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[PMID]:29184209
[Au] Autor:Rodriguez E; Sakurai K; Xu J; Chen Y; Toda K; Zhao S; Han BX; Ryu D; Yin H; Liedtke W; Wang F
[Ad] Endereço:Department of Neurobiology, Duke University Medical Center, Durham, NC, USA.
[Ti] Título:A craniofacial-specific monosynaptic circuit enables heightened affective pain.
[So] Source:Nat Neurosci;20(12):1734-1743, 2017 Dec.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Humans often rank craniofacial pain as more severe than body pain. Evidence suggests that a stimulus of the same intensity induces stronger pain in the face than in the body. However, the underlying neural circuitry for the differential processing of facial versus bodily pain remains unknown. Interestingly, the lateral parabrachial nucleus (PB ), a critical node in the affective pain circuit, is activated more strongly by noxious stimulation of the face than of the hindpaw. Using a novel activity-dependent technology called CANE developed in our laboratory, we identified and selectively labeled noxious-stimulus-activated PB neurons and performed comprehensive anatomical input-output mapping. Surprisingly, we uncovered a hitherto uncharacterized monosynaptic connection between cranial sensory neurons and the PB -nociceptive neurons. Optogenetic activation of this monosynaptic craniofacial-to-PB projection induced robust escape and avoidance behaviors and stress calls, whereas optogenetic silencing specifically reduced facial nociception. The monosynaptic circuit revealed here provides a neural substrate for heightened craniofacial affective pain.
[Mh] Termos MeSH primário: Dor Facial/fisiopatologia
Dor Facial/psicologia
Nociceptores
Sinapses
[Mh] Termos MeSH secundário: Afeto
Vias Aferentes/fisiopatologia
Animais
Comportamento Animal
Condicionamento Operante
Feminino
Genes fos/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Optogenética
Estimulação Física
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1038/s41593-017-0012-1


  2 / 10602 MEDLINE  
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[PMID]:28977586
[Au] Autor:Payrits M; Sághy É; Cseko K; Pohóczky K; Bölcskei K; Ernszt D; Barabás K; Szolcsányi J; Ábrahám IM; Helyes Z; Szoke É
[Ad] Endereço:Department of Pharmacology and Pharmacotherapy, University of Pécs Medical School, H-7624 Pécs, Hungary.
[Ti] Título:Estradiol Sensitizes the Transient Receptor Potential Vanilloid 1 Receptor in Pain Responses.
[So] Source:Endocrinology;158(10):3249-3258, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sex differences exist in chronic pain pathologies, and gonadal estradiol (E2) alters the pain sensation. The nocisensor transient receptor potential vanilloid 1 (TRPV1) receptor plays a critical role in triggering pain. Here we examined the impact of E2 on the function of TRPV1 receptor in mice sensory neurons in vitro and in vivo. Both mechano- and thermonociceptive thresholds of the plantar surface of the paw of female mice were significantly lower in proestrus compared with the estrus phase. These thresholds were higher in ovariectomized (OVX) mice and significantly lower in sham-operated mice in proestrus compared with the sham-operated mice in estrus phase. This difference was absent in TRPV1 receptor-deficient mice. Furthermore, E2 potentiated the TRPV1 receptor activation-induced mechanical hyperalgesia in OVX mice. Long pretreatment (14 hours) with E2 induced a significant increase in TRPV1 receptor messenger RNA expression and abolished the capsaicin-induced TRPV1 receptor desensitization in primary sensory neurons. The short E2 incubation (10 minutes) also prevented the desensitization, which reverted after coadministration of E2 and the tropomyosin-related kinase A (TrkA) receptor inhibitor. Our study provides in vivo and in vitro evidence for E2-induced TRPV1 receptor upregulation and sensitization mediated by TrkAR via E2-induced genomic and nongenomic mechanisms. The sensitization and upregulation of TRPV1 receptor by E2 in sensory neurons may explain the greater pain sensitivity in female mice.
