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Pesquisa : A08.186.854.697 [Categoria DeCS]
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[PMID]:29311559
[Au] Autor:Dulin JN; Adler AF; Kumamaru H; Poplawski GHD; Lee-Kubli C; Strobl H; Gibbs D; Kadoya K; Fawcett JW; Lu P; Tuszynski MH
[Ad] Endereço:Department of Neurosciences, University of California, San Diego, La Jolla, CA, 92093, USA.
[Ti] Título:Injured adult motor and sensory axons regenerate into appropriate organotypic domains of neural progenitor grafts.
[So] Source:Nat Commun;9(1):84, 2018 01 08.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Neural progenitor cell (NPC) transplantation has high therapeutic potential in neurological disorders. Functional restoration may depend on the formation of reciprocal connections between host and graft. While it has been reported that axons extending out of neural grafts in the brain form contacts onto phenotypically appropriate host target regions, it is not known whether adult, injured host axons regenerating into NPC grafts also form appropriate connections. We report that spinal cord NPCs grafted into the injured adult rat spinal cord self-assemble organotypic, dorsal horn-like domains. These clusters are extensively innervated by regenerating adult host sensory axons and are avoided by corticospinal axons. Moreover, host axon regeneration into grafts increases significantly after enrichment with appropriate neuronal targets. Together, these findings demonstrate that injured adult axons retain the ability to recognize appropriate targets and avoid inappropriate targets within neural progenitor grafts, suggesting that restoration of complex circuitry after SCI may be achievable.
[Mh] Termos MeSH primário: Axônios/fisiologia
Neurônios Motores/fisiologia
Regeneração Nervosa/fisiologia
Células-Tronco Neurais/transplante
Células Receptoras Sensoriais/fisiologia
Corno Dorsal da Medula Espinal/fisiologia
Traumatismos da Medula Espinal/terapia
[Mh] Termos MeSH secundário: Animais
Feminino
Masculino
Células-Tronco Neurais/fisiologia
Ratos
Medula Espinal/citologia
Transplante de Células-Tronco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180211
[Lr] Data última revisão:
180211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02613-x


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[PMID]:29020118
[Au] Autor:Marmiroli P; Riva B; Pozzi E; Ballarini E; Lim D; Chiorazzi A; Meregalli C; Distasi C; Renn CL; Semperboni S; Morosi L; Ruffinatti FA; Zucchetti M; Dorsey SG; Cavaletti G; Genazzani A; Carozzi VA
[Ad] Endereço:Experimental Neurology Unit, School of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy.
[Ti] Título:Susceptibility of different mouse strains to oxaliplatin peripheral neurotoxicity: Phenotypic and genotypic insights.
[So] Source:PLoS One;12(10):e0186250, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peripheral neurotoxicity is one of the most distressing side effects of oxaliplatin therapy for cancer. Indeed, most patients that received oxaliplatin experience acute and/or chronic severe sensory peripheral neuropathy. However, despite similar co-morbidities, cancer stage, demographics and treatment schedule, patients develop oxaliplatin-induced peripheral neurotoxicity with remarkably different severity. This suggests individual genetic variability, which might be used to glean the mechanistic insights into oxaliplatin neurotoxicity. We characterized the susceptibility of different mice strains to oxaliplatin neurotoxicity investigating the phenotypic features of neuropathy and gene expression profiles in dorsal root ganglia of six genetically different mice strains (Balb-c, C57BL6, DBA/2J, AJ, FVB and CD1) exposed to the same oxaliplatin schedule. Differential gene expression in dorsal root ganglia from each mice strain were assayed using a genome-wide expression analysis and selected genes were validated by RT-PCR analysis. The demonstration of consistent differences in the phenotypic response to oxaliplatin across different strains is interesting to allow the selection of the appropriate strain based on the pre-defined read-out parameters. Further investigation of the correlation between gene expression changes and oxaliplatin-induced neurotoxicity phenotype in each strain will be useful to deeper investigate the molecular mechanisms of oxaliplatin neurotoxicity.
