Neurobiology of Pain最新文献

{"title":"Low-intensity pulsed ultrasound phonophoresis with diclofenac alleviated inflammation and pain via downregulation of M1 macrophages in rats with carrageenan-induced knee joint arthritis","authors":"Ryo Sasaki ,&nbsp;Junya Sakamoto ,&nbsp;Yuichiro Honda ,&nbsp;Satoko Motokawa ,&nbsp;Hideki Kataoka ,&nbsp;Tomoki Origuchi ,&nbsp;Minoru Okita","doi":"10.1016/j.ynpai.2023.100148","DOIUrl":"10.1016/j.ynpai.2023.100148","url":null,"abstract":"<div><h3>Objective</h3><p>This study aimed to investigate the effects of low-intensity pulsed ultrasound (LIPUS) phonophoresis with diclofenac on inflammation and pain in the acute phase of carrageenan-induced arthritis in rats.</p></div><div><h3>Design</h3><p>60 male Wistar rats were randomly divided into the arthritis, diclofenac, LIPUS, phonophoresis, and sham-arthritis control groups. LIPUS and transdermal diclofenac gel were applied to the lateral side of the inflamed knee for 7 days, initiated postinjection day 1. In the phonophoresis group, diclofenac gel was rubbed onto the skin, followed by LIPUS application over the medication. Knee joint transverse diameters, pressure pain thresholds (PPTs), and paw withdrawal thresholds (PWT) were evaluated. The number of CD68-, CD11c-, and CD206-positive cells, and IL-1β and COX-2 mRNA expression were analyzed 8 days after injection.</p></div><div><h3>Results</h3><p>In the phonophoresis group, the transverse diameter, PPT, PWT significantly recovered at the day 8 compared to those in the LIPUS and diclofenac groups. The number of CD68- and CD11c-positive cells in the phonophoresis group was significantly lower than that in the LIPUS and diclofenac groups, but no significant differences were observed among three groups in CD206-positive cells. IL-1β and COX-2 mRNA levels were lower in the phonophoresis group than in the arthritis group, although there were no differences among the LIPUS, diclofenac, and phonophoresis groups.</p></div><div><h3>Conclusion</h3><p>LIPUS phonophoresis with diclofenac is more effective to ameliorate inflammation and pain compared to diclofenac or LIPUS alone, and the mechanism involves the decrease of M1 macrophages.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"15 ","pages":"Article 100148"},"PeriodicalIF":0.0,"publicationDate":"2023-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452073X23000351/pdfft?md5=36d1e1ea99ee9ec31cf3b62e82f7fc75&pid=1-s2.0-S2452073X23000351-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138515099","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":"Percutaneous electric nerve field stimulation alters cortical thickness in a pilot study of veterans with fibromyalgia","authors":"Anna Woodbury ,&nbsp;Lisa C. Krishnamurthy ,&nbsp;Anastasia Bohsali ,&nbsp;Venkatagiri Krishnamurthy ,&nbsp;Jeremy L. Smith ,&nbsp;Melat Gebre ,&nbsp;Kari Tyler ,&nbsp;Mark Vernon ,&nbsp;Bruce Crosson ,&nbsp;Jerry P. Kalangara ,&nbsp;Vitaly Napadow ,&nbsp;Jason W. Allen ,&nbsp;Daniel Harper","doi":"10.1016/j.ynpai.2022.100093","DOIUrl":"10.1016/j.ynpai.2022.100093","url":null,"abstract":"<div><h3>Objective</h3><p>To evaluate changes in cortical thickness and right posterior insula (r-pIns) gamma-aminobutyric acid (GABA) concentrations in veterans with fibromyalgia treated with auricular percutaneous electric nerve field stimulation (PENFS).</p></div><div><h3>Materials &amp; methods</h3><p>This was a randomized, controlled, open label investigation conducted in a government hospital. Twenty-one<!--> <!-->veterans with fibromyalgia were<!--> <!-->randomized to receive either standard therapy (ST; i.e., 4 weekly visits with a pain practitioner) or ST with<!--> <!-->auricular PENFS (ST + PENFS). Neuroimaging data was collected at baseline (i.e. before the first treatment session) and again within 2 weeks post-treatment.​ Clinical pain and physical function were also assessed at<!--> <!-->these timepoints. Single-voxel magnetic resonance spectroscopy was carried out in r-pIns to assess changes in r-pIns GABA concentrations and high-resolution T1-weighted images were collected to assess changes in regional gray matter volume using cortical thickness.</p></div><div><h3>Results</h3><p>Both the ST + PENFS and ST groups reported a decrease in pain with treatment. <strong>Volumetric:</strong> Cortical thickness significantly decreased in the left middle posterior cingulate (p = 0.018) and increased in the left cuneus (p = 0.014) following ST + PENFS treatment. These findings were significant following FDR correction for multiple comparisons. ST group right hemisphere insula cortical thickness increased post-treatment and was significantly (p = 0.02) inversely correlated with pain scores. ST + PENFS group right hemisphere posterior dorsal cingulate size significantly (p = 0.044) positively correlated with pain scores. <strong>GABA</strong>: There were no significant correlations with GABA, though a trend was noted towards increased GABA following treatment in both groups (p = 0.083) using a linear mixed effects model.