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[PMID]:29295980
[Au] Autor:Barragán-Iglesias P; Lou TF; Bhat VD; Megat S; Burton MD; Price TJ; Campbell ZT
[Ad] Endereço:School of Behavioral and Brain Sciences, University of Texas at Dallas, Richardson, TX, 75080, USA.
[Ti] Título:Inhibition of Poly(A)-binding protein with a synthetic RNA mimic reduces pain sensitization in mice.
[So] Source:Nat Commun;9(1):10, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nociceptors rely on cap-dependent translation to rapidly induce protein synthesis in response to pro-inflammatory signals. Comparatively little is known regarding the role of the regulatory factors bound to the 3' end of mRNA in nociceptor sensitization. Poly(A)-binding protein (PABP) stimulates translation initiation by bridging the Poly(A) tail to the eukaryotic initiation factor 4F complex associated with the mRNA cap. Here, we use unbiased assessment of PABP binding specificity to generate a chemically modified RNA-based competitive inhibitor of PABP. The resulting RNA mimic, which we designated as the Poly(A) SPOT-ON, is more stable than unmodified RNA and binds PABP with high affinity and selectivity in vitro. We show that injection of the Poly(A) SPOT-ON at the site of an injury can attenuate behavioral response to pain. Collectively, these results suggest that PABP is integral for nociceptive plasticity. The general strategy described here provides a broad new source of mechanism-based inhibitors for RNA-binding proteins and is applicable for in vivo studies.
[Mh] Termos MeSH primário: Dor/metabolismo
Poli A/metabolismo
Proteínas de Ligação a Poli(A)/metabolismo
RNA/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Células Cultivadas
Gânglios Espinais/citologia
Seres Humanos
Camundongos
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Dor Nociceptiva/metabolismo
Dor Nociceptiva/prevenção & controle
Dor/prevenção & controle
Medição da Dor
Poli A/química
Poli A/farmacologia
Proteínas de Ligação a Poli(A)/química
Ligação Proteica
RNA/química
RNA/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Poly(A)-Binding Proteins); 24937-83-5 (Poly A); 63231-63-0 (RNA)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02449-5


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[PMID]:28854251
[Au] Autor:Soon B; Vicenzino B; Schmid AB; Coppieters MW
[Ad] Endereço:Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, The University of Queensland, Brisbane, Australia.
[Ti] Título:Facilitatory and inhibitory pain mechanisms are altered in patients with carpal tunnel syndrome.
[So] Source:PLoS One;12(8):e0183252, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Preliminary evidence from studies using quantitative sensory testing suggests the presence of central mechanisms in patients with carpal tunnel syndrome (CTS) as apparent by widespread hyperalgesia. Hallmarks of central mechanisms after nerve injuries include nociceptive facilitation and reduced endogenous pain inhibition. Methods to study nociceptive facilitation in CTS so far have been limited to quantitative sensory testing and the integrity of endogenous inhibition remains unexamined. The aim of this study was therefore to investigate changes in facilitatory and inhibitory processing in patients with CTS by studying hypersensitivity following experimentally induced pain (facilitatory mechanisms) and the efficacy of conditioned pain modulation (CPM, inhibitory mechanisms). Twenty-five patients with mild to moderate CTS and 25 age and sex matched control participants without CTS were recruited. Increased pain facilitation was evaluated via injection of hypertonic saline into the upper trapezius. Altered pain inhibition through CPM was investigated through cold water immersion of the foot as the conditioning stimulus and pressure pain threshold over the thenar and hypothenar eminence bilaterally as the test stimulus. The results demonstrated that patients with CTS showed a greater duration (p = 0.047), intensity (p = 0.044) and area (p = 0.012) of pain in response to experimentally induced pain in the upper trapezius and impaired CPM compared to the control participants (p = 0.006). Although typically considered to be driven by peripheral mechanisms, these findings indicate that CTS demonstrates characteristics of altered central processing with increased pain facilitation and reduced endogenous pain inhibition.
