Molecular Pain最新文献

{"title":"Methylglyoxal activates transient receptor potential A1/V1 via reactive oxygen species in the spinal dorsal horn.","authors":"Takeru Ueno, Manabu Yamanaka, Wataru Taniguchi, Naoko Nishio, Yuki Matsuyama, Ryo Miyake, Yuta Kaimochi, Terumasa Nakatsuka, Hiroshi Yamada","doi":"10.1177/17448069241233744","DOIUrl":"10.1177/17448069241233744","url":null,"abstract":"<p><p>Methylglyoxal (MGO), a highly reactive dicarbonyl metabolite of glucose primarily formed during the glycolytic pathway, is a precursor of advanced glycation end-products (AGEs). Recently, numerous studies have shown that MGO accumulation can cause pain and hyperalgesia. However, the mechanism through which MGO induces pain in the spinal dorsal horn remains unclear. The present study investigated the effect of MGO on spontaneous excitatory postsynaptic currents (sEPSC) in rat spinal dorsal horn neurons using blind whole-cell patch-clamp recording. Perfusion of MGO increased the frequency and amplitude of sEPSC in spinal horn neurons in a concentration-dependent manner. Additionally, MGO administration increased the number of miniature EPSC (mEPSC) in the presence of tetrodotoxin, a sodium channel blocker. However, 6-cyano-7-nitroqiunocaline-2,3-dione (CNQX), an AMPA/kainate receptor antagonist, blocked the enhancement of sEPSC by MGO. HC-030031, a TRP ankyrin-1 (TRPA1) antagonist, and capsazepine, a TRP vanilloid-1 (TRPV1) antagonist, inhibited the action of MGO. Notably, the effects of MGO were completely inhibited by HC-030031 and capsazepine. MGO generates reactive oxygen species (ROS) via AGEs. ROS also potentially induce pain via TRPA1 and TRPV1 in the spinal dorsal horn. Furthermore, we examined the effect of MGO in the presence of N-tert-butyl-α-phenylnitrone (PBN), a non-selective ROS scavenger, and found that the effect of MGO was completely inhibited. These results suggest that MGO increases spontaneous glutamate release from the presynaptic terminal to spinal dorsal horn neurons through TRPA1, TRPV1, and ROS and could enhance excitatory synaptic transmission.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069241233744"},"PeriodicalIF":3.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10868495/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139697885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methylene blue dose-dependently induces cutaneous inflammation and heat hyperalgesia in a novel rat model.","authors":"Ratan K Banik, Twan Sia, Malcolm E Johns, Phu V Tran, Andrew Y Cheng, Sudarshan Setty, Donald A Simone","doi":"10.1177/17448069241259535","DOIUrl":"10.1177/17448069241259535","url":null,"abstract":"<p><p>Methylene blue (MB) has been shown to reduce mortality and morbidity in vasoplegic patients after cardiac surgery. Though MB is considered to be safe, extravasation of MB leading to cutaneous toxicity has been reported. In this study, we sought to characterize MB-induced cutaneous toxicity and investigate the underlying mechanisms. To induce MB-induced cutaneous toxicity, we injected 64 adult male Sprague-Dawley rates with 200 µL saline (vehicle) or 1%, 0.1%, or 0.01% MB in the plantar hind paws. Paw swelling, skin histologic changes, and heat and mechanical hyperalgesia were measured. Injection of 1%, but not 0.1% or 0.01% MB, produced significant paw swelling compared to saline. Injection of 1% MB produced heat hyperalgesia but not mechanical hyperalgesia. Pain behaviors were unchanged following injections of 0.1% or 0.01% MB. Global transcriptomic analysis by RNAseq identified 117 differentially expressed genes (111 upregulated, 6 downregulated). Ingenuity Pathway Analysis showed an increased quantity of leukocytes, increased lipids, and decreased apoptosis of myeloid cells and phagocytes with activation of IL-1β and Fos as the two major regulatory hubs. qPCR showed a 16-fold increase in IL-6 mRNA. Thus, using a novel rat model of MB-induced cutaneous toxicity, we show that infiltration of 1% MB into cutaneous tissue causes a dose-dependent pro-inflammatory response, highlighting potential roles of IL-6, IL-1β, and Fos. Thus, anesthesiologists should administer dilute MB intravenously through peripheral venous catheters. Higher concentrations of MB (1%) should be administered through a central venous catheter to minimize the risk of cutaneous toxicity.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069241259535"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11162129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141076271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optotagging and characterization of GABAergic rostral ventromedial medulla (RVM) neurons.","authors":"Taylor Follansbee, Henry Le Chang, Mirela Iodi Carstens, Yun Guan, Earl Carstens, Xinzhong Dong","doi":"10.1177/17448069241270295","DOIUrl":"10.1177/17448069241270295","url":null,"abstract":"<p><p>The transmission of nociceptive and pruriceptive signals in the spinal cord is greatly influenced by descending modulation from brain areas such as the rostral ventromedial medulla (RVM). Within the RVM three classes of neurons have been discovered which are relevant to spinal pain modulation, the On, Off, and Neutral cells. These neurons were discovered due to their functional response to nociceptive stimulation. On cells are excited, Off cells are inhibited, and Neutral cells have no response to noxious stimulation. Since these neurons are identified by functional response characteristics it has been difficult to molecularly identify them. In the present study, we leverage our ability to perform optotagging within the RVM to determine whether RVM On, Off, and Neutral cells are GABAergic. We found that 27.27% of RVM On cells, 47.37% of RVM Off cells, and 42.6% of RVM Neutral cells were GABAergic. These results demonstrate that RVM On, Off, and Neutral cells represent a heterogeneous population of neurons and provide a reliable technique for the molecular identification of these neurons.