Neurobiology of Pain最新文献

{"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":"2025-03-06","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":"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":"2025-02-28","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":"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":"2025-02-27","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":"The contribution of clock genes BMAL1 and PER2 in osteoarthritis-associated pain","authors":"Erick J. Rodríguez-Palma ,&nbsp;Santiago Loya-Lopez ,&nbsp;Kyle Allen ,&nbsp;Yenisel Cruz-Almeida ,&nbsp;Rajesh Khanna","doi":"10.1016/j.ynpai.2024.100177","DOIUrl":"10.1016/j.ynpai.2024.100177","url":null,"abstract":"<div><div>Joint pain is the primary symptom of osteoarthritis (OA) and the main motivator for patients to seek medical care. OA-related pain significantly restricts joint function and diminishes quality of life. Despite the availability of various pain-relieving medications for OA, current treatment strategies often fall short in delivering adequate pain relief. Furthermore, long-term use of pain medications for OA management is frequently linked with notable side effects and toxicities, suggesting the need to explore new potential targets to treat pain in OA patients. In this context, clock genes, particularly brain and muscle aryl hydrocarbon receptor nuclear translocator-like 1 (BMAL1) and period circadian protein homolog 2 (PER2), known for their role in circadian rhythms, represent promising opportunities for pharmacological interventions due to their involvement in both the development and maintenance of OA pain. While BMAL1 and PER2 have been extensively studied in neuropathic and inflammatory pain, their specific contributions to OA pain remain less clear, demanding further investigation. This narrative review aims to synthesize the relationship between OA pain and the BMAL1 and PER2 signaling pathways, ultimately exploring the potential therapeutic role of clock genes in addressing this challenging condition.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"17 ","pages":"Article 100177"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11754085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143030301","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":"Glial activation and nociceptive neuropeptide elevation associated with the development of chronic post-traumatic headache following repetitive blast exposure","authors":"Amirah Wright ,&nbsp;Susan F. Murphy ,&nbsp;Pamela J. VandeVord","doi":"10.1016/j.ynpai.2024.100178","DOIUrl":"10.1016/j.ynpai.2024.100178","url":null,"abstract":"<div><div>Chronic headaches and pain are prevalent in those who are exposure to blast events, yet there is a gap in fundamental data that identifies the pathological mechanism for the chronification of pain. Blast-related post-traumatic headaches (PTH) are understudied and chronic pain behaviors in preclinical models can be vital to help elucidate PTH mechanisms. The descending pain modulatory system controls pain perception and involves<!--> <!-->specific brain regions such as the cortex, thalamus, pons, and medulla. In this study, male rats were exposed to repeated blast events to induce traumatic brain injury (bTBI) and subsequently assessed for the development of PTH by testing for chronic pain behaviors and examining the neuropathology of the descending pain pathway. The results demonstrated that facial hypersensitivity developed as early as week two following bTBI and persisted throughout the study (12 weeks). Depressive-like behaviors were observed at 12 weeks following bTBI, and these behaviors were associated with neuropathologies such as microglia ramification and neuropeptide elevation (Calcitonin Gene-Related Peptide, CGRP; Substance P, SP). Overall, these findings support the hypothesis that bTBI causes the activation of microglia and elevation of neuropeptides, which contribute to the development of chronic PTH behaviors.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"17 ","pages":"Article 100178"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11754688/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143030299","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":"Critical reflections on medication overuse headache in patients with migraine: An unsolved riddle in nociception","authors":"Alberto Chiarugi ,&nbsp;Daniela Buonvicino","doi":"10.1016/j.ynpai.2025.100179","DOIUrl":"10.1016/j.ynpai.2025.100179","url":null,"abstract":"<div><div>Migraine chronification very frequently exposes patients to the inevitable risk of excessive symptomatic intake that, in turn, prompts development of medication overuse headache (MOH). The latter further compromises headache severity establishing a vicious cycle of symptomatic intake and relapsing head pain that critically worsens the overall clinical status of patients. A great deal of attention has been focused on MOH pathogenesis, and thanks to preclinical and clinical studies knowledge about this disorder is now remarkably advanced. Still, some open questions remain regarding issues related to the neurobiology and neurochemistry underpinning pain chronification in MOH patients, as well as the remedies capable of interrupting pronociceptive cephalic sensitization and drug overuse. Here, a critical reappraisal of these issues is provided in an attempt to gain deeper insight and promote debate on a pain disorder that still represents a conundrum in the field of nociception.