[Mh] Termos MeSH primário: Predisposição Genética para Doença
Síndromes Neurotóxicas/genética
Síndromes Neurotóxicas/patologia
Compostos Organoplatínicos/efeitos adversos
Sistema Nervoso Periférico/patologia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Biópsia
Doença Crônica
Gânglios Espinais/efeitos dos fármacos
Gânglios Espinais/patologia
Regulação da Expressão Gênica/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos
Bainha de Mielina/metabolismo
Condução Nervosa/efeitos dos fármacos
Neuralgia/complicações
Neuralgia/genética
Neuralgia/patologia
Neurônios/metabolismo
Neurônios/patologia
Síndromes Neurotóxicas/complicações
Síndromes Neurotóxicas/fisiopatologia
Medição da Dor
Sistema Nervoso Periférico/fisiopatologia
Reação em Cadeia da Polimerase em Tempo Real
Nervo Isquiático/patologia
Nervo Isquiático/fisiopatologia
Pele/patologia
Corno Dorsal da Medula Espinal/efeitos dos fármacos
Corno Dorsal da Medula Espinal/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Organoplatinum Compounds); 04ZR38536J (oxaliplatin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186250


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[PMID]:28822786
[Au] Autor:Chang KT; Lin YL; Lin CT; Hong CJ; Tsai MJ; Huang WC; Shih YH; Lee YY; Cheng H; Huang MC
[Ad] Endereço:Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan; Neural Regeneration Laboratory, Department of Neurosurgery, Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan.
[Ti] Título:Leptin is essential for microglial activation and neuropathic pain after preganglionic cervical root avulsion.
[So] Source:Life Sci;187:31-41, 2017 Oct 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Preganglionic cervical root avulsion (PCRA) affects both the peripheral and central nervous systems and is often associated with neuropathic pain. Unlike peripheral nerve injuries (PNI), central lesions caused by disruption of cervical roots from the spinal cord following PCRA contribute to the generation of neuropathic pain. Leptin is involved in the development of neuropathic pain after PNI by affecting neurons. However, whether leptin is involved in microglial activation leading to neuropathic pain after PCRA is unknown. MAIN METHODS: Preganglionic avulsion of the left 6 -8 cervical roots was performed in C57B/6J mice and leptin-deficient mice. A leptin antagonist or leptin was administered to C57B/6J mice and leptin-deficient mice after injury, respectively. The expression pattern of spinal and supraspinal microglia was examined by immunofluorescent staining. Von Frey filaments were used to test pain sensitivity. KEY FINDINGS: Leptin is essential for the development of neuropathic pain after PCRA. Allodynia was absent in the leptin-deficient mice and the mice administered the leptin antagonist. We also found that leptin deficiency or the administration of its antagonist inhibited the development of microgliosis in the dorsal horn and brainstem. Furthermore, increase in the expression of CD86 and iNOS, and Wallerian degeneration were noted in the spinal cord. The administration of exogenous leptin to leptin-deficient mice reversed these effects. SIGNIFICANCE: We concluded that leptin is involved in the proliferation and activation of microglia, which in turn enhances the development of neuropathic pain. Blocking the effects of leptin might be a target for the treatment of neuropathic pain after PCRA.
[Mh] Termos MeSH primário: Fratura Avulsão/fisiopatologia
Leptina/fisiologia
Microglia/fisiologia
Neuralgia/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Antígeno B7-2/biossíntese
Tronco Encefálico/efeitos dos fármacos
Tronco Encefálico/patologia
Proliferação Celular/fisiologia
Medula Cervical/lesões
Feminino
Fratura Avulsão/complicações
Fratura Avulsão/patologia
Gliose/prevenção & controle
Leptina/antagonistas & inibidores
Leptina/genética
Leptina/farmacologia
Masculino
Camundongos
Camundongos Transgênicos
Microglia/efeitos dos fármacos
Neuralgia/complicações
Óxido Nítrico Sintase Tipo II/biossíntese
Medição da Dor/efeitos dos fármacos
Medula Espinal/efeitos dos fármacos
Medula Espinal/metabolismo
Medula Espinal/patologia
Corno Dorsal da Medula Espinal/efeitos dos fármacos
Corno Dorsal da Medula Espinal/patologia
Degeneração Walleriana/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-2 Antigen); 0 (Leptin); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170821
[St] Status:MEDLINE


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[PMID]:28652182
[Au] Autor:Shi Y; Qin W; Nie F; Wen H; Lu K; Cui J
[Ad] Endereço:Department of Pain Care, Southwest Hospital, Third Military Medical University, Chongqing 400038, China; Department of Anesthesia, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
[Ti] Título:Ulinastatin attenuates neuropathic pain via the ATP/P2Y2 receptor pathway in rat models.
