain-induced anxiety and its relationship with PV⁺ neurons, perineuronal nets (PNNs, labeled with Wisteria floribunda agglutinin [WFA]), and microglia in the corticolimbic regions. Male Wistar rats with partial sciatic nerve ligation (PSL) were given access to running wheels either from 3 days (early voluntary exercise [EEx]) or from 4 weeks (late voluntary exercise [LEx]) postoperatively. Nociceptive behaviors were assessed using the von Frey and acetone tests, while anxiety-like behaviors were assessed using the open field and elevated plus maze tests. Brain sections were histologically analyzed using immunohistochemistry and immunofluorescence 8 weeks post-surgery. Both early and late exercise partially restored the paw withdrawal thresholds and the arousal response. PSL-EEx rats did not exhibit anxiety-like behaviors. PSL-LEx rats transiently showed anxiety-like behaviors, but these were eradicated by exercise. PSL altered PV⁺ neurons and PNNs in specific corticolimbic subregions. Notably, voluntary exercise restored the densities of PV⁺-strong WFA⁺ neurons in the basolateral amygdala, PV⁺-WFA^-, and PV⁺-WFA⁺ neurons in the anterior cingulate cortex, and PV⁺-WFA⁺ neurons in the hippocampal cornu ammonis 1. These changes correlated with reduced anxiety-like behaviors. Exercise modulated PSL-induced microglial activation and interacted differently with these neurons. These findings suggest that voluntary exercise prevents and eliminates chronic pain-induced anxiety through neuronal mechanisms other than analgesic effects, potentially involving PV⁺ neurons, PNNs, and microglia in the corticolimbic subregions.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"18 ","pages":"Article 100181"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143601363","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":"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}