Molecular Pain最新文献_第2页

Long-term plasticity of NMDA GluN2B (NR2B) receptor in anterior cingulate cortical synapses. 前扣带回皮质突触中 NMDA GluN2B (NR2B) 受体的长期可塑性。

IF 3.3 3区医学

Molecular Pain Pub Date : 2024-01-01 DOI: 10.1177/17448069241230258

Min Zhuo

引用次数: 0

The analgesic effects of botulinum neurotoxin by modulating pain-related receptors; A literature review. 肉毒杆菌神经毒素通过调节疼痛相关受体产生的镇痛效果；文献综述。

IF 2.8 3区医学

Molecular Pain Pub Date : 2024-01-01 DOI: 10.1177/17448069241275099

Saereh Hosseindoost, Maziyar Askari Rad, Seyed Hassan Inanloo, Mojgan Rahimi, Samaneh Dehghan, Amirhossein Orandi, Ahmad Reza Dehpour, Hossein Majedi

{"title":"The analgesic effects of botulinum neurotoxin by modulating pain-related receptors; A literature review.","authors":"Saereh Hosseindoost, Maziyar Askari Rad, Seyed Hassan Inanloo, Mojgan Rahimi, Samaneh Dehghan, Amirhossein Orandi, Ahmad Reza Dehpour, Hossein Majedi","doi":"10.1177/17448069241275099","DOIUrl":"10.1177/17448069241275099","url":null,"abstract":"Botulinum neurotoxins (BoNTs), produced by Clostridium botulinum, have been used for the treatment of various central and peripheral neurological conditions. Recent studies have suggested that BoNTs may also have a beneficial effect on pain conditions. It has been hypothesized that one of the mechanisms underlying BoNTs' analgesic effects is the inhibition of pain-related receptors' transmission to the neuronal cell membrane. BoNT application disrupts the integration of synaptic vesicles with the cellular membrane, which is responsible for transporting various receptors, including pain receptors such as TRP channels, calcium channels, sodium channels, purinergic receptors, neurokinin-1 receptors, and glutamate receptors. BoNT also modulates the opioidergic system and the GABAergic system, both of which are involved in the pain process. Understanding the cellular and molecular mechanisms underlying these effects can provide valuable insights for the development of novel therapeutic approaches for pain management. This review aims to summarize the experimental evidence of the analgesic functions of BoNTs and discuss the cellular and molecular mechanisms by which they can act on pain conditions by inhibiting the transmission of pain-related receptors.","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11339750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141879071","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}

引用次数: 0

Effects of systemic oxytocin administration on ultraviolet B-induced nociceptive hypersensitivity and tactile hyposensitivity in mice. 全身注射催产素对紫外线诱导的小鼠痛觉超敏和触觉减敏的影响

IF 3.3 3区医学

Molecular Pain Pub Date : 2024-01-01 DOI: 10.1177/17448069241226553

M Danilo Boada, Silvia Gutierrez, James C Eisenach

{"title":"Effects of systemic oxytocin administration on ultraviolet B-induced nociceptive hypersensitivity and tactile hyposensitivity in mice.","authors":"M Danilo Boada, Silvia Gutierrez, James C Eisenach","doi":"10.1177/17448069241226553","DOIUrl":"10.1177/17448069241226553","url":null,"abstract":"Ultraviolet B (UVB) radiation induces cutaneous inflammation, leading to thermal and mechanical hypersensitivity. Here, we examine the mechanical properties and profile of tactile and nociceptive peripheral afferents functionally disrupted by this injury and the role of oxytocin (OXT) as a modulator of this disruption. We recorded intracellularly from L4 afferents innervating the irradiated area (5.1 J/cm2) in 4-6 old week male mice (C57BL/6J) after administering OXT intraperitoneally, 6 mg/Kg. The distribution of recorded neurons was shifted by UVB radiation to a pattern observed after acute and chronic injuries and reduced mechanical thresholds of A and C- high threshold mechanoreceptors while reducing tactile sensitivity. UVB radiation did not change somatic membrane electrical properties or fiber conduction velocity. OXT systemic administration rapidly reversed these peripheral changes toward normal in both low and high-threshold mechanoreceptors and shifted recorded neuron distribution toward normal. OXT and V1aR receptors were present on the terminals of myelinated and unmyelinated afferents innervating the skin. We conclude that UVB radiation, similar to local tissue surgical injury, cancer metastasis, and peripheral nerve injury, alters the distribution of low and high threshold mechanoreceptors afferents and sensitizes nociceptors while desensitizing tactile units. Acute systemic OXT administration partially returns all of those effects to normal.","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10846038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139087632","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}

