Eleri L.F. McEachern , Maria Zilic , Susana G. Sotocinal , Nader Ghasemlou , Jeffrey S. Mogil
{"title":"The timing of the mouse hind paw incision does not influence postsurgical pain","authors":"Eleri L.F. McEachern , Maria Zilic , Susana G. Sotocinal , Nader Ghasemlou , Jeffrey S. Mogil","doi":"10.1016/j.ynpai.2024.100161","DOIUrl":"10.1016/j.ynpai.2024.100161","url":null,"abstract":"<div><p>Chronobiological approaches have emerged as tools to study pain and inflammation. Although time–of-day effects on the expression of pain after injury have been studied, it remains unaddressed whether the timing of the injury itself can alter subsequent pain behaviors. The aim of this study was to assess postsurgical pain behaviors in a mouse hind paw incision assay in a circadian-dependent manner. Incisions were made at one of four equally spaced time points over a 24-hour period, with evoked and spontaneous pain behaviors measured using the von Frey mechanical sensitivity test, Hargreaves’ radiant heat paw-withdrawal test, and the Mouse Grimace Scale. Algesiometric testing was performed in C57BL/6 mice prior to and at multiple time points after incision injury, at the same time of day, until pain resolution. No statistically significant differences were observed between groups. This study adds to the literature on circadian rhythms and their influence on pain in the pursuit of more biologically informed pre- and postoperative care.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"16 ","pages":"Article 100161"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452073X24000126/pdfft?md5=45cbc5cc70c3527e23264fe25bc82b00&pid=1-s2.0-S2452073X24000126-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141940518","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}
Khalid W. Freij , Fiona B.A.T. Agbor , Kiari R. Kinnie , Vinodh Srinivasasainagendra , Tammie L. Quinn , Hemant K. Tiwari , Robert E. Sorge , Burel R. Goodin , Edwin N. Aroke
{"title":"The pace of biological aging significantly mediates the relationship between internalized stigma of chronic pain and chronic low back pain severity among non-hispanic black but not non-hispanic white adults","authors":"Khalid W. Freij , Fiona B.A.T. Agbor , Kiari R. Kinnie , Vinodh Srinivasasainagendra , Tammie L. Quinn , Hemant K. Tiwari , Robert E. Sorge , Burel R. Goodin , Edwin N. Aroke","doi":"10.1016/j.ynpai.2024.100170","DOIUrl":"10.1016/j.ynpai.2024.100170","url":null,"abstract":"<div><div>This study aimed to determine the nature of the relationship between the internalized stigma of chronic pain (ISCP), the pace of biological aging, and racial disparities in nonspecific chronic low back pain (CLBP). We used Dunedin Pace of Aging from the Epigenome (DunedinPACE), Horvath’s, Hannum’s, and PhenoAge clocks to determine the pace of biological aging in adults, ages 18 to 82 years: 74 no pain, 56 low-impact pain, and 76 high-impact pain. Individuals with high-impact pain reported higher levels of ISCP and DunedinPACE compared to those with low-impact or no pain (p < 0.001). There was no significant relationship between ISCP and epigenetic age acceleration from Horvath, Hannum, and PhenoAge clocks (<em>p</em> > 0.05). Mediation analysis showed that an association between ISCP and pain severity and interference was mediated by the pace of biological aging (<em>p</em> ≤ 0.001). We further found that race moderated the indirect effect of ISCP on pain severity and interference, with ISCP being a stronger positive predictor of the pace of biological aging for non-Hispanic Blacks (NHBs) than for non-Hispanic Whites (NHWs). Future bio-behavioral interventions targeting internalized stigma surrounding chronic pain at various levels are necessary. A deeper understanding of the biological aging process could lead to improvements in managing nonspecific chronic low back pain (CLBP), particularly within underserved minority populations.