[So] Source:Gene;627:263-270, 2017 Sep 05.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Ulinastatin, a serine protease inhibitor, which has anti-inflammatory properties and neuroprotective effects, is used to treat acute inflammatory disorders. Recent evidence indicates that administration of ulinastatin alleviates pain in rat model of neuropathic pain (NPP). However, its effect on NPP and the underlying mechanism requires further study. In this study, we evaluated the role of intrathecal administration of ulinastatin in rats with sciatic nerve ligation and observed the effect of ulinastatin on the ATP/P2Y2 receptor pathway. We performed mechanical and thermal sensitivity measurements, immunohistochemistry and double-label immunofluoresence studies to evaluate P2Y2 receptor and adenosine 5'-monophosphate-activated protein kinase (AMPK) expression in the dorsal horn of the lumbar enlargement region of the spinal cord, and a luciferase assay for the detection of ATP levels in the cerebrospinal fluid. The results showed that ulinastatin prevented the development of mechanical allodynia and thermal hypersensitivity in the rat sciatic nerve ligation model. Ulinastatin reduced the level of extracellular ATP, down-regulated P2Y2 receptor and AMPK expression in the spinal dorsal horn of the chronic constrictive injury model. We found that increased expression of P2Y2 receptor in microglia was likely involved in the activation of microglia after nerve injury, and ulinastatin inhibited the abnormal microglia activation in the dorsal horn after nerve injury. These findings demonstrated that ulinastatin might be a potential and effective drug for the treatment of NPP via the suppression of the ATP/P2Y2 receptor pathway.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Glicoproteínas/uso terapêutico
Neuralgia/tratamento farmacológico
Receptores Purinérgicos P2Y2/metabolismo
Inibidores de Serino Proteinase/uso terapêutico
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/genética
Proteínas Quinases Ativadas por AMP/metabolismo
Trifosfato de Adenosina/líquido cefalorraquidiano
Animais
Glicoproteínas/farmacologia
Masculino
Microglia/efeitos dos fármacos
Microglia/metabolismo
Neuralgia/metabolismo
Ratos
Ratos Sprague-Dawley
Receptores Purinérgicos P2Y2/genética
Inibidores de Serino Proteinase/farmacologia
Transdução de Sinais
Corno Dorsal da Medula Espinal/efeitos dos fármacos
Corno Dorsal da Medula Espinal/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycoproteins); 0 (Receptors, Purinergic P2Y2); 0 (Serine Proteinase Inhibitors); 8L70Q75FXE (Adenosine Triphosphate); EC 2.7.11.31 (AMP-Activated Protein Kinases); OR3S9IF86U (urinastatin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE


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[PMID]:28617705
[Au] Autor:Xu J; Feng YW; Liu L; Wang W; Zhong XX; Wei XH; Liu XG
[Ad] Endereço:From the Department of Physiology and Pain Research Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, People's Republic of China (J.X., Y.-W.F., W.W., X.-X.Z., X.-H.W., X.-G.L.); Guangdong Provincial Key Laboratory of Brain Function and Disease, Guangzhou, Guangdong, People's Republic of China (X.-H.W., X.-G.L.); and Department of Anesthesiology, Guangzhou Hospital of Traditional Chinese Medicine, Guangzhou, Guangdong, People's Republic of China (L.L.).
[Ti] Título:Liver X Receptor α Is Involved in Counteracting Mechanical Allodynia by Inhibiting Neuroinflammation in the Spinal Dorsal Horn.
[So] Source:Anesthesiology;127(3):534-547, 2017 Sep.