</p></div><div><h3>Conclusions</h3><p>Results suggest a novel effect of PENFS reflected by differential volumetric changes compared to ST. The changes in GABA that occur in both groups are more likely related to ST. Insular GABA and cortical thickness in key regions of interest may be developed as potential biomarkers for evaluating chronic pain pathology and treatment outcomes.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"12 ","pages":"Article 100093"},"PeriodicalIF":0.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9207563/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10347402","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":"Anandamide in the dorsal periaqueductal gray inhibits sensory input without a correlation to sympathoexcitation","authors":"Christopher J. Roberts ,&nbsp;Francis A. Hopp ,&nbsp;Quinn H. Hogan ,&nbsp;Caron Dean","doi":"10.1016/j.ynpai.2022.100104","DOIUrl":"10.1016/j.ynpai.2022.100104","url":null,"abstract":"<div><p>There is growing literature supporting cannabinoids as a potential therapeutic for pain conditions. The development of chronic pain has been associated with reduced concentrations of the endogenous cannabinoid anandamide (AEA) in the midbrain dorsal periaqueductal gray (dPAG), and microinjections of synthetic cannabinoids into the dPAG are antinociceptive. Therefore, the goal of this study was to examine the role of the dPAG in cannabinoid-mediated sensory inhibition. Given that cannabinoids in the dPAG also elicit sympathoexcitation, a secondary goal was to assess coordination between sympathetic and antinociceptive responses. AEA was microinjected into the dPAG while recording single unit activity of wide dynamic range (WDR) dorsal horn neurons (DHNs) evoked by high intensity mechanical stimulation of the hindpaw, concurrently with renal sympathetic nerve activity (RSNA), in anesthetized male rats. AEA microinjected into the dPAG decreased evoked DHN activity (n = 24 units), for half of which AEA also elicited sympathoexcitation. AEA actions were mediated by cannabinoid 1 receptors as confirmed by local pretreatment with the cannabinoid receptor antagonist AM281. dPAG microinjection of the synaptic excitant DL-homocysteic acid (DLH) also decreased evoked DHN activity (n = 27 units), but in all cases this was accompanied by sympathoexcitation. Thus, sensory inhibition elicited from the dPAG is not exclusively linked with sympathoexcitation, suggesting discrete neuronal circuits. The rostrocaudal location of sites may affect evoked responses as AEA produced sensory inhibition without sympathetic effects at 86 % of caudal compared to 25 % of rostral sites, supporting anatomically distinct neurocircuits. These data indicate that spatially selective manipulation of cannabinoid signaling could provide analgesia without potentially harmful autonomic activation.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"12 ","pages":"Article 100104"},"PeriodicalIF":0.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6c/fd/main.PMC9755024.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10688035","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 neurobiology of social stress resulting from Racism: Implications for pain disparities among racialized minorities","authors":"Joanna M. Hobson ,&nbsp;Myles D. Moody ,&nbsp;Robert E. Sorge ,&nbsp;Burel R. Goodin","doi":"10.1016/j.ynpai.2022.100101","DOIUrl":"10.1016/j.ynpai.2022.100101","url":null,"abstract":"<div><p>Extant literature posits that humans experience two types of threat: physical threat and social threat. While describing pain as “physical” or “social” can be helpful for understanding pain origins (i.e., broken bone versus lost relationship), this dichotomy is largely artificial and not particularly helpful for understanding how the human brain experiences pain. One real world example of social exclusion and rejection that is threatening and likely to bring about significant stress is racism. Racism is a system of beliefs, practices, and policies that operates to disadvantage racialized minorities while providing advantage to those with historical power, particularly White people in the United States and most other Western nations. The objective of this Mini-Review is to present evidence in support of the argument that racism promotes physical pain in racialized minorities, which in turn promotes chronic pain disparities. First, we provide a theoretical framework describing how racism is a potent stressor that affects the health and well-being of racialized minorities. We will then address the neurobiological underpinnings linking racism to social threat, as well as that linking social threats and physical pain. Finally, we will discuss how the perception of social threat brought about by racism may undermine pain management efforts.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"12 ","pages":"Article 100101"},"PeriodicalIF":0.