[Mh] Termos MeSH primário: Estradiol/farmacologia
Dor/fisiopatologia
Canais de Cátion TRPV/efeitos dos fármacos
Canais de Cátion TRPV/fisiologia
[Mh] Termos MeSH secundário: Animais
Capsaicina/farmacologia
Células Cultivadas
Tolerância a Medicamentos
Estro/fisiologia
Feminino
Expressão Gênica/efeitos dos fármacos
Temperatura Alta
Masculino
Mecanorreceptores/efeitos dos fármacos
Mecanorreceptores/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Nociceptores/efeitos dos fármacos
Nociceptores/fisiologia
Ovariectomia
Proestro/fisiologia
RNA Mensageiro/análise
Células Receptoras Sensoriais/química
Células Receptoras Sensoriais/fisiologia
Caracteres Sexuais
Canais de Cátion TRPV/genética
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (TRPV Cation Channels); 0 (TRPV1 receptor); 4TI98Z838E (Estradiol); S07O44R1ZM (Capsaicin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00101


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[PMID]:28972120
[Au] Autor:Melo-Carrillo A; Strassman AM; Nir RR; Schain AJ; Noseda R; Stratton J; Burstein R
[Ad] Endereço:Department of Anesthesia, Critical Care & Pain Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215.
[Ti] Título:Fremanezumab-A Humanized Monoclonal Anti-CGRP Antibody-Inhibits Thinly Myelinated (Aδ) But Not Unmyelinated (C) Meningeal Nociceptors.
[So] Source:J Neurosci;37(44):10587-10596, 2017 Nov 01.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Calcitonin gene-related peptide (CGRP), the most abundant neuropeptide in primary afferent sensory neurons, is strongly implicated in the pathophysiology of migraine headache, but its role in migraine is still equivocal. As a new approach to migraine treatment, humanized anti-CGRP monoclonal antibodies (CGRP-mAbs) were developed to reduce the availability of CGRP, and were found effective in reducing the frequency of chronic and episodic migraine. We recently tested the effect of fremanezumab (TEV-48125), a CGRP-mAb, on the activity of second-order trigeminovascular dorsal horn neurons that receive peripheral input from the cranial dura, and found a selective inhibition of high-threshold but not wide-dynamic range class of neurons. To investigate the basis for this selective inhibitory effect, and further explore the mechanism of action of CGRP-mAbs, we tested the effect of fremanezumab on the cortical spreading depression-evoked activation of mechanosensitive primary afferent meningeal nociceptors that innervate the cranial dura, using single-unit recording in the trigeminal ganglion of anesthetized male rats. Fremanezumab pretreatment selectively inhibited the responsiveness of Aδ neurons, but not C-fiber neurons, as reflected in a decrease in the percentage of neurons that showed activation by cortical spreading depression. These findings identify Aδ meningeal nociceptors as a likely site of action of fremanezumab in the prevention of headache. The selectivity in its peripheral inhibitory action may partly account for fremanezumab's selective inhibition of high-threshold, as a result of a predominant A-δ input to high-threshold neurons, but not wide dynamic-range dorsal horn neurons, and why it may not be effective in all migraine patients. Recently, we reported that humanized CGRP monoclonal antibodies (CGRP-mAbs) prevent activation and sensitization of high-threshold (HT) but not wide-dynamic range trigeminovascular neurons by cortical spreading depression (CSD). In the current paper, we report that CGRP-mAbs prevent the activation of Aδ but not C-type meningeal nociceptors by CSD. This is the first identification of an anti-migraine drug that appears to be selective for Aδ-fibers (peripherally) and HT neurons (centrally). As the main CGRP-mAb site of action appears to be situated outside the brain, we conclude that the initiation of the headache phase of migraine depends on activation of meningeal nociceptors, and that for selected patients, activation of the Aδ-HT pain pathway may be sufficient for the generation of headache perception.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Peptídeo Relacionado com Gene de Calcitonina/antagonistas & inibidores
Bainha de Mielina/efeitos dos fármacos
Fibras Nervosas Mielinizadas/efeitos dos fármacos
Fibras Nervosas Amielínicas/efeitos dos fármacos
Nociceptores/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Peptídeo Relacionado com Gene de Calcitonina/fisiologia
Seres Humanos
Masculino
Bainha de Mielina/fisiologia
Fibras Nervosas Mielinizadas/fisiologia
Fibras Nervosas Amielínicas/fisiologia
Nociceptores/fisiologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (TEV-48125); 83652-28-2 (Calcitonin Gene-Related Peptide)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2211-17.2017


  4 / 10602 MEDLINE  
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[PMID]:28855331
[Au] Autor:Follansbee TL; Gjelsvik KJ; Brann CL; McParland AL; Longhurst CA; Galko MJ; Ganter GK
[Ad] Endereço:Department of Biology, College of Arts and Sciences, University of New England, Biddeford, Maine 04005.