[Is] ISSN:1528-1175
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Liver X receptors, including α and ß isoforms, are ligand-activated transcription factors. Whether liver X receptor α plays a role in neuropathic pain is unknown. METHODS: A spared nerve injury model was established in adult male rats and mice. Von Frey tests were performed to evaluate the neuropathic pain behavior; Western blot and immunohistochemistry were performed to understand the underlying mechanisms. RESULTS: Intrathecal injection of a specific liver X receptor agonist T0901317 or GW3965 could either prevent the development of mechanical allodynia or alleviate the established mechanical allodynia, both in rats and wild-type mice. GW3965 could inhibit the activation of glial cells and the expression of tumor necrosis factor-α (mean ± SD: 196 ± 48 vs. 119 ± 57; n = 6; P < 0.01) and interleukin 1ß (mean ± SD: 215 ± 69 vs. 158 ± 74; n = 6; P < 0.01) and increase the expression of interleukin 10 in the spinal dorsal horn. All of the above effects of GW3965 could be abolished by liver X receptor α mutation. Moreover, more glial cells were activated, and more interleukin 1ß was released in the spinal dorsal horn in liver X receptor α knockout mice than in wild-type mice after spared nerve injury. Aminoglutethimide, a neurosteroid synthesis inhibitor, blocked the inhibitory effect of T0901317 on mechanical allodynia, on the activation of glial cells, and on the expression of cytokines. CONCLUSIONS: Activation of liver X receptor α inhibits mechanical allodynia by inhibiting the activation of glial cells and rebalancing cytokines in the spinal dorsal horn via neurosteroids.
[Mh] Termos MeSH primário: Hiperalgesia/prevenção & controle
Inflamação/prevenção & controle
Receptores X do Fígado/metabolismo
Neuralgia/prevenção & controle
Corno Dorsal da Medula Espinal/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Citocinas
Modelos Animais de Doenças
Imuno-Histoquímica
Interleucina-1beta/metabolismo
Masculino
Camundongos
Camundongos Knockout
Neuroglia/metabolismo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukin-1beta); 0 (Liver X Receptors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1097/ALN.0000000000001718


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[PMID]:28570125
[Au] Autor:Zhang E; Kim JJ; Shin N; Yin Y; Nan Y; Xu Y; Hong J; Hsu TM; Chung W; Ko Y; Lee W; Lim K; Kim DW; Lee SY
[Ad] Endereço:1 Department of Anatomy, Medical Science, Brain Research Institute, Chungnam National University School of Medicine , Daejeon, South Korea .
[Ti] Título:High Omega-3 Polyunsaturated Fatty Acids in fat-1 Mice Reduce Inflammatory Pain.
[So] Source:J Med Food;20(6):535-541, 2017 Jun.
[Is] ISSN:1557-7600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Omega-3 and omega-6 polyunsaturated fatty acids (PUFAs), such as α-linolenic and linoleic acids, are essential fatty acids in mammals, because they cannot be synthesized de novo. However, fat-1 transgenic mice can synthesize omega-3 PUFAs from omega-6 PUFAs without dietary supplementation of omega-3, leading to abundant omega-3 PUFA accumulation in various tissues. In this study, we used fat-1 transgenic mice to investigate the role of omega-3 PUFAs in response to inflammatory pain. A high omega-3 PUFA tissue content attenuated formalin-induced pain sensitivity, microglial activation, inducible nitric oxide synthase expression, and the phosphorylation of NR2B, a subunit of the N-methyl-d-aspartate (NMDA) receptor. Our findings suggest that elevated omega-3 PUFA levels inhibit NMDA receptor activity in the spinal dorsal horn and modulate inflammatory pain transmission by regulating signal transmission at the spinal dorsal horn, leading to the attenuation of chemically induced inflammatory pain.
[Mh] Termos MeSH primário: Ácidos Graxos Ômega-3/administração & dosagem
Dor/tratamento farmacológico
Dor/imunologia
[Mh] Termos MeSH secundário: Animais
Suplementos Nutricionais/análise
Ácidos Graxos Ômega-6/administração & dosagem
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
N-Metilaspartato/metabolismo
Receptores de N-Metil-D-Aspartato/imunologia
Corno Dorsal da Medula Espinal/efeitos dos fármacos
Corno Dorsal da Medula Espinal/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids, Omega-3); 0 (Fatty Acids, Omega-6); 0 (Receptors, N-Methyl-D-Aspartate); 6384-92-5 (N-Methylaspartate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE
[do] DOI:10.1089/jmf.2016.3871


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[PMID]:28542572
[Au] Autor:Banno T; Omura T; Masaki N; Arima H; Xu D; Okamoto A; Costigan M; Latremoliere A; Matsuyama Y; Setou M
[Ad] Endereço:Department of Orthopaedic Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan.