[Mh] Termos MeSH primário: Síndrome do Túnel Carpal/fisiopatologia
Dor Crônica/fisiopatologia
Hiperalgesia/fisiopatologia
Dor Nociceptiva/fisiopatologia
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Condicionamento (Psicologia)
Feminino
Mãos/inervação
Mãos/fisiopatologia
Seres Humanos
Injeções Intramusculares
Masculino
Meia-Idade
Músculo Esquelético/inervação
Músculo Esquelético/fisiopatologia
Medição da Dor
Limiar da Dor
Estimulação Física
Pressão
Solução Salina Hipertônica/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Saline Solution, Hypertonic)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183252


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[PMID]:28674170
[Au] Autor:Moy JK; Khoutorsky A; Asiedu MN; Black BJ; Kuhn JL; Barragán-Iglesias P; Megat S; Burton MD; Burgos-Vega CC; Melemedjian OK; Boitano S; Vagner J; Gkogkas CG; Pancrazio JJ; Mogil JS; Dussor G; Sonenberg N; Price TJ
[Ad] Endereço:School of Behavioral and Brain Sciences, and.
[Ti] Título:The MNK-eIF4E Signaling Axis Contributes to Injury-Induced Nociceptive Plasticity and the Development of Chronic Pain.
[So] Source:J Neurosci;37(31):7481-7499, 2017 Aug 02.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Injury-induced sensitization of nociceptors contributes to pain states and the development of chronic pain. Inhibiting activity-dependent mRNA translation through mechanistic target of rapamycin and mitogen-activated protein kinase (MAPK) pathways blocks the development of nociceptor sensitization. These pathways convergently signal to the eukaryotic translation initiation factor (eIF) 4F complex to regulate the sensitization of nociceptors, but the details of this process are ill defined. Here we investigated the hypothesis that phosphorylation of the 5' cap-binding protein eIF4E by its specific kinase MAPK interacting kinases (MNKs) 1/2 is a key factor in nociceptor sensitization and the development of chronic pain. Phosphorylation of ser209 on eIF4E regulates the translation of a subset of mRNAs. We show that pronociceptive and inflammatory factors, such as nerve growth factor (NGF), interleukin-6 (IL-6), and carrageenan, produce decreased mechanical and thermal hypersensitivity, decreased affective pain behaviors, and strongly reduced hyperalgesic priming in mice lacking eIF4E phosphorylation ( ). Tests were done in both sexes, and no sex differences were found. Moreover, in patch-clamp electrophysiology and Ca imaging experiments on dorsal root ganglion neurons, NGF- and IL-6-induced increases in excitability were attenuated in neurons from mice. These effects were recapitulated in mice and with the MNK1/2 inhibitor cercosporamide. We also find that cold hypersensitivity induced by peripheral nerve injury is reduced in and mice and following cercosporamide treatment. Our findings demonstrate that the MNK1/2-eIF4E signaling axis is an important contributing factor to mechanisms of nociceptor plasticity and the development of chronic pain. Chronic pain is a debilitating disease affecting approximately one in three Americans. Chronic pain is thought to be driven by changes in the excitability of peripheral nociceptive neurons, but the precise mechanisms controlling these changes are not elucidated. Emerging evidence demonstrates that mRNA translation regulation pathways are key factors in changes in nociceptor excitability. Our work demonstrates that a single phosphorylation site on the 5' cap-binding protein eIF4E is a critical mechanism for changes in nociceptor excitability that drive the development of chronic pain. We reveal a new mechanistic target for the development of a chronic pain state and propose that targeting the upstream kinase, MAPK interacting kinase 1/2, could be used as a therapeutic approach for chronic pain.