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9449662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33461327","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":"Enrichment of genomic pathways based on differential DNA methylation profiles associated with knee osteoarthritis pain","authors":"Soamy Montesino-Goicolea ,&nbsp;Lingsong Meng ,&nbsp;Asha Rani ,&nbsp;Zhiguang Huo ,&nbsp;Thomas C. Foster ,&nbsp;Roger B. Fillingim ,&nbsp;Yenisel Cruz-Almeida","doi":"10.1016/j.ynpai.2022.100107","DOIUrl":"10.1016/j.ynpai.2022.100107","url":null,"abstract":"<div><p>Our study aimed to identify differentially methylated regions (i.e., genomic region where multiple adjacent CpG sites show differential methylation) and their enriched genomic pathways associated with knee osteoarthritis pain (KOA). We recruited cognitively healthy middle to older aged (age 45–85) adults with (n = 182) and without (n = 31) self-reported KOA pain. We also extracted DNA from peripheral blood that was analyzed using MethylationEPIC arrays. The R package <em>minfi</em> (<span>Aryee et al., 2014</span>) was used to perform methylation data preprocessing and quality control. To investigate biological pathways impacted by differential methylation, we performed pathway enrichment analysis using Ingenuity Pathway Analysis (IPA) to identify canonical pathways and upstream regulators. Annotated genes within ± 5 kb of the putative differentially methylated regions (DMRs, p &lt; 0.05) were subjected to the IPA analysis. There was no significant difference in age, sex, study site between no pain and pain group (p &gt; 0.05). Non-Hispanic black individuals were overrepresented in the pain group (p = 0.003). At raw p &lt; 0.05 cutoff, we identified a total of 19,710 CpG probes, including 13,951 hypermethylated CpG probes, for which DNA methylation level was higher in the groups with highest pain grades. We also identified 5,759 hypomethylated CpG probes for which DNA methylation level was lower in the pain groups with higher pain grades. IPA revealed that pain-related DMRs were enriched across multiple pathways and upstream regulators. The top 10 canonical pathways were linked to cellular signaling processes related to immune responses (i.e., antigen presentation, PD-1, PD-L1 cancer immunotherapy, B cell development, IL-4 signaling, Th1 and Th2 activation pathway, and phagosome maturation). Moreover, in terms of upstream regulators, NDUFAF3 was the most significant (p = 8.6E-04) upstream regulator. Our findings support previous preliminary work suggesting the importance of epigenetic regulation of the immune system in knee pain and the need for future work to understand the epigenetic contributions to chronic pain.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"12 ","pages":"Article 100107"},"PeriodicalIF":0.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9755025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10638422","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":"Sex-distinct microglial activation and myeloid cell infiltration in the spinal cord after painful peripheral injury","authors":"Nolan A. Huck ,&nbsp;Lauren J. Donovan ,&nbsp;Huaishuang Shen ,&nbsp;Claire E. Jordan ,&nbsp;Gabriella P.B. Muwanga ,&nbsp;Caldwell M. Bridges ,&nbsp;Thomas E. Forman ,&nbsp;Stephanie A. Cordonnier ,&nbsp;Elena S. Haight ,&nbsp;Fiona Dale-Huang ,&nbsp;Yoshinori Takemura ,&nbsp;Vivianne L. Tawfik","doi":"10.1016/j.ynpai.2022.100106","DOIUrl":"10.1016/j.ynpai.2022.100106","url":null,"abstract":"<div><p>Chronic pain is a common and often debilitating problem that affects 100 million Americans. A better understanding of pain’s molecular mechanisms is necessary for developing safe and effective therapeutics. Microglial activation has been implicated as a mediator of chronic pain in numerous preclinical studies; unfortunately, translational efforts using known glial modulators have largely failed, perhaps at least in part due to poor specificity of the compounds pursued, or an incomplete understanding of microglial reactivity. In order to achieve a more granular understanding of the role of microglia in chronic pain as a means of optimizing translational efforts, we utilized a clinically-informed mouse model of complex regional pain syndrome (CRPS), and monitored microglial activation throughout pain progression. We discovered that while both males and females exhibit spinal cord microglial activation as evidenced by increases in Iba1, activation is attenuated and delayed in females. We further evaluated the expression of the newly identified microglia-specific marker, TMEM119, and identified two distinct populations in the spinal cord parenchyma after peripheral injury: TMEM119+ microglia and TMEM119- infiltrating myeloid lineage cells, which are comprised of Ly6G + neutrophils and Ly6G- macrophages/monocytes. Neurons are sensitized by inflammatory mediators released in the CNS after injury; however, the cellular source of these cytokines remains somewhat unclear. Using multiplex <em>in situ</em> hybridization in combination with immunohistochemistry, we demonstrate that spinal cord TMEM119+ microglia are the cellular source of cytokines IL6 and IL1β after peripheral injury. Taken together, these data have important implications for translational studies: 1) microglia remain a viable analgesic target for males and females, so long as duration after injury is considered; 2) the analgesic properties of microglial modulators are likely at least in part related to their suppression of microglial-released cytokines, and 3) a limited number of neutrophils and macrophages/monocytes infiltrate the spinal cord after peripheral injury but have unknown impact on pain persistence or resolution. Further studies to uncover glial-targeted therapeutic interventions will need to consider sex, timing after injury, and the exact target population of interest to have the specificity necessary for translation.