[Ti] Título:Arachidonic acid containing phosphatidylcholine increases due to microglial activation in ipsilateral spinal dorsal horn following spared sciatic nerve injury.
[So] Source:PLoS One;12(5):e0177595, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peripheral nerve injury induces substantial molecular changes in the somatosensory system that leads to maladaptive plasticity and cause neuropathic pain. Understanding the molecular pathways responsible for the development of neuropathic pain is essential to the development of novel rationally designed therapeutics. Although lipids make up to half of the dry weight of the spinal cord, their relation with the development of neuropathic pain is poorly understood. We aimed to elucidate the regulation of spinal lipids in response to neuropathic peripheral nerve injury in mice by utilizing matrix-assisted laser desorption/ionization imaging mass spectrometry, which allows visualization of lipid distribution within the cord. We found that arachidonic acid (AA) containing [PC(diacyl-16:0/20:4)+K]+ was increased temporarily at superficial ipsilateral dorsal horn seven days after spared nerve injury (SNI). The spatiotemporal changes in lipid concentration resembled microglia activation as defined by ionized calcium binding adaptor molecule 1 (Iba1) immunohistochemistry. Suppression of microglial function through minocycline administration resulted in attenuation of hypersensitivity and reduces [PC(diacyl-16:0/20:4)+K]+ elevation in the spinal dorsal horn. These data suggested that AA containing [PC(diacyl-16:0/20:4)+K]+ is related to hypersensitivity evoked by SNI and implicate microglial cell activation in this lipid production.
[Mh] Termos MeSH primário: Ácido Araquidônico/metabolismo
Microglia/metabolismo
Fosfatidilcolinas/metabolismo
Nervo Isquiático/lesões
Corno Dorsal da Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas de Ligação ao Cálcio/metabolismo
Metabolismo dos Lipídeos/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteínas dos Microfilamentos/metabolismo
Microglia/efeitos dos fármacos
Minociclina/farmacologia
Neuralgia/etiologia
Neuralgia/metabolismo
Espectrometria de Massas por Ionização e Dessorção a Laser Assistida por Matriz
Corno Dorsal da Medula Espinal/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, mouse); 0 (Calcium-Binding Proteins); 0 (Microfilament Proteins); 0 (Phosphatidylcholines); 27YG812J1I (Arachidonic Acid); FYY3R43WGO (Minocycline)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177595


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[PMID]:28542001
[Au] Autor:Ohashi N; Uta D; Sasaki M; Ohashi M; Kamiya Y; Kohno T
[Ad] Endereço:Division of Anesthesiology (N.O., T.K.) and Division of Orthopedic Surgery, Department of Regenerative and Transplant Medicine (M.O.), Niigata University Graduate School of Medical and Dental Sciences, Niigata City, Japan; Department of Applied Pharmacology, Toyama University Graduate School of Medicine and Pharmaceutical Sciences, Toyama City, Japan (D.U.); and Division of Anesthesiology, Niigata University Medical and Dental Hospital, Uonuma Institute of Community Medicine, Minami-Uonuma City, Japan (M.S., Y.K.).
[Ti] Título:Acetaminophen Metabolite N-Acylphenolamine Induces Analgesia via Transient Receptor Potential Vanilloid 1 Receptors Expressed on the Primary Afferent Terminals of C-fibers in the Spinal Dorsal Horn.
[So] Source:Anesthesiology;127(2):355-371, 2017 Aug.