[Mh] Termos MeSH primário: Adenosina Trifosfatases/metabolismo
Proteínas de Transporte de Cátions/metabolismo
Dor Crônica/fisiopatologia
Fator de Iniciação 4E em Eucariotos/metabolismo
Gânglios Espinais/fisiopatologia
Hiperalgesia/fisiopatologia
Plasticidade Neuronal
Nociceptividade
[Mh] Termos MeSH secundário: Animais
Dor Crônica/etiologia
ATPases Transportadoras de Cobre
Progressão da Doença
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Dor Nociceptiva/etiologia
Dor Nociceptiva/fisiopatologia
Células Receptoras Sensoriais/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cation Transport Proteins); 0 (Eukaryotic Initiation Factor-4E); 0 (eIF4E protein, mouse); EC 3.6.1.- (Adenosine Triphosphatases); EC 3.6.3.4 (Atp7a protein, mouse); EC 3.6.3.54 (Copper-transporting ATPases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0220-17.2017


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[PMID]:28520835
[Au] Autor:Schneiderhan J; Clauw D; Schwenk TL
[Ad] Endereço:University of Michigan Health System, Ann Arbor.
[Ti] Título:Primary Care of Patients With Chronic Pain.
[So] Source:JAMA;317(23):2367-2368, 2017 Jun 20.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Analgésicos Opioides/uso terapêutico
Dor Crônica/terapia
Atenção Primária à Saúde
[Mh] Termos MeSH secundário: Dor Aguda/fisiopatologia
Dor Aguda/terapia
Dor Crônica/epidemiologia
Dor Crônica/fisiopatologia
Progressão da Doença
Acesso aos Serviços de Saúde
Seres Humanos
Neuralgia/diagnóstico
Neuralgia/fisiopatologia
Dor Nociceptiva/diagnóstico
Dor Nociceptiva/fisiopatologia
Transtornos Relacionados ao Uso de Opioides/epidemiologia
Manejo da Dor/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics, Opioid)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.5787


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[PMID]:28446160
[Au] Autor:Boakye-Gyasi E; Henneh IT; Abotsi WKM; Ameyaw EO; Woode E
[Ad] Endereço:Department of Pharmacology, Faculty of Pharmacy and Pharmaceutical Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana. ebgyasi.pharm@knust.edu.gh.
[Ti] Título:Hydro-ethanolic leaf extract of Ziziphus abyssinica Hochst Ex A. Rich (Rhamnaceae) exhibits anti-nociceptive effects in murine models.
[So] Source:BMC Complement Altern Med;17(1):231, 2017 Apr 26.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Despite substantial advances in pain research and treatment, millions of people continue to suffer from pain and this has been attributed mainly to the unavailability of effective and safer analgesics. The use of plants as medicines is still widespread and plants constitute a large source of novel phytocompounds that might become leads for the discovery of newer, effective and safer alternatives. Various parts of Ziziphus abyssinica have been used in folk medicine in several African countries as painkillers. However, there is no report on the possible anti-nociceptive effects of this plant especially the leaves, hence the need for this current study. METHODS: The possible anti-nociceptive activity of hydro-ethanolic leaf extract of Ziziphus abyssinica (EthE) was assessed in rodents using chemical (acetic acid, formalin and glutamate), thermal (tail-immersion test) and mechanical/inflammatory (carrageenan) models of nociception. RESULTS: EthE (30-300 mg/kg, p.o.) dose-dependently and significantly inhibited chemical-induced nociception with a maximum inhibition of 86.29 ± 2.27%, 76.34 ± 5.67%, 84.97 ± 5.35%, and 82.81 ± 5.97% respectively for acetic acid, formalin (phase 1), formalin (phase 2) and glutamate tests at its highest dose. EthE also dose-dependently and significantly increased reaction times in both tail-immersion and carrageenan-induced hypernociceptive tests. The activities of the extract in the various models were comparable with the effect of morphine hydrochloride and diclofenac sodium used as standard analgesic drugs. CONCLUSION: Oral administration of hydro-ethanolic leaf extract of Ziziphus abyssinica ameliorates nocifensive behaviours associated with chemical-, thermal- and mechanical/inflammatory - induced nociceptive pain.