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069241270295"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11301720/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141759923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between migraine and mitochondria: A Mendelian randomization study.","authors":"Ming-Yang Hong, Yu-Xin Chen, Yi-Cheng Xiong, Yi-Han Sun, Abdullah Al Mamun, Jian Xiao","doi":"10.1177/17448069241298849","DOIUrl":"10.1177/17448069241298849","url":null,"abstract":"<p><strong>Background and objective: </strong>Mitochondria are important organelles functioning in metabolic processes, inflammatory response and neurological disorders. Migraines are chronic and paroxysmal neurological disorders characterized by recurrent episodes of severe headache and other neurological symptoms. We explored whether mitochondria may be genetically and/or causally associated with migraine.</p><p><strong>Methods: </strong>Summary-level statistics of mitochondrial DNA copy number (mtDNA-CN), 69 mitochondria related exposures and migraine with aura, migraine without aura, migraine with aura and triptan purchases, migraine with aura, drug-induced, migraine without aura and triptan purchases and migraine without aura, drug-induced, were collected from genome-wide association studies (GWAS). The analysis employed two-sample Mendelian randomization, utilizing various methods including MR-Egger, inverse-variance weighted (IVW), MR-PRESSO (MR-pleiotropy residual sum and outlier), maximum likelihood, and weighted median.</p><p><strong>Results: </strong>We observed a potential association with decreased levels of mtDNA-CN with the risk of migraine without aura (Odds ratio (OR) 1.517, 95% Confidence interval (CI) 1.072-2.147, <i>p</i> = 0.019). Besides, for every 1 unit in NAD-dependent protein deacylase sirtuin-5 (SIRT5), relative risk of migraine without aura increased by 16.4%. For every 1 unit increase in Phenylalanine-transfer RNA (tRNA) ligase, relative risk of migraine without aura increased by 13.5%. For every 1 unit increase in Apoptosis-inducing factor 1, relative risk of migraine without aura increased by 27.4%.</p><p><strong>Conclusion: </strong>This study indicates fresh evidence of association between mtDNA-CN, mitochondrial related exposures and migraine especially migraine without aura. The findings may shed light on developing interventions targeting on the causal pathway from mitochondria to migraine.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":"20 ","pages":"17448069241298849"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11672378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predicting long-term pain by combining brain imaging, genetics and health questionnaire data with Swedish national registries using a prospective superstruct design.","authors":"Filip Gedin, Sebastian Blomé, Granit Kastrati, Maria Lalouni, Fredrik Åhs, Peter Fransson, Jörgen Rosén, William Hedley Thompson, Karin Jensen","doi":"10.1177/17448069241301628","DOIUrl":"10.1177/17448069241301628","url":null,"abstract":"<p><strong>Background: </strong>Long-term pain is a common health problem that results in disability for patients of all ages, leading to an enormous economic burden. Over 20% of the population suffer from long-term pain. Unfortunately, there are no clinical tests that predicts who will develop long-term pain. The overall aim is to predict future pain incidence based on brain function, pain behavior, health status, and genetic variability.</p><p><strong>Method: </strong>PrePain utilizes a superstruct design, which involves recruiting participants from ongoing research projects. Eligible individuals for participation in PrePain were over 18 years old and free from long-term pain. During the baseline visit, participants provide pain and health-related questionnaires, undergo structural and functional MRI scans, and provide a saliva sample for DNA extraction. Individual baseline measures are then routinely followed-up via national registries.</p><p><strong>Result: </strong>We present quality-assessed data from over 300 participants. The average age was 34 years, and most participants were women (75%). Participants rated their pain sensitivity above average and reported low avoidance. Catastrophizing thoughts during painful episodes were rated as moderate. Assessments of (f)MRI data indicated generally good image quality. In this first follow-up, we found that 45 participants had a pain-related diagnoses.</p><p><strong>Conclusion: </strong>Results indicate that a superstruct design is feasible for collecting a large number of high-quality data. The incidence of long-term pain indicates that a sufficient number of participants have been recruited to complete the prediction analyses. PrePain is a unique prospective pain database with a fair prognosis to determine risk factors of long-term pain.