</div></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"16 ","pages":"Article 100170"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142533682","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":"Is exercise therapy the first-line treatment for chronic pain?","authors":"Emiko Senba","doi":"10.1016/j.ynpai.2024.100154","DOIUrl":"10.1016/j.ynpai.2024.100154","url":null,"abstract":"","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"15 ","pages":"Article 100154"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452073X24000059/pdfft?md5=aed02ef2d1dea3e3b637ab7c3e690d22&pid=1-s2.0-S2452073X24000059-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140407502","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":"A review of dorsal root ganglia and primary sensory neuron plasticity mediating inflammatory and chronic neuropathic pain","authors":"Kyeongran Jang, Sandra M. Garraway","doi":"10.1016/j.ynpai.2024.100151","DOIUrl":"10.1016/j.ynpai.2024.100151","url":null,"abstract":"<div><p>Pain is a sensory state resulting from complex integration of peripheral nociceptive inputs and central processing. Pain consists of adaptive pain that is acute and beneficial for healing and maladaptive pain that is often persistent and pathological. Pain is indeed heterogeneous, and can be expressed as nociceptive, inflammatory, or neuropathic in nature. Neuropathic pain is an example of maladaptive pain that occurs after spinal cord injury (SCI), which triggers a wide range of neural plasticity. The nociceptive processing that underlies pain hypersensitivity is well-studied in the spinal cord. However, recent investigations show maladaptive plasticity that leads to pain, including neuropathic pain after SCI, also exists at peripheral sites, such as the dorsal root ganglia (DRG), which contains the cell bodies of sensory neurons. This review discusses the important role DRGs play in nociceptive processing that underlies inflammatory and neuropathic pain. Specifically, it highlights nociceptor hyperexcitability as critical to increased pain states. Furthermore, it reviews prior literature on glutamate and glutamate receptors, voltage-gated sodium channels (VGSC), and brain-derived neurotrophic factor (BDNF) signaling in the DRG as important contributors to inflammatory and neuropathic pain. We previously reviewed BDNF’s role as a bidirectional neuromodulator of spinal plasticity. Here, we shift focus to the periphery and discuss BDNF-TrkB expression on nociceptors, non-nociceptor sensory neurons, and non-neuronal cells in the periphery as a potential contributor to induction and persistence of pain after SCI. Overall, this review presents a comprehensive evaluation of large bodies of work that individually focus on pain, DRG, BDNF, and SCI, to understand their interaction in nociceptive processing.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"15 ","pages":"Article 100151"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452073X24000023/pdfft?md5=08c83cca77407d35cd8633c8460651e0&pid=1-s2.0-S2452073X24000023-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139517322","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":"Pain-sensorimotor interactions: New perspectives and a new model","authors":"Greg M. Murray , Barry J. Sessle","doi":"10.1016/j.ynpai.2024.100150","DOIUrl":"10.1016/j.ynpai.2024.100150","url":null,"abstract":"<div><p>How pain and sensorimotor behavior interact has been the subject of research and debate for many decades. This article reviews theories bearing on pain-sensorimotor interactions and considers their strengths and limitations in the light of findings from experimental and clinical studies of pain-sensorimotor interactions in the spinal and craniofacial sensorimotor systems. A strength of recent theories is that they have incorporated concepts and features missing from earlier theories to account for the role of the sensory-discriminative, motivational-affective, and cognitive-evaluative dimensions of pain in pain-sensorimotor interactions. Findings acquired since the formulation of these recent theories indicate that additional features need to be considered to provide a more comprehensive conceptualization of pain-sensorimotor interactions. These features include biopsychosocial influences that range from biological factors such as genetics and epigenetics to psychological factors and social factors encompassing environmental and cultural influences. Also needing consideration is a mechanistic framework that includes other biological factors reflecting nociceptive processes and glioplastic and neuroplastic changes in sensorimotor and related brain and spinal cord circuits in acute or chronic pain conditions. The literature reviewed and the limitations of previous theories bearing on pain-sensorimotor interactions have led us to provide new perspectives on these interactions, and this has prompted our development of a new concept, the Theory of Pain-Sensorimotor Interactions (TOPSMI) that we suggest gives a more comprehensive framework to consider the interactions and their complexity. This theory states that <strong><em>pain is associated with plastic changes in the central nervous system (CNS) that lead to an activation pattern of motor units that contributes to the