[Mh] Termos MeSH primário: Analgésicos/farmacologia
Dor Nociceptiva/tratamento farmacológico
Fitoterapia
Extratos Vegetais/uso terapêutico
Ziziphus
[Mh] Termos MeSH secundário: Ácido Acético
África
Analgésicos/uso terapêutico
Animais
Anti-Inflamatórios/farmacologia
Anti-Inflamatórios/uso terapêutico
Comportamento Animal
Carragenina
Modelos Animais de Doenças
Feminino
Formaldeído
Ácido Glutâmico
Temperatura Alta
Inflamação/complicações
Masculino
Camundongos Endogâmicos ICR
Dor Nociceptiva/induzido quimicamente
Dor Nociceptiva/etiologia
Dor
Extratos Vegetais/farmacologia
Folhas de Planta
Ratos Sprague-Dawley
Tempo de Reação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Anti-Inflammatory Agents); 0 (Plant Extracts); 1HG84L3525 (Formaldehyde); 3KX376GY7L (Glutamic Acid); 9000-07-1 (Carrageenan); Q40Q9N063P (Acetic Acid)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1750-z


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[PMID]:28437360
[Au] Autor:Pan Z; Xue ZY; Li GF; Sun ML; Zhang M; Hao LY; Tang QQ; Zhu LJ; Cao JL
[Ad] Endereço:From Jiangsu Province Key Laboratory of Anesthesiology (Z.P., Z.-Y.X., G.-F.L., M.-L.S., M.Z., L.-Y.H., Q.-Q.T., L.-J.Z., J.-L.C.) and Jiangsu Province Key Laboratory of Anesthesia and Analgesia Application Technology (Z.P., Z.-Y.X., G.-F.L., M.-L.S., M.Z., L.-Y.H., Q.-Q.T., L.-J.Z., J.-L.C.), Xuzhou Medical University, Xuzhou; and Department of Anesthesiology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou (J.-L.C.), China.
[Ti] Título:DNA Hydroxymethylation by Ten-eleven Translocation Methylcytosine Dioxygenase 1 and 3 Regulates Nociceptive Sensitization in a Chronic Inflammatory Pain Model.
[So] Source:Anesthesiology;127(1):147-163, 2017 Jul.
[Is] ISSN:1528-1175
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ten-eleven translocation methylcytosine dioxygenase converts 5-methylcytosine in DNA to 5-hydroxymethylcytosine, which plays an important role in gene transcription. Although 5-hydroxymethylcytosine is enriched in mammalian neurons, its regulatory function in nociceptive information processing is unknown. METHODS: The global levels of 5-hydroxymethylcytosine and ten-eleven translocation methylcytosine dioxygenase were measured in spinal cords in mice treated with complete Freund's adjuvant. Immunoblotting, immunohistochemistry, and behavioral tests were used to explore the downstream ten-eleven translocation methylcytosine dioxygenase-dependent signaling pathway. RESULTS: Complete Freund's adjuvant-induced nociception increased the mean levels (± SD) of spinal 5-hydroxymethylcytosine (178 ± 34 vs. 100 ± 21; P = 0.0019), ten-eleven translocation methylcytosine dioxygenase-1 (0.52 ± 0.11 vs. 0.36 ± 0.064; P = 0.0088), and ten-eleven translocation methylcytosine dioxygenase-3 (0.61 ± 0.13 vs. 0.39 ± 0.08; P = 0.0083) compared with levels in control mice (n = 6/group). The knockdown of ten-eleven translocation methylcytosine dioxygenase-1 or ten-eleven translocation methylcytosine dioxygenase-3 alleviated thermal hyperalgesia and mechanical allodynia, whereas overexpression cytosinethem in naïve mice (n = 6/group). Down-regulation of spinal ten-eleven translocation methylcytosine dioxygenase-1 and ten-eleven translocation methylcytosine dioxygenase-3 also reversed the increases in Fos expression (123 ± 26 vs. 294 ± 6; P = 0.0031; and 140 ± 21 vs. 294 ± 60; P = 0.0043, respectively; n = 6/group), 5-hydroxymethylcytosine levels in the Stat3 promoter (75 ± 16.1 vs. 156 ± 28.9; P = 0.0043; and 91 ± 19.1 vs. 156 ± 28.9; P = 0.0066, respectively; n = 5/group), and consequent Stat3 expression (93 ± 19.6 vs. 137 ± 27.5; P = 0.035; and 72 ± 15.2 vs. 137 ± 27.5; P = 0.0028, respectively; n = 5/group) in complete Freund's adjuvant-treated mice. CONCLUSIONS: This study reveals a novel epigenetic mechanism for ten-eleven translocation methylcytosine dioxygenase-1 and ten-eleven translocation methylcytosine dioxygenase-3 in the modulation of spinal nociceptive information via targeting of Stat3.