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":"20 ","pages":"17448069241301628"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11605748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Newly discovered functions of miRNAs in neuropathic pain: Transitioning from recent discoveries to innovative underlying mechanisms.","authors":"Hasan Golmakani, Amir Azimian, Ebrahim Golmakani","doi":"10.1177/17448069231225845","DOIUrl":"10.1177/17448069231225845","url":null,"abstract":"<p><p>Neuropathic pain is a widespread clinical issue caused by somatosensory nervous system damage, affecting numerous individuals. It poses considerable economic and public health challenges, and managing it can be challenging due to unclear underlying mechanisms. Nevertheless, emerging evidence suggests that neurogenic inflammation and neuroinflammation play a role in developing pain patterns. Emerging evidence suggests that neurogenic inflammation and neuroinflammation play significant roles in developing neuropathic pain within the nervous system. Increased/decreased miRNA expression patterns could affect the progression of neuropathic and inflammatory pain by controlling nerve regeneration, neuroinflammation, and the expression of abnormal ion channels. However, our limited knowledge of miRNA targets hinders a complete grasp of miRNA's functions. Meanwhile, exploring exosomal miRNA, a recently uncovered role, has significantly advanced our comprehension of neuropathic pain's pathophysiology in recent times. In this review, we present a comprehensive overview of the latest miRNA studies and explore the possible ways miRNAs might play a role in the development of neuropathic pain.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069231225845"},"PeriodicalIF":3.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10851769/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139040276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal associations of immune cell phenotypes with migraine: A mendelian randomization study.","authors":"Weifang Chai, Weihao Chai, Fei Guo","doi":"10.1177/17448069241274679","DOIUrl":"10.1177/17448069241274679","url":null,"abstract":"<p><p>The interaction between the immune system and the brain, crucial for blood-brain barrier integrity, is a potential factor in migraine development. Although there's evidence of a connection between immune dysregulation and migraine, a clear causal link has been lacking. To bridge this knowledge gap, we performed a two-sample Mendelian randomization (MR) analysis of 731 immune cell phenotypes to determine their causality with migraine, of which parameters included fluorescence, cell abundance, count, and morphology. Sensitivity and pleiotropy checks validated our findings. After applying a false discovery rate correction, our MR study identified 35 of 731 immune phenotypes with a significant causal link to migraine (<i>p</i> < 0.05). Of these, 24 showed a protective effect (inverse variance weighting : <i>p</i> < 0.05, odds ratio <1), and 11 were risk factors (inverse variance weighting : <i>p</i> < 0.05, odds ratio >1). Although limited by population sample size and potential population-specific genetic variations, our study uncovers a significant genetic link between certain immune cell markers and migraine, providing new insights into the disorder's pathophysiology. These discoveries are crucial for developing targeted biomarkers and personalized treatments. The research enhances our understanding of immune cells' role in migraine and may substantially improve patient outcomes and lessen its socio-economic impact.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069241274679"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11316964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141860356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characteristics of immune cells and causal relationship with chondromalacia: A two-sample, bidirectional mendelian randomization study.","authors":"Weiwei Chai, Mengwei Zhang, Yan He, Weihao Chai","doi":"10.1177/17448069241289962","DOIUrl":"10.1177/17448069241289962","url":null,"abstract":"<p><p>Chondromalacia, characterized by the softening of cartilage, is a prevalent condition affecting joint health with complex etiology. The immune system's role in its pathogenesis has been implicated but remains to be fully elucidated. To address a critical knowledge gap, we conducted a two-sample Mendelian randomization analysis of 731 immune cell phenotypes, assessing parameters like fluorescence, cell count, and morphology. After sensitivity and pleiotropy checks, and applying a false discovery rate correction, our study linked 17 phenotypes to chondromalacia (<i>p</i> < .05). Among them, seven immune cell phenotypes were found to have a protective effect against chondromalacia (IVW: <i>p</i> < .05, OR <1), while 10 were considered risk factors (IVW:<i>p</i> < .05, OR >1). Despite the constraints of sample size and possible genetic differences among populations, our research has identified a notable genetic correlation between specific immune cell indicators and chondromalacia. This breakthrough sheds light on the pathophysiological mechanisms of the condition. The identification of protective and risk-associated immune cell phenotypes provides a foundation for further exploration of immunological mechanisms in chondromalacia and may pave the way for targeted interventions. Future research is warranted to validate these findings and explore their clinical implications.