individual’s adaptive sensorimotor behavior. This activation pattern takes account of the biological, psychological, and social influences on the musculoskeletal tissues involved in sensorimotor behavior and on the plastic changes and the experience of pain in that individual. The pattern is normally optimized in terms of biomechanical advantage and metabolic cost related to the features of the individual’s musculoskeletal tissues and aims to minimize pain and any associated sensorimotor changes, and thereby maintain homeostasis. However, adverse biopsychosocial factors and their interactions may result in plastic CNS changes leading to less optimal, even maladaptive, sensorimotor changes producing motor unit activation patterns associated with the development of further pain.</em></strong> This more comprehensive theory points towards customized treatment strategies, in line with the management approaches to pain proposed in the biopsychosocial model of pain.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"15 ","pages":"Article 100150"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452073X24000011/pdfft?md5=7c27b7d26972c1b32b2102ac81886c3d&pid=1-s2.0-S2452073X24000011-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139506162","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}
Adam B. Willits , Leena Kader , Olivia Eller , Emily Roberts , Bailey Bye , Taylor Strope , Bret D. Freudenthal , Shahid Umar , Sree Chintapalli , Kartik Shankar , Dong Pei , Julie Christianson , Kyle M. Baumbauer , Erin E. Young
{"title":"Spinal cord injury-induced neurogenic bowel: A role for host-microbiome interactions in bowel pain and dysfunction","authors":"Adam B. Willits , Leena Kader , Olivia Eller , Emily Roberts , Bailey Bye , Taylor Strope , Bret D. Freudenthal , Shahid Umar , Sree Chintapalli , Kartik Shankar , Dong Pei , Julie Christianson , Kyle M. Baumbauer , Erin E. Young","doi":"10.1016/j.ynpai.2024.100156","DOIUrl":"https://doi.org/10.1016/j.ynpai.2024.100156","url":null,"abstract":"<div><h3>Background and aims</h3><p>Spinal cord injury (SCI) affects roughly 300,000 Americans with 17,000 new cases added annually. In addition to paralysis, 60% of people with SCI develop neurogenic bowel (NB), a syndrome characterized by slow colonic transit, constipation, and chronic abdominal pain. The knowledge gap surrounding NB mechanisms after SCI means that interventions are primarily symptom-focused and largely ineffective. The goal of the present studies was to identify mechanism(s) that initiate and maintain NB after SCI as a critical first step in the development of evidence-based, novel therapeutic treatment options.</p></div><div><h3>Methods</h3><p>Following spinal contusion injury at T9, we observed alterations in bowel structure and function reflecting key clinical features of NB. We then leveraged tissue-specific whole transcriptome analyses (RNAseq) and fecal 16S rRNA amplicon sequencing in combination with histological, molecular, and functional (Ca<sup>2+</sup> imaging) approaches to identify potential mechanism(s) underlying the generation of the NB phenotype.</p></div><div><h3>Results</h3><p>In agreement with prior reports focused on SCI-induced changes in the skin, we observed a rapid and persistent increase in expression of calcitonin gene-related peptide (CGRP) expression in the colon. This is suggestive of a neurogenic inflammation-like process engaged by antidromic activity of below-level primary afferents following SCI. CGRP has been shown to disrupt colon homeostasis and negatively affect peristalsis and colon function. As predicted, contusion SCI resulted in increased colonic transit time, expansion of lymphatic nodules, colonic structural and genomic damage, and disruption of the inner, sterile intestinal mucus layer corresponding to increased CGRP expression in the colon. Gut microbiome colonization significantly shifted over 28 days leading to the increase in <em>Anaeroplasma,</em> a pathogenic, gram-negative microbe. Moreover, colon specific vagal afferents and enteric neurons were hyperresponsive after SCI to different agonists including fecal supernatants.</p></div><div><h3>Conclusions</h3><p>Our data suggest that SCI results in overexpression of colonic CGRP which could alter colon structure and function. Neurogenic inflammatory-like processes and gut microbiome dysbiosis can also sensitize vagal afferents, providing a mechanism for visceral pain despite the loss of normal sensation post-SCI. These data may shed light on novel therapeutic interventions targeting this process to prevent NB development in patients.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"15 ","pages":"Article 100156"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452073X24000072/pdfft?md5=3dd815ed0045b8a4173ed2ba539f6627&pid=1-s2.0-S2452073X24000072-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140533825","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}