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"17 ","pages":"Article 100179"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143427655","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":"Targeting Nav1.7 and Nav1.8 with a PIKfyve inhibitor to reverse inflammatory and neuropathic pain","authors":"Erick J. Rodríguez-Palma ,&nbsp;Santiago Loya-Lopez ,&nbsp;Sophia M. Min ,&nbsp;Aida Calderon-Rivera ,&nbsp;Kimberly Gomez ,&nbsp;Rajesh Khanna ,&nbsp;Alison D. Axtman","doi":"10.1016/j.ynpai.2024.100174","DOIUrl":"10.1016/j.ynpai.2024.100174","url":null,"abstract":"<div><div>PIKfyve (1-phosphatidylinositol 3-phosphate 5-kinase), a lipid kinase, plays an important role in generating phosphatidylinositol (3,5)-bisphosphate (PI(3,5)P₂). SGC-PIKFYVE-1, a potent and selective inhibitor of PIKfyve, has been used as a chemical probe to explore pathways dependent on PIKfyve activity. Based on reported changes in membrane dynamics and ion transport in response to PIKfyve inhibition, we hypothesized that pharmacological inhibition of PIKfyve could modulate pain. Acute treatment with SGC-PIKFYVE-1 (10 µM) inhibited voltage-gated sodium currents through the inhibition of Na_v1.7 and Na_v1.8 channels, without affecting voltage-gated calcium or potassium currents in sensory neurons. Additionally, systemic administration of SGC-PIKFYVE-1 (30 mg/kg) alleviated mechanical and cold sensitivity induced by neuropathic or inflammatory pain in both male and female mice, without causing motor impairments. Although other functions of PIKfyve are well characterized, its role in inhibiting chronic pain has not been fully elucidated. Our study provides proof-of-concept for this alternative approach to pain management. Collectively, these results highlight the inhibitory effects of PIKfyve as a promising avenue for further exploration in chronic pain treatment.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"17 ","pages":"Article 100174"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11665415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142886485","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":"Evidence for glial reactivity using positron-emission tomography imaging of translocator Protein-18 kD [TSPO] in both sham and nerve-injured rats in a preclinical model of orofacial neuropathic pain","authors":"Gaelle M. Emvalomenos ,&nbsp;James W.M. Kang ,&nbsp;Sabrina Salberg ,&nbsp;Crystal Li ,&nbsp;Bianca Jupp ,&nbsp;Matthew Long ,&nbsp;Mohammad B. Haskali ,&nbsp;Sunil Kellapatha ,&nbsp;OIivia I. Davanzo ,&nbsp;Hyunsol Lim ,&nbsp;Richelle Mychasiuk ,&nbsp;Kevin A. Keay ,&nbsp;Luke A. Henderson","doi":"10.1016/j.ynpai.2024.100175","DOIUrl":"10.1016/j.ynpai.2024.100175","url":null,"abstract":"<div><div>Chronic neuropathic pain is a debilitating condition that results from damage to the nervous system. Current treatments are largely ineffective, with limited understanding of the underlying mechanisms hindering development of effective treatments. Preclinical models of neuropathic pain have revealed that non-neural changes are important for the development of neuropathic pain, although these data are derived almost exclusively from post-mortem histological analyses. Although these static snapshots have provided valuable data, they cannot provide insights into non-neural cell changes that could be also assessed in human patients with chronic pain. In this study we used translocator protein 18 kDa (TSPO) PET imaging with [¹⁸F]PBR06 to visualise in-vivo, the activity of macrophages and microglia in a rodent preclinical model of trigeminal neuropathic pain. Using chronic constriction injury of the infraorbital nerve (ION-CCI) we compared temporal changes in TSPO binding in male rats, prior to, and up to 28 days after ION-CCI compared with both sham-injured and naïve counterparts. Unexpectedly, we found significant increases in TSPO signal in both ION-CCI and sham-injured rats within the trigeminal ganglion, spinal trigeminal nucleus and paratrigeminal nucleus during the initial phase following surgery and/or nerve injury. This increased TSPO binding returned to control levels by day 28. Qualitative histological appraisal of macrophage accumulation and glial reactivity in both ION-CCI and sham-injured rats indicated macrophage accumulation in the trigeminal ganglion and microglial reactivity in the brainstem trigeminal complex. These findings show, glial changes in the peripheral nerve and brain in both nerve-injured and sham-injured rats in a preclinical model of neuropathic pain which provides a platform for translation into human patients.