[Mh] Termos MeSH primário: Citosina/análogos & derivados
Citosina/metabolismo
Metilação de DNA/fisiologia
Dioxigenases/metabolismo
Inflamação/fisiopatologia
Dor Nociceptiva/fisiopatologia
[Mh] Termos MeSH secundário: 5-Metilcitosina/metabolismo
Animais
Dor Crônica/fisiopatologia
Proteínas de Ligação a DNA/metabolismo
Modelos Animais de Doenças
Masculino
Camundongos
Proteínas Proto-Oncogênicas/metabolismo
Transdução de Sinais
Medula Espinal/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Proto-Oncogene Proteins); 6R795CQT4H (5-Methylcytosine); 8J337D1HZY (Cytosine); EC 1.13.11.- (Dioxygenases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE
[do] DOI:10.1097/ALN.0000000000001632


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[PMID]:28428504
[Au] Autor:Osawa G; Aruga E
[Ad] Endereço:Dept. of Palliative Medicine, Teikyo University School of Medicine.
[Ti] Título:[Assessment and Strategy for Nociceptive Pain in Cancer].
[So] Source:Gan To Kagaku Ryoho;44(4):278-282, 2017 Apr.
[Is] ISSN:0385-0684
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Pain is classified as either nociceptive pain, which results from a nociceptor stimulation, or neuropathic pain, which results from a lesion of the neural pathway. Clinically, in many cases, pain consists of a single origin but multiple origins are also possible. In this paper, we outline an assessment and strategy for nociceptive pain in cancer. The onset time, location, feature, strength, and etiology were included as categories for the assessment of pain. Furthermore, we added a psychosocial assessment to the physical assessment, which ensured comprehensive pain evaluation. We performed the investigation according to the WHO method for cancer pain relief. According to the effects and adverse effects, we chose a non-opioid analgesic and an opioid analgesic as medications. However, nonpharmacological therapy, such as radiotherapy and nerve block, is not a concern with the WHO analgesic ladder. It is important that a multi-disciplinary team, which includes physicians, nurses, physiotherapists, and pharmacists, support the patients to manage their pain by themselves through the knowledge of the factors affecting their pain and the medication methods for easing it when it gets worse. Although we cannot ease pain completely, it is important to define the goal of treatment with patients and to examine the strategy for maximum pain relief.
[Mh] Termos MeSH primário: Dor do Câncer/tratamento farmacológico
Neoplasias/complicações
Dor Nociceptiva/tratamento farmacológico
[Mh] Termos MeSH secundário: Dor do Câncer/etiologia
Seres Humanos
Manejo da Dor
Medição da Dor
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170422
[St] Status:MEDLINE


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[PMID]:28389699
[Au] Autor:Albury CL; Stuart S; Haupt LM; Griffiths LR
[Ad] Endereço:Genomics Research Centre, Institute for Biomedical Health and Innovation, Queensland University of Technology, Brisbane, QLD, 4059, Australia.
[Ti] Título:Ion channelopathies and migraine pathogenesis.
[So] Source:Mol Genet Genomics;292(4):729-739, 2017 Aug.
[Is] ISSN:1617-4623
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Migraine is a common neurological disorder that affects approximately 12-20% of the general adult population. Migraine pathogenesis is complex and not wholly understood. Molecular genetic investigations, imaging and biochemical studies, have unveiled a number of interconnected neurological pathways which seem to have a cause and effect component integral to its cause. Much weight of migraine attack initiation can be placed on the initial trigger and the pathways involved in its neuronal counter reaction. Ion channels play a large role in the generation, portrayal and mitigation of the brains response to external triggers. Several genetic studies have identified and implicated a number of ion channelopathy genes which may contribute to this generalised process. This review will focus on the genetics of migraine with particular emphasis placed on the potentially important role genes HEPH (responsible for iron transport and homeostasis) and KCNK18 (important for the transport and homeostasis of potassium) play in migraine cause.