引用次数: 0

Acute pulpitis promotes purinergic signaling to induce pain in rats via P38MAPK/NF-κB signaling pathway. 急性牙髓炎通过 P38MAPK/NF-κB 信号通路促进嘌呤能信号传导以诱发大鼠疼痛

IF 3.3 3区医学

Molecular Pain Pub Date : 2024-01-01 DOI: 10.1177/17448069241234451

Yangxi Chen, Jun Hu, Fang Qi, Yiqun Kang, Tiejun Zhang, Li Wang

{"title":"Acute pulpitis promotes purinergic signaling to induce pain in rats via P38MAPK/NF-κB signaling pathway.","authors":"Yangxi Chen, Jun Hu, Fang Qi, Yiqun Kang, Tiejun Zhang, Li Wang","doi":"10.1177/17448069241234451","DOIUrl":"10.1177/17448069241234451","url":null,"abstract":"Toothache is one of the most common types of pain, but the mechanisms underlying pulpitis-induced pain remain unknown. The ionotropic purinergic receptor family (P2X) is reported to mediate nociception in the nervous system. This study aims to investigate the involvement of P2X3 in the sensitisation of the trigeminal ganglion (TG) and the inflammation caused by acute pulpitis. An acute tooth inflammation model was established by applying LPS to the pulp of SD rats. We found that the increased expression of P2X3 was induced by acute pulpitis. A selective P2X3 inhibitor (A-317491) reduced pain-like behavior in the maxillofacial region of rats and depressed the activation of neurons in the trigeminal ganglion induced by pulpitis. The upregulated MAPK signaling (p-p38, p-ERK1/2) expression in the ipsilateral TG induced by pulpitis could also be depressed by the application of the P2X3 inhibitor. Furthermore, the expression of markers of inflammatory processes, such as NF-κB, TNF-α and IL-1β, could be induced by acute pulpitis and deduced by the intraperitoneal injection of P2X3 antagonists. Our findings demonstrate that purinergic P2X3 receptor signaling in TG neurons contributes to pulpitis-induced pain in rats and that P2X3 signaling may be a potential therapeutic target for tooth pain.","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10868473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139702915","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}

引用次数: 0

Isolectin B4 (IB4)-conjugated streptavidin for the selective knockdown of proteins in IB4-positive (+) nociceptors. 等选蛋白 B4 (IB4) 连接链霉亲和素用于选择性敲除 IB4 阳性（+）神经感受器中的蛋白质。

IF 3.3 3区医学

Molecular Pain Pub Date : 2024-01-01 DOI: 10.1177/17448069241230419

Oliver Bogen, Dionéia Araldi, Anatol Sucher, Kord Kober, Peter T Ohara, Jon D Levine

{"title":"Isolectin B4 (IB4)-conjugated streptavidin for the selective knockdown of proteins in IB4-positive (+) nociceptors.","authors":"Oliver Bogen, Dionéia Araldi, Anatol Sucher, Kord Kober, Peter T Ohara, Jon D Levine","doi":"10.1177/17448069241230419","DOIUrl":"10.1177/17448069241230419","url":null,"abstract":"In vivo analysis of protein function in nociceptor subpopulations using antisense oligonucleotides and short interfering RNAs is limited by their non-selective cellular uptake. To address the need for selective transfection methods, we covalently linked isolectin B4 (IB4) to streptavidin and analyzed whether it could be used to study protein function in IB4(+)-nociceptors. Rats treated intrathecally with IB4-conjugated streptavidin complexed with biotinylated antisense oligonucleotides for protein kinase C epsilon (PKCε) mRNA were found to have: (a) less PKCε in dorsal root ganglia (DRG), (b) reduced PKCε expression in IB4(+) but not IB4(-) DRG neurons, and (c) fewer transcripts of the PKCε gene in the DRG. This knockdown in PKCε expression in IB4(+) DRG neurons is sufficient to reverse hyperalgesic priming, a rodent model of chronic pain that is dependent on PKCε in IB4(+)-nociceptors. These results establish that IB4-streptavidin can be used to study protein function in a defined subpopulation of nociceptive C-fiber afferents.","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10851726/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139513385","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}