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"17 ","pages":"Article 100175"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699482/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142933485","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":"Keratinocyte-derived extracellular vesicles in painful diabetic neuropathy","authors":"James Coy-Dibley ,&nbsp;Nirupa D. Jayaraj ,&nbsp;Dongjun Ren ,&nbsp;Paola Pacifico ,&nbsp;Abdelhak Belmadani ,&nbsp;Yi-Zhi Wang ,&nbsp;Kamil K. Gebis ,&nbsp;Jeffrey N. Savas ,&nbsp;Amy S. Paller ,&nbsp;Richard J. Miller ,&nbsp;Daniela M. Menichella","doi":"10.1016/j.ynpai.2024.100176","DOIUrl":"10.1016/j.ynpai.2024.100176","url":null,"abstract":"<div><div>Painful diabetic neuropathy (PDN) is a challenging complication of diabetes with patients experiencing a painful and burning sensation in their extremities. Existing treatments provide limited relief without addressing the underlying mechanisms of the disease. PDN involves the gradual degeneration of nerve fibers in the skin. Keratinocytes, the most abundant epidermal cell type, are closely positioned to cutaneous nerve terminals, suggesting the possibility of bi-directional communication. Extracellular vesicles are lipid-bilayer encapsulated nanovesicles released from many cell types that mediate cell to cell communication. The role of keratinocyte-derived extracellular vesicles (KDEVs) in influencing signaling between the skin and cutaneous nerve terminals and their contribution to the genesis of PDN has not been explored. In this study, we characterized KDEVs in a well-established high-fat diet mouse model of PDN using primary adult mouse keratinocyte cultures. We obtained highly enriched KDEVs through size-exclusion chromatography and then analyzed their molecular cargo using proteomic analysis and small RNA sequencing. We found significant differences in the protein and microRNA content of high-fat diet KDEVs compared to KDEVs obtained from control mice on a regular diet, including pathways involved in axon guidance and synaptic transmission. Additionally, using an <em>in vivo</em> conditional extracellular vesicle reporter mouse model, we demonstrated that epidermal-originating GFP-tagged KDEVs are retrogradely trafficked into the dorsal root ganglion (DRG) neuron cell bodies. This study presents the first comprehensive isolation and molecular characterization of the KDEV protein and microRNA cargo in RD and HFD mice. Our findings suggest a potential novel communication pathway between keratinocytes and DRG neurons in the skin, which could have implications for PDN.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"17 ","pages":"Article 100176"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11731614/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985262","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":"Neuronal activation patterns during self-referential pain imagination","authors":"Annabel Vetterlein ,&nbsp;Thomas Plieger ,&nbsp;Merlin Monzel ,&nbsp;Svea A. Hogeterp ,&nbsp;Lilli Wagner ,&nbsp;Thomas Grünhage ,&nbsp;Andrea Felten ,&nbsp;Peter Trautner ,&nbsp;Jana Karneboge ,&nbsp;Martin Reuter","doi":"10.1016/j.ynpai.2024.100158","DOIUrl":"10.1016/j.ynpai.2024.100158","url":null,"abstract":"<div><p>In clinical assessments and pain therapy, patients are asked to imagine themselves in pain. However, the underlying neuronal processes remain poorly understood. Prior research has focused on empathy for pain or reported small sample sizes. Thus, the present study aimed to promote the neurobiological understanding of self-referential pain imagination. We hypothesised to find activation contrasts (pain vs. no pain) across pain-related areas and expected two of the most prominent predictors of chronic pain, pain sensitivity (PS) and locus of control (LoC), to be moderators.</p><p>In an fMRI study, <em>N</em> = 82 participants completed a pain imagination task, in which they were asked to imagine themselves in painful and non-painful situations presented in the form of pictures and texts. After each trial, they were instructed to give painfulness ratings. As a laboratory measure of PS, electrical pain thresholds were assessed. A questionnaire was completed to measure LoC.</p><p>Across presentation modes we found activity contrasts in previously pain-related regions, such as the prefrontal, supplementary motor, primary motor, somatosensory and posterior parietal cortices, and the cerebellum. We found positive associations of PS and external LoC with painfulness ratings, and a negative correlation between PS and internal LoC. Despite our hypotheses, neither PS nor internal LoC were significant predictors of the BOLD-signal contrasts.</p><p>Though future studies are needed to draw further conclusions, our results provide preliminary evidence of a potential neuronal imagination-perception overlap in pain.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"16 ","pages":"Article 100158"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452073X24000096/pdfft?md5=8a9c2603322477b07469a22e7aeb5eea&pid=1-s2.0-S2452073X24000096-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141784323","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}