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"12 ","pages":"Article 100106"},"PeriodicalIF":0.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f8/b4/main.PMC9755061.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9517375","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":"Towards a deeper understanding of pain: How machine learning and deep learning algorithms are needed to provide the next generation of pain medicine for use in the clinic","authors":"Scott Alexander Holmes ,&nbsp;Joud Mar'i ,&nbsp;Stephen Green ,&nbsp;David Borsook","doi":"10.1016/j.ynpai.2022.100108","DOIUrl":"10.1016/j.ynpai.2022.100108","url":null,"abstract":"<div><p>As our definition of pain evolves, the factors implicit in defining and predicting pain status grow. These factors each have unique data characteristics and their outcomes each have unique target attributes. The clinical characterization of pain does not, as defined in the most recent IASP definition, require any tissue pathology, suggesting that the experience of pain can be uniquely psychological in nature. Predicting a persons pain status may be optimized through integration of multiple independent observations; however, how they are integrated has direct relevance towards predicting chronic pain development, clinical application, and research investigation. The current challenge is to find clinically-mindful ways of integrating clinical pain rating scales with neuroimaging of the peripheral and central nervous system with the biopsychocial environment and improving our capacity for diagnostic flexibility and knowledge translation through data modeling. This commentary addresses how our current knowledge of pain phenotypes and risk factors interacts with statistical models and how we can proceed forward in a clinically responsible way.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"12 ","pages":"Article 100108"},"PeriodicalIF":0.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/93/c9/main.PMC10039383.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9204616","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":"Nitroglycerin as a model of migraine: Clinical and preclinical review","authors":"Paula Sureda-Gibert ,&nbsp;Marcela Romero-Reyes ,&nbsp;Simon Akerman","doi":"10.1016/j.ynpai.2022.100105","DOIUrl":"10.1016/j.ynpai.2022.100105","url":null,"abstract":"<div><p>Migraine stands as one of the most disabling neurological conditions worldwide. It is a disorder of great challenge to study given its heterogeneous representation, cyclic nature, and complexity of neural networks involved. Despite this, clinical and preclinical research has greatly benefitted from the use of the nitric oxide donor, nitroglycerin (NTG), to model this disorder, dissect underlying mechanisms, and to facilitate the development and screening of effective therapeutics. NTG is capable of triggering a migraine attack, only in migraineurs or patients with a history of migraine and inducing migraine-like phenotypes in rodent models. It is however unclear to what extent NTG and NO, as its breakdown product, is a determinant factor in the underlying pathophysiology of migraine, and importantly, whether it really does facilitate the translation from the bench to the bedside, and vice-versa. This review provides an insight into the evidence supporting the strengths of this model, as well as its limitations, and shines a light into the possible role of NO-related mechanisms in altered molecular signalling pathways.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"12 ","pages":"Article 100105"},"PeriodicalIF":0.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6c/60/main.PMC10039393.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10298127","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":"Magnetic resonance spectroscopy studies in migraine","authors":"Simona Nikolova,&nbsp;Todd J. Schwedt","doi":"10.1016/j.ynpai.2022.100102","DOIUrl":"10.1016/j.ynpai.2022.100102","url":null,"abstract":"<div><p></p><ul><li><span><p>This review summarizes major findings and recent advances in magnetic resonance spectroscopy (MRS) of migraine. A multi database search of PubMed, EMBASE, and Web of Science was performed with variations of magnetic resonance spectroscopy and headache until 20th September 2021. The search generated 2897 studies, 676 which were duplicates and 1836 were not related to headache. Of the remaining 385 studies examined, further exclusions for not migraine (n = 114), and not MRS of human brain (n = 128), and non-original contributions (n = 51) or conferences (n = 24) or case studies (n = 11) or non-English (n = 3), were applied. The manuscripts of all resulting reports were reviewed for their possible inclusion in this manuscript (n = 54). The reference lists of all included reports were carefully reviewed and articles relevant to this review were added (n = 2).