引用次数: 0

Electroacupuncture attenuates nociceptive behaviors in a mouse model of cancer pain. 电针可减轻癌痛小鼠模型的痛觉行为

IF 3.3 3区医学

Molecular Pain Pub Date : 2024-01-01 DOI: 10.1177/17448069241240692

Yu-Xue Zhao, Ming-Jiang Yao, Jian-Wu Shen, Wen-Xi Zhang, Yuan-Xi Zhou

{"title":"Electroacupuncture attenuates nociceptive behaviors in a mouse model of cancer pain.","authors":"Yu-Xue Zhao, Ming-Jiang Yao, Jian-Wu Shen, Wen-Xi Zhang, Yuan-Xi Zhou","doi":"10.1177/17448069241240692","DOIUrl":"10.1177/17448069241240692","url":null,"abstract":"Pain is a major symptom in cancer patients, and cancer-induced bone pain (CIBP) is the most common type of moderate and severe cancer-related pain. The current available analgesic treatments for CIBP have adverse effects as well as limited therapeutic effects. Acupuncture is proved effective in pain management as a safe alternative therapy. We evaluated the analgesic effect of acupuncture in treatment of cancer pain and try to explore the underlying analgesic mechanisms. Nude mice were inoculated with cancer cells into the left distal femur to establish cancer pain model. Electroacupuncture (EA) treatment was applied for the xenograft animals. Pain behaviors of mice were evaluated, followed by the detections of neuropeptide-related and inflammation-related indicators in peripheral and central levels. EA treatment alleviated cancer-induced pain behaviors covering mechanical allodynia, thermal hyperalgesia and spontaneous pain, and also down-regulated immunofluorescence expressions of neuropeptide CGRP and p75 in the skin of affected plantar area in xenograft mice, and inhibited expressions of overexpressed neuropeptide-related and inflammation-related protein in the lumbar spinal cord of xenograft mice. Overall, our findings suggest that EA treatment ameliorated cancer-induced pain behaviors in the mouse xenograft model of cancer pain, possibly through inhibiting the expressions of neuropeptide-related and inflammation-related protein in central level following tumor cell xenografts.","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11010748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140039827","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}

引用次数: 0

Rapid cleavage of IL-1β in DRG neurons produces tissue injury-induced pain hypersensitivity. DRG 神经元中 IL-1β 的快速裂解会产生组织损伤诱导的痛觉过敏。

IF 2.8 3区医学

Molecular Pain Pub Date : 2024-01-01 DOI: 10.1177/17448069241285357

Daisuke Fujita, Yutaka Matsuoka, Shunsuke Yamakita, Yasuhiko Horii, Daiki Ishikawa, Kohsuke Kushimoto, Hiroaki Amino, Fumimasa Amaya

{"title":"Rapid cleavage of IL-1β in DRG neurons produces tissue injury-induced pain hypersensitivity.","authors":"Daisuke Fujita, Yutaka Matsuoka, Shunsuke Yamakita, Yasuhiko Horii, Daiki Ishikawa, Kohsuke Kushimoto, Hiroaki Amino, Fumimasa Amaya","doi":"10.1177/17448069241285357","DOIUrl":"10.1177/17448069241285357","url":null,"abstract":"Background: IL-1β plays a critical role in the pathophysiology of neuroinflammation. The presence of cleaved IL-1β (cIL-1β) in the neurons of the dorsal root ganglion (DRG) implicates its function in biological signaling arising from the sensory neuron. This study was conducted to analyze the role of IL-1β in nociceptive transduction after tissue injury. Methods: A plantar incision was made in C57BL/6 mice, following which immunohistochemistry and RNA scope in situ hybridization were performed at various time points to analyze cIL-1β, caspase-1, and IL-1 receptor 1 (IL-1R1) expression in the DRG. The effect of intrathecal administration of a caspase-1 inhibitor or regional anesthesia using local anesthetics on cIL-1β expression and pain hypersensitivity was analyzed by immunohistochemistry and behavioral analysis. ERK phosphorylation was also analyzed to investigate the effect of IL-1β on the activity of spinal dorsal horn neurons. Results: cIL-1β expression was significantly increased in caspase-1-positive DRG neurons 5 min after the plantar incision. Intrathecal caspase-1 inhibitor treatment inhibited IL-1β cleavage and pain hypersensitivity after the plantar incision. IL-1R1 was also detected in the DRG neurons, although the majority of IL-1R1-expressing neurons lacked cIL-1β expression. Regional anesthesia using local anesthetics prevented cIL-1β processing. Plantar incision-induced phosphorylation of ERK was inhibited by the caspase-1 inhibitor. Conclusion: IL-1β in the DRG neuron undergoes rapid cleavage in response to tissue injury in an activity-dependent manner. Cleaved IL-1β causes injury-induced functional activation of sensory neurons and pain hypersensitivity. IL-1β in the primary afferent neurons is involved in physiological nociceptive signal transduction.","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11394351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140598","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}