[Mh] Termos MeSH primário: Canalopatias/genética
Proteínas de Membrana/genética
Transtornos de Enxaqueca/genética
Dor Nociceptiva/genética
Canais de Potássio/genética
[Mh] Termos MeSH secundário: Adulto
Canalopatias/patologia
Feminino
Seres Humanos
Masculino
Transtornos de Enxaqueca/patologia
Dor Nociceptiva/patologia
Canais de Potássio/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (HEPH protein, human); 0 (KCNK18 protein, human); 0 (Membrane Proteins); 0 (Potassium Channels)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170409
[St] Status:MEDLINE
[do] DOI:10.1007/s00438-017-1317-1


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[PMID]:28330877
[Au] Autor:Kuo YL; Cheng JK; Hou WH; Chang YC; Du PH; Jian JJ; Rau RH; Yang JH; Lien CC; Tsaur ML
[Ad] Endereço:Institute of Neuroscience, Brain Research Center, National Yang-Ming University, Taipei 112, Taiwan.
[Ti] Título:K Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control.
[So] Source:J Neurosci;37(16):4391-4404, 2017 Apr 19.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The K channel pore-forming subunit Kv4.3 is expressed in a subset of nonpeptidergic nociceptors within the dorsal root ganglion (DRG), and knockdown of Kv4.3 selectively induces mechanical hypersensitivity, a major symptom of neuropathic pain. K channel modulatory subunits KChIP1, KChIP2, and DPP10 are coexpressed in Kv4.3 DRG neurons, but whether they participate in Kv4.3-mediated pain control is unknown. Here, we show the existence of a Kv4.3/KChIP1/KChIP2/DPP10 complex (abbreviated as the Kv4 complex) in the endoplasmic reticulum and cell surface of DRG neurons. After intrathecal injection of a gene-specific antisense oligodeoxynucleotide to knock down the expression of each component in the Kv4 complex, mechanical hypersensitivity develops in the hindlimbs of rats in parallel with a reduction in all components in the lumbar DRGs. Electrophysiological data further indicate that the excitability of nonpeptidergic nociceptors is enhanced. The expression of all Kv4 complex components in DRG neurons is downregulated following spinal nerve ligation (SNL). To rescue Kv4 complex downregulation, cDNA constructs encoding Kv4.3, KChIP1, and DPP10 were transfected into the injured DRGs (defined as DRGs with injured spinal nerves) of living SNL rats. SNL-evoked mechanical hypersensitivity was attenuated, accompanied by a partial recovery of Kv4.3, KChIP1, and DPP10 surface levels in the injured DRGs. By showing an interdependent regulation among components in the Kv4 complex, this study demonstrates that K channel modulatory subunits KChIP1, KChIP2, and DPP10 participate in Kv4.3-mediated mechanical pain control. Thus, these modulatory subunits could be potential drug targets for neuropathic pain. Neuropathic pain, a type of moderate to severe chronic pain resulting from nerve injury or disorder, affects 6.9%-10% of the global population. However, less than half of patients report satisfactory pain relief from current treatments. K channels, which act to reduce nociceptor activity, have been suggested to be novel drug targets for neuropathic pain. This study is the first to show that K channel modulatory subunits KChIP1, KChIP2, and DPP10 are potential drug targets for neuropathic pain because they form a channel complex with the K channel pore-forming subunit Kv4.3 in a subset of nociceptors to selectively inhibit mechanical hypersensitivity, a major symptom of neuropathic pain.