Jacquelyn R. Dayton , Jose Marquez , Alejandra K. Romo , Yi-Je Chen , Jorge E. Contreras , Theanne N. Griffith
{"title":"Thermal escape box: A cost-benefit evaluation paradigm for investigating thermosensation and thermal pain","authors":"Jacquelyn R. Dayton , Jose Marquez , Alejandra K. Romo , Yi-Je Chen , Jorge E. Contreras , Theanne N. Griffith","doi":"10.1016/j.ynpai.2024.100155","DOIUrl":"https://doi.org/10.1016/j.ynpai.2024.100155","url":null,"abstract":"<div><p>Thermosensation, the ability to detect and estimate temperature, is an evolutionarily conserved process that is essential for survival. Thermosensing is impaired in various pain syndromes, resulting in thermal allodynia, the perception of an innocuous temperature as painful, or thermal hyperalgesia, an exacerbated perception of a painful thermal stimulus. Several behavioral assays exist to study thermosensation and thermal pain in rodents, however, most rely on reflexive withdrawal responses or the subjective quantification of spontaneous nocifensive behaviors. Here, we created a new apparatus, the thermal escape box, which can be attached to temperature-controlled plates and used to assess temperature-dependent effort-based decision-making. The apparatus consists of a light chamber with an opening that fits around temperature-controlled plates, and a small entryway into a dark chamber. A mouse must choose to stay in a brightly lit aversive area or traverse the plates to escape to the enclosed dark chamber. We quantified escape latencies of adult C57Bl/6 mice at different plate temperatures from video recordings and found they were significantly longer at 5 °C, 18 °C, and 52 °C, compared to 30 °C, a mouse’s preferred ambient temperature. Differences in escape latencies were abolished in male Trpm8<sup>−/−</sup> mice and in male Trpv1<sup>−/−</sup> animals. Finally, we show that chronic constriction injury procedures or oxaliplatin treatement significantly increased escape latencies at cold temperatures compared to controls, the later of which was prevented by the analgesic meloxicam. This demonstrates the utility of this assay in detecting cold pain. Collectively, our study has identified a new and effective tool that uses cost-benefit valuations to study thermosensation and thermal pain.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"15 ","pages":"Article 100155"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452073X24000060/pdfft?md5=dabe2e0a6bc09d3753d5d78632ccb495&pid=1-s2.0-S2452073X24000060-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140350865","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}
Sandoval Ortega Raquel Adaia , Renard Margot , Cohen Michael X. , Nevian Thomas
{"title":"Interactive effects of pain and arousal state on heart rate and cortical activity in the mouse anterior cingulate and somatosensory cortices","authors":"Sandoval Ortega Raquel Adaia , Renard Margot , Cohen Michael X. , Nevian Thomas","doi":"10.1016/j.ynpai.2024.100157","DOIUrl":"10.1016/j.ynpai.2024.100157","url":null,"abstract":"<div><p>Sensory disconnection is a hallmark of sleep, yet the cortex retains some ability to process sensory information. Acute noxious stimulation during sleep increases the heart rate and the likelihood of awakening, indicating that certain mechanisms for pain sensing and processing remain active. However, processing of somatosensory information, including pain, during sleep remains underexplored. To assess somatosensation in natural sleep, we simultaneously recorded heart rate and local field potentials in the anterior cingulate (ACC) and somatosensory (S1) cortices of naïve, adult male mice, while applying noxious and non-noxious stimuli to their hind paws throughout their sleep-wake cycle. Noxious stimuli evoked stronger heart rate increases in both wake and non-rapid eye movement sleep (NREMS), and resulted in larger awakening probability in NREMS, as compared to non-noxious stimulation, suggesting differential processing of noxious and non-noxious information during sleep. Somatosensory information differentially reached S1 and ACC in sleep, eliciting complex transient and sustained responses in the delta, alpha, and gamma frequency bands as well as somatosensory evoked potentials. These dynamics depended on sleep state, the behavioral response to the stimulation and stimulation intensity (non-noxious vs. noxious). Furthermore, we found a correlation of the heart rate with the gamma band in S1 in the absence of a reaction in wake and sleep for noxious stimulation. These findings confirm that somatosensory information, including nociception, is sensed and processed during sleep even in the absence of a behavioral response.