引用次数: 0

Fat mass and obesity-related protein contributes to the development and maintenance of bone cancer pain in rats by abrogating m6A methylation of RNA. 脂肪量和肥胖相关蛋白通过减弱 RNA 的 m6A 甲基化，促进大鼠骨癌疼痛的发展和维持。

IF 2.8 3区医学

Molecular Pain Pub Date : 2024-01-01 DOI: 10.1177/17448069241295987

Beibei Liu, Danyang Meng, Man Luo, Longsheng Xu, Ming Yao

{"title":"Fat mass and obesity-related protein contributes to the development and maintenance of bone cancer pain in rats by abrogating m6A methylation of RNA.","authors":"Beibei Liu, Danyang Meng, Man Luo, Longsheng Xu, Ming Yao","doi":"10.1177/17448069241295987","DOIUrl":"10.1177/17448069241295987","url":null,"abstract":"Effective prevention and treatment options for bone cancer-related pain (BCP) are lacking. In recent years, numerous studies have investigated the association between m6A epigenetic modifications and pain, revealing their significant role in pain initiation and maintenance. This study aimed to provide theoretical support for the treatment of BCP and to identify target drugs for future development. Specifically, we investigated the involvement of fat mass and obesity-related protein (FTO) in rat models of BCP by administering varying doses (1/5/10 mg/kg) of the FTO inhibitor meclofenamic acid (MA) and assessing changes in mechanical sensitivity through domain analysis, gait analysis, and open-field experiments. After successfully establishing the BCP model, we verified it by performing mechanical sensitivity assessments. We observed significantly increased expression levels of the demethylase FTO within the spinal dorsal horn accompanied by decreased m6A methylation levels in the model. Compared with untreated BCP rats, remarkably improved behavioral responses indicative of reduced pain were observed in the model rats after administration of 10 mg/kg MA, concomitant with decreased expression levels of FTO and increased m6A methylation levels. Compared with untreated BCP rats, the expression levels of p-ERK and pro-inflammatory cytokines were also significantly decreased after MA administration. Taken together, FTO can downregulate m6A methylation level and activate ERK/inflammatory cytokines signaling pathway to maintain BCP in rats.","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11490980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470491","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}

引用次数: 0

Methylglyoxal activates transient receptor potential A1/V1 via reactive oxygen species in the spinal dorsal horn. 甲基乙二酸通过脊髓背角的活性氧激活瞬时受体电位 A1/V1

IF 3.3 3区医学

Molecular Pain Pub Date : 2024-01-01 DOI: 10.1177/17448069241233744

Takeru Ueno, Manabu Yamanaka, Wataru Taniguchi, Naoko Nishio, Yuki Matsuyama, Ryo Miyake, Yuta Kaimochi, Terumasa Nakatsuka, Hiroshi Yamada

{"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":"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.","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":null,"pages":null},"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}

引用次数: 0

Optotagging and characterization of GABAergic rostral ventromedial medulla (RVM) neurons. GABA能颅内外侧髓质（RVM）神经元的光标记和特征描述。

IF 2.8 3区医学

Molecular Pain Pub Date : 2024-01-01 DOI: 10.1177/17448069241270295

Taylor Follansbee, Henry Le Chang, Mirela Iodi Carstens, Yun Guan, Earl Carstens, Xinzhong Dong

{"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":"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.","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":null,"pages":null},"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}

引用次数: 0