[Is] ISSN:1528-1175
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The widely used analgesic acetaminophen is metabolized to N-acylphenolamine, which induces analgesia by acting directly on transient receptor potential vanilloid 1 or cannabinoid 1 receptors in the brain. Although these receptors are also abundant in the spinal cord, no previous studies have reported analgesic effects of acetaminophen or N-acylphenolamine mediated by the spinal cord dorsal horn. We hypothesized that clinical doses of acetaminophen induce analgesia via these spinal mechanisms. METHODS: We assessed our hypothesis in a rat model using behavioral measures. We also used in vivo and in vitro whole cell patch-clamp recordings of dorsal horn neurons to assess excitatory synaptic transmission. RESULTS: Intravenous acetaminophen decreased peripheral pinch-induced excitatory responses in the dorsal horn (53.1 ± 20.7% of control; n = 10; P < 0.01), while direct application of acetaminophen to the dorsal horn did not reduce these responses. Direct application of N-acylphenolamine decreased the amplitudes of monosynaptic excitatory postsynaptic currents evoked by C-fiber stimulation (control, 462.5 ± 197.5 pA; N-acylphenolamine, 272.5 ± 134.5 pA; n = 10; P = 0.022) but not those evoked by stimulation of Aδ-fibers. These phenomena were mediated by transient receptor potential vanilloid 1 receptors, but not cannabinoid 1 receptors. The analgesic effects of acetaminophen and N-acylphenolamine were stronger in rats experiencing an inflammatory pain model compared to naïve rats. CONCLUSIONS: Our results suggest that the acetaminophen metabolite N-acylphenolamine induces analgesia directly via transient receptor potential vanilloid 1 receptors expressed on central terminals of C-fibers in the spinal dorsal horn and leads to conduction block, shunt currents, and desensitization of these fibers.
[Mh] Termos MeSH primário: Acetaminofen/farmacologia
Analgesia/métodos
Neurônios Aferentes/efeitos dos fármacos
Dor/prevenção & controle
Corno Dorsal da Medula Espinal/efeitos dos fármacos
Canais de Cátion TRPV/efeitos dos fármacos
[Mh] Termos MeSH secundário: Analgésicos não Entorpecentes/farmacologia
Animais
Modelos Animais de Doenças
Masculino
Fibras Nervosas Amielínicas/efeitos dos fármacos
Ratos
Ratos Wistar
Canais de Cátion TRPV/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics, Non-Narcotic); 0 (TRPV Cation Channels); 0 (Trpv1 protein, rat); 362O9ITL9D (Acetaminophen)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1097/ALN.0000000000001700


  9 / 268 MEDLINE  
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[PMID]:28535564
[Au] Autor:Gao Z; Feng Y; Ju H
[Ad] Endereço:Peking University People's Hospital & Peking University International Hospital, Beijing, China.
[Ti] Título:The Different Dynamic Changes of Nerve Growth Factor in the Dorsal Horn and Dorsal Root Ganglion Leads to Hyperalgesia and Allodynia in Diabetic Neuropathic Pain.
[So] Source:Pain Physician;20(4):E551-E561, 2017 May.
[Is] ISSN:2150-1149
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Diabetic peripheral neuropathy (DPN) is the most common complication of diabetes and more than half of the patients with DPN have self-reported symptoms referring to painful diabetic neuropathy (PDN). Nerve growth factor (NGF) is a key factor for the nervous system, but the role of it in the neuropathic pain of diabetic patients is unclear. OBJECTIVE: This study aimed to investigate the relationship between the dynamic expression of NGF in dorsal horn and dorsal root ganglion (DRG) of diabetic rats and hyperalgesia and allodynia in diabetic neuropathic pain. It also aimed to explore the effects of exogenous mouse NGF (mNGF) on NGF expression in dorsal horn, DRG, and mechanical pain threshold. STUDY DESIGN: Animal research study. SETTING: Experimental research laboratory. METHODS: The model of diabetes was established by a single intraperitoneal injection of streptozocin (STZ 55 mg/kg). Firstly, the rats were randomly divided into 2 groups: control group (n = 10) and diabetes group (n = 40). The diabetes group contained 4 subgroups: diabetes week 1 group (DM1, n = 10), diabetes week 2 group (DM2, n = 10), diabetes week 4 group (DM4, n = 10), and diabetes week 8 group (DM8, n = 10). Then, the other rats were randomly divided into 2 groups: control group (n = 10) and treatment group (n = 30). The treatment group contained 3 subgroups: saline group (n = 10), low dose mNGF group (mNGF1, n = 10), and high dose mNGF group (mNGF2, n = 10). Mechanical pain threshold was assessed using Von Frey hairs, before the establishment of the diabetes model and 1, 2, 4, and 8 weeks after