</p></span></li></ul>Included are 56 studies of migraine with and without aura that involve magnetic resonance spectroscopy of the human brain. The topics are presented in the form of a narrative review. This review aims to provide a summary of the metabolic changes measured by MRS in patients with migraine. Despite the variability reported between studies, common findings focused on regions functionally relevant to migraine such as occipital cortices, thalamic nuclei, cerebellum and cingulate. The most reproducible results were decreased <em>N</em>-acetyl-aspartate (NAA) in cerebellum in patients with hemiplegic migraine and in the thalamus of chronic migraine patients. Increased lactate (Lac) in the occipital cortex was found for migraine with aura but not in subjects without aura. MRS studies support the hypothesis of impaired energetics and mitochondrial dysfunction in migraine. Although results regarding GABA and Glu were less consistent, studies suggest there might be an imbalance of these important inhibitory and excitatory neurotransmitters in the migraine brain. Multinuclear imaging studies in migraine with and without aura, predominantly investigating phosphorous, report alterations of PCr in occipital, parietal, and posterior brain regions. There have been too few studies to assess the diagnostic relevance of sodium imaging in migraine.</div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"12 ","pages":"Article 100102"},"PeriodicalIF":0.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5b/a2/main.PMC9755026.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10399024","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":"Comparison of Pain-Like behaviors in two surgical incision animal models in C57BL/6J mice","authors":"Esad Ulker ,&nbsp;Martial Caillaud ,&nbsp;Eda Koseli ,&nbsp;Katherine Contreras ,&nbsp;Yasmin Alkhlaif ,&nbsp;Eric Lindley ,&nbsp;Mitali Barik ,&nbsp;Sofia Ghani ,&nbsp;Camron D. Bryant ,&nbsp;M. Imad Damaj","doi":"10.1016/j.ynpai.2022.100103","DOIUrl":"10.1016/j.ynpai.2022.100103","url":null,"abstract":"<div><h3>Background</h3><p>Management of pain post-surgery is crucial for tissue healing in both veterinary and human medicine. Overuse of some analgesics such as opioids may lead to addictions and worsen pain syndromes (opioid-induced hyperalgesia), while underuse of it may affect the welfare of the patient. Therefore, the importance of using surgery models in laboratory animals is increasing, with the goal of improving our understanding of pain neurobiology and developing safer analgesics.</p></div><div><h3>Methods</h3><p>We compared the widely used plantar incision model with the laparotomy surgery model and measured pain-related behaviors using both spontaneous and evoked responses in female and male C57BL/6J mice. Additionally, we assessed conditioned place preference (CPP) and sucrose preference tests to measure pain-induced motivation for the analgesic ketoprofen and anhedonia-like behavior.</p></div><div><h3>Results</h3><p>Laparotomized mice showed increased abdominal sensitivity while paw-incised mice showed increased paw thermal and mechanical sensitivity up to seven days post-surgery. Laparotomy surgery reduced all spontaneous behaviors in our study however this effect dissipated by 24 h post-laparotomy. On the other hand, paw incision only reduced the percentage of cage hanging in a sex-dependent manner at 6 h post-incision. We also showed that both surgery models increased conditioned place preference for ketoprofen while preference for sucrose was only reduced at 24 h post-laparotomy. Laporatomy, but not paw incision, induced a decrease in body weight at 24 h post-surgery. Neither surgery model affected fluid intake.</p></div><div><h3>Conclusion</h3><p>Our results indicate that post-surgery hypersensitivity and behavioral deficits may differ by the incision site. Furthermore, factors associated with the surgery including length of the incision, duration of the anesthesia, and the layers that received stitches may affect subsequent spontaneous behaviors. These findings may help to improve drug development or the choice of the effective analgesic, depending on the surgery type.</p></div>","PeriodicalId":52177,"journal":{"name":"Neurobiology of Pain","volume":"12 ","pages":"Article 100103"},"PeriodicalIF":0.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0e/27/main.PMC9755018.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10404949","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}