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069241289962"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11528737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142308165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered intra- and inter-network functional activity among migraine, chronic migraine, and trigeminal neuralgia.","authors":"Qichen Zhou, Rong Zhao, Zhaoxia Qin, Yapeng Qi, Wenshuang Tang, Lan Liu, Weikan Wang, Jian-Ren Liu, Xiaoxia Du","doi":"10.1177/17448069241300939","DOIUrl":"10.1177/17448069241300939","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the specific manifestations and differences in brain network activity and functional connectivity between brain networks in patients with trigeminal neuralgia and migraine, aiming to reveal the neural basis of these two diseases.</p><p><strong>Background: </strong>Head and facial pain, including trigeminal neuralgia and migraine, is prevalent globally. However, the underlying neural mechanisms of these conditions remain unclear. Resting-state functional connectivity studies based on independent component analysis (ICA) may offer new insights into these diseases.</p><p><strong>Methods: </strong>The study involved 23 chronic migraine, 37 episodic migraine, 21 trigeminal neuralgia patients, and 33 age- and gender-matched controls. Resting-state functional magnetic resonance imaging was performed, and five sets of brain network components were extracted through ICA. Neuronal activity indicators were calculated for each participant's independent components, including amplitudes of low-frequency fluctuation (ALFF) and regional homogeneity (ReHo). Functional connectivity was also assessed and compared among the four groups.</p><p><strong>Results: </strong>Trigeminal neuralgia patients showed reduced ALFF in the dorsal attention network versus episodic migraine patients and controls. Both trigeminal neuralgia and chronic migraine patients had decreased ReHo in this network. Migraine patients had weaker connectivity between the default mode and visual networks than controls. Trigeminal neuralgia patients also showed higher connectivity between the somatosensory motor and dorsal attention networks. Compared to episodic migraine, trigeminal neuralgia, and chronic migraine patients had increased connectivity between the visual and dorsal attention networks.</p><p><strong>Conclusion: </strong>The study provides evidence that long-term chronic head and facial pain may contribute to abnormalities in the activation and connectivity of the dorsal attention network. Compared to migraine patients, trigeminal neuralgia patients exhibit abnormal brain network connectivity, particularly within the somatomotor network, which may explain the presence of significant \"trigger points.\" These findings offer new perspectives for understanding the characteristics of different head and facial pain subtypes.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":"20 ","pages":"17448069241300939"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629411/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of calcium-stimulated adenylyl cyclase subtype 1 (AC1) for the treatment of pain and anxiety symptoms in Parkinson's disease mice model.","authors":"Zhaoxiang Zhou, Qi-Yu Chen, Min Zhuo, Ping-Yi Xu","doi":"10.1177/17448069241266683","DOIUrl":"10.1177/17448069241266683","url":null,"abstract":"<p><p>Pain and anxiety are two common and undertreated non-motor symptoms in Parkinson's disease (PD), which affect the life quality of PD patients, and the underlying mechanisms remain unclear. As an important subtype of adenylyl cyclases (ACs), adenylyl cyclase subtype 1 (AC1) is critical for the induction of cortical long-term potentiation (LTP) and injury induced synaptic potentiation in the cortical areas including anterior cingulate cortex (ACC) and insular cortex (IC). Genetic deletion of AC1 or pharmacological inhibition of AC1 improved chronic pain and anxiety in different animal models. In this study, we proved the motor deficit, pain and anxiety symptoms of PD in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice model. As a lead candidate AC1 inhibitor, oral administration (1 dose and seven doses) of NB001 (20 and 40 mg/kg) showed significant analgesic effect in MPTP-treated mice, and the anxiety behavior was also reduced (40 mg/kg). By using genetic knockout mice, we found that AC1 knockout mice showed reduced pain and anxiety symptoms after MPTP administration, but not AC8 knockout mice. In summary, genetic deletion of AC1 or pharmacological inhibition of AC1 improved pain and anxiety symptoms in PD model mice, but didn't affect motor function. These results suggest that NB001 is a potential drug for the treatment of pain and anxiety symptoms in PD patients by inhibiting AC1 target.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069241266683"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11282525/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141443091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}