[Mh] Termos MeSH primário: Dipeptidil Peptidases e Tripeptidil Peptidases/metabolismo
Proteínas Interatuantes com Canais de Kv/metabolismo
Dor Nociceptiva/metabolismo
Canais de Potássio Shal/metabolismo
[Mh] Termos MeSH secundário: Animais
Dipeptidil Peptidases e Tripeptidil Peptidases/genética
Gânglios Espinais/citologia
Gânglios Espinais/metabolismo
Gânglios Espinais/fisiologia
Proteínas Interatuantes com Canais de Kv/genética
Masculino
Neurônios/metabolismo
Neurônios/fisiologia
Dor Nociceptiva/fisiopatologia
Ratos
Ratos Sprague-Dawley
Canais de Potássio Shal/genética
Tato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Kv Channel-Interacting Proteins); 0 (Shal Potassium Channels); EC 3.4.14.- (DPP10 protein, rat); EC 3.4.14.- (Dipeptidyl-Peptidases and Tripeptidyl-Peptidases)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1619-16.2017


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[PMID]:28282295
[Au] Autor:Hashemzaei M; Abdollahzadeh M; Iranshahi M; Golmakani E; Rezaee R; Tabrizian K
[Ti] Título:Effects of luteolin and luteolin-morphine co-administration on acute and chronic pain and sciatic nerve ligated-induced neuropathy in mice.
[So] Source:J Complement Integr Med;14(1), 2017 Mar 01.
[Is] ISSN:1553-3840
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Background Neuropathic pain (NP) is a common condition accompanied by nerve injury. To date, there is no definite treatment approved for this disorder. In addition, many drugs that are used for NP cause adverse reactions. Luteolin is a naturally occurring flavonoid with diverse pharmacological properties such as anti-inflammatory, antioxidant and anticancer. We sought to investigate luteolin effects on chronic, acute and neuropathic pain as well as its potential to increase morphine anti-nociceptive effects in mice. Methods Albino mice (20-25 g) were randomly divided into 14 groups (n=7) including morphine 1 mg/kg body weight +luteolin (5 mg/kg body weight), morphine (9 mg/kg body weight, i.p.), luteolin (2.5, 5 and 10 mg/kg body weight), imipramine 40 mg/kg body weight and normal saline (NS) (0.9 %) as vehicle and subjected to hot plate test. Formalin test was done in the following groups: NS, diclofenac sodium (10 mg/kg body weight, i.p.), morphine (9 mg/kg body weight, i.p.) and luteolin (2.5, 5 and 10 mg/kg body weight). Results Administration of luteolin single dose (5 and 10 mg/kg body weight) significantly reduced neuropathic pain ( p<0.05$\rm{p}<0.05$) in comparison to negative control. Anti-nociceptive effects of luteolin were comparable to imipramine as the standard positive control ( p<0.001$\rm{p}<0.001$). Co-administration of luteolin and morphine potentiated morphine 1 mg/kg body weight painkilling effects ( p<0.001$\rm{p}<0.001$). Conclusions Our results showed that luteolin alone reduces neuropathic pain. Furthermore, when co-administered with morphine 1 mg/kg body weight, luteolin potentiates morphine effects. Therefore, luteolin-morphine co-administration might be a valuable alternative for the conventional treatment.
[Mh] Termos MeSH primário: Analgésicos/uso terapêutico
Dor Crônica/tratamento farmacológico
Luteolina/uso terapêutico
Morfina/uso terapêutico
Dor Nociceptiva/tratamento farmacológico
Extratos Vegetais/uso terapêutico
Neuropatia Ciática/tratamento farmacológico
[Mh] Termos MeSH secundário: Doença Aguda
Analgésicos/farmacologia
Animais
Modelos Animais de Doenças
Quimioterapia Combinada
Formaldeído
Interações Ervas-Drogas
Temperatura Alta
Luteolina/farmacologia
Camundongos
Morfina/farmacologia
Dor/tratamento farmacológico
Manejo da Dor
Traumatismos dos Nervos Periféricos/complicações
Fitoterapia
Extratos Vegetais/farmacologia
Nervo Isquiático
Ciática/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Plant Extracts); 1HG84L3525 (Formaldehyde); 76I7G6D29C (Morphine); KUX1ZNC9J2 (Luteolin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170311
[St] Status:MEDLINE



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