the establishment. The NGF expression in dorsal horn and DRG was measured by western blot. RESULTS: The mechanical pain threshold decreased one week after the establishment of the diabetes model, which continued for 8 weeks. The NGF expression in the dorsal horn was reduced 2 weeks after diabetes induction and the decreased NGF expression continued for 4 weeks. However, the NGF expression in DRG was reduced one week after diabetes induction and remained at a low level for 8 weeks. Hyperalgesia occurred when the NGF expression in the DRG decreased and further reduction in the NGF expression in the dorsal horn caused concomitant allodynia. The mechanical pain threshold was significantly elevated 2 weeks after mNGF treatment. LIMITATIONS: The course of diabetes should be much longer and there is not a precise analysis of the quantitative relation between the NGF expression in the dorsal horn/DRG and hyperalgesia/allodynia. CONCLUSION: In diabetic neuropathic pain, the dynamic changes of the NGF expression in dorsal horn and DRG is involved in the development of hyperalgesia and allodynia respectively. Exogenous mNGF may relieve diabetic neuropathic pain by increasing the NGF expression in dorsal horn and DRG.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/complicações
Gânglios Espinais/metabolismo
Hiperalgesia/etiologia
Fator de Crescimento Neural/metabolismo
Neuralgia/etiologia
Corno Dorsal da Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Hiperalgesia/metabolismo
Camundongos
Fator de Crescimento Neural/farmacologia
Neuralgia/metabolismo
Limiar da Dor
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
9061-61-4 (Nerve Growth Factor)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE


  10 / 268 MEDLINE  
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[PMID]:28385947
[Au] Autor:Tamai K; Suzuki A; Takahashi S; Akhgar J; Rahmani MS; Hayashi K; Ohyama S; Nakamura H
[Ad] Endereço:Osaka City University Graduate School of Medicine, 1-5-7, Asahimachi, Abenoku, Osaka 545-8585, Japan.
[Ti] Título:The incidence of nerve root injury by high-speed drill can be reduced by chilled saline irrigation in a rabbit model.
[So] Source:Bone Joint J;99-B(4):554-560, 2017 Apr.
[Is] ISSN:2049-4408
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIMS: We aimed to evaluate the temperature around the nerve root during drilling of the lamina and to determine whether irrigation during drilling can reduce the chance of nerve root injury. MATERIALS AND METHODS: Lumbar nerve roots were exposed to frictional heat by high-speed drilling of the lamina in a live rabbit model, with saline (room temperature (RT) or chilled saline) or without saline (control) irrigation. We measured temperatures surrounding the nerve root and made histological evaluations. RESULTS: In the control group, the mean temperature around the nerve root was 52.0°C (38.0°C to 75.5°C) after 60 seconds of drilling, and nerve root injuries were found in one out of 13 (7.7%) immediately, three out of 14 (21.4%) at three days, and 11 out of 25 (44.0%) at seven days post-operatively. While the RT group showed a significantly lower temperature around the nerve root compared with the control group (mean 46.5°C; 34.5°C to 66.9°C, p < 0.001), RT saline failed to significantly reduce the incidence of nerve root injury (ten out of 26; 38.5%; odds ratio (OR) 0.96; 95% confidence interval (CI) 0.516 to 1.785; p = 0.563). However, chilled saline irrigation resulted in a significantly lower temperature than the control group (mean 39.0°C; 35.3°C to 52.3°C; p < 0.001) and a lower rate of nerve root injury (two out of 21; 9.5%, OR 0.13; 95% CI 0.02 to 0.703, p = 0.010). CONCLUSION: Frictional heat caused by a high-speed drill can cause histological nerve root injury. Chilled saline irrigation had a more prominent effect than RT in reducing the incidence of the thermal injury during extended drilling. Cite this article: 2017;99-B:554-60.
[Mh] Termos MeSH primário: Laminectomia/efeitos adversos
Traumatismos dos Nervos Periféricos/prevenção & controle
Corno Dorsal da Medula Espinal/cirurgia
Raízes Nervosas Espinhais/lesões
Irrigação Terapêutica/métodos
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Hipotermia Induzida/métodos
Laminectomia/instrumentação
Laminectomia/métodos
Masculino
Traumatismos dos Nervos Periféricos/etiologia
Traumatismos dos Nervos Periféricos/patologia
Coelhos
Corno Dorsal da Medula Espinal/patologia
Raízes Nervosas Espinhais/patologia
Temperatura Ambiente
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170408
[St] Status:MEDLINE
[do] DOI:10.1302/0301-620X.99B4.BJJ-2016-0841.R1



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