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"15 ","pages":"Article 100157"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452073X24000084/pdfft?md5=1d867902815cd56c53eb4fb7bf001383&pid=1-s2.0-S2452073X24000084-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140788448","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}
Randal A. Serafini , Aarthi Ramakrishnan , Li Shen , Venetia Zachariou
{"title":"Desipramine induces anti-inflammatory dorsal root ganglion transcriptional signatures in the murine spared nerve injury model","authors":"Randal A. Serafini , Aarthi Ramakrishnan , Li Shen , Venetia Zachariou","doi":"10.1016/j.ynpai.2024.100153","DOIUrl":"https://doi.org/10.1016/j.ynpai.2024.100153","url":null,"abstract":"<div><p>Monoamine-targeting antidepressants serve as frontline medications for chronic pain and associated comorbidities. While persistent anti-allodynic properties of antidepressants generally require weeks of treatment, several groups have demonstrated acute analgesic effects within hours of administration, suggesting a role in non-mesocorticolimbic pain processing regions such as the peripheral nervous system. To further explore this possibility, after four weeks of spared nerve injury or sham surgeries, we systemically administered desipramine or saline for an additional three weeks and performed whole transcriptome RNA sequencing on L3-6 dorsal root ganglia. Along with alterations in molecular pathways associated with neuronal activity, we observed a robust immunomodulatory transcriptional signature in the desipramine treated group. Cell subtype deconvolution predicted that these changes were associated with A- and C-fibers. Of note, differentially expressed genes from the dorsal root ganglia of DMI-treated, injured mice were largely unique compared to those from the nucleus accumbens of the same animals. These observations suggest that, under peripheral nerve injury conditions, desipramine induces specific gene expression changes across various regions of the nociceptive circuitry.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"15 ","pages":"Article 100153"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452073X24000047/pdfft?md5=d65d525a01a8a6d98785e12760320e17&pid=1-s2.0-S2452073X24000047-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140190896","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}
Zachary M.S. Waarala , Logan Comins , Sophie Laumet , Joseph K. Folger , Geoffroy Laumet
{"title":"Massage-like stroking produces analgesia in mice","authors":"Zachary M.S. Waarala , Logan Comins , Sophie Laumet , Joseph K. Folger , Geoffroy Laumet","doi":"10.1016/j.ynpai.2023.100149","DOIUrl":"10.1016/j.ynpai.2023.100149","url":null,"abstract":"<div><p>Chronic pain treatment remains a major challenge and pharmacological interventions are associated with important side effects. Manual medicine treatments such as massage, acupuncture, manipulation of the fascial system (MFS), and osteopathic manipulative treatments produce pain relief in humans, but the underlying mechanism is poorly understood limiting leverage and optimization of manual medicine techniques as safe pain therapy. To decipher the physiological mechanisms of manipulative medicine treatments, we have established a preclinical model. Here, we established a murine model of massage-like stroking (MLS)-induced analgesia. We characterized that the analgesia effects were present in both sexes, and were independent of the experimenters, handling, consciousness, and opioid receptors. MLS alleviates thermal pain in naive mice and postoperative pain hypersensitivity. This novel model will allow discovery of the physiological mechanisms involved in MLS-induced analgesia and identification of new therapeutic strategies.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"15 ","pages":"Article 100149"},"PeriodicalIF":0.0,"publicationDate":"2023-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452073X23000363/pdfft?md5=f8237574284af1873e7905191ae13bb8&pid=1-s2.0-S2452073X23000363-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139027257","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}