[Ti] Título: Nociceptive Sensitization Requires BMP Signaling via the Canonical SMAD Pathway.
[So] Source:J Neurosci;37(35):8524-8533, 2017 Aug 30.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nociceptive sensitization is a common feature in chronic pain, but its basic cellular mechanisms are only partially understood. The present study used the model system and a candidate gene approach to identify novel components required for modulation of an injury-induced nociceptive sensitization pathway presumably downstream of Hedgehog. This study demonstrates that RNAi silencing of a member of the Bone Morphogenetic Protein (BMP) signaling pathway, Decapentaplegic (Dpp), specifically in the Class IV multidendritic nociceptive neuron, significantly attenuated ultraviolet injury-induced sensitization. Furthermore, overexpression of Dpp in Class IV neurons was sufficient to induce thermal hypersensitivity in the absence of injury. The requirement of various BMP receptors and members of the SMAD signal transduction pathway in nociceptive sensitization was also demonstrated. The effects of BMP signaling were shown to be largely specific to the sensitization pathway and not associated with changes in nociception in the absence of injury or with changes in dendritic morphology. Thus, the results demonstrate that Dpp and its pathway play a crucial and novel role in nociceptive sensitization. Because the BMP family is so strongly conserved between vertebrates and invertebrates, it seems likely that the components analyzed in this study represent potential therapeutic targets for the treatment of chronic pain in humans. This report provides a genetic analysis of primary nociceptive neuron mechanisms that promote sensitization in response to injury. larvae whose primary nociceptive neurons were reduced in levels of specific components of the BMP signaling pathway, were injured and then tested for nocifensive responses to a normally subnoxious stimulus. Results suggest that nociceptive neurons use the BMP2/4 ligand, along with identified receptors and intracellular transducers to transition to a sensitized state. These findings are consistent with the observation that BMP receptor hyperactivation correlates with bone abnormalities and pain sensitization in fibrodysplasia ossificans progressiva (Kitterman et al., 2012). Because nociceptive sensitization is associated with chronic pain, these findings indicate that human BMP pathway components may represent targets for novel pain-relieving drugs.
[Mh] Termos MeSH primário: Proteínas Morfogenéticas Ósseas/metabolismo
Sensibilização do Sistema Nervoso Central/fisiologia
Proteínas de Drosophila/metabolismo
Drosophila/fisiologia
Nociceptividade/fisiologia
Nociceptores/fisiologia
Proteínas Smad/metabolismo
[Mh] Termos MeSH secundário: Animais
Limiar da Dor/fisiologia
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Drosophila Proteins); 0 (Smad Proteins); 0 (dpp protein, Drosophila)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3458-16.2017


  5 / 10602 MEDLINE  
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[PMID]:28817806
[Au] Autor:Ghitani N; Barik A; Szczot M; Thompson JH; Li C; Le Pichon CE; Krashes MJ; Chesler AT
[Ad] Endereço:National Center for Complementary and Integrative Health (NCCIH), National Institutes of Health (NIH), Bethesda MD, USA.
[Ti] Título:Specialized Mechanosensory Nociceptors Mediating Rapid Responses to Hair Pull.
[So] Source:Neuron;95(4):944-954.e4, 2017 Aug 16.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The somatosensory system provides animals with the ability to detect, distinguish, and respond to diverse thermal, mechanical, and irritating stimuli. While there has been progress in defining classes of neurons underlying temperature sensation and gentle touch, less is known about the neurons specific for mechanical pain. Here, we use in vivo functional imaging to identify a class of cutaneous sensory neurons that are selectively activated by high-threshold mechanical stimulation (HTMRs). We show that their optogenetic excitation evokes rapid protective and avoidance behaviors. Unlike other nociceptors, these HTMRs are fast-conducting Aδ-fibers with highly specialized circumferential endings wrapping the base of individual hair follicles. Notably, we find that Aδ-HTMRs innervate unique but overlapping fields and can be activated by stimuli as precise as the pulling of a single hair. Together, the distinctive features of this class of Aδ-HTMRs appear optimized for accurate and rapid localization of mechanical pain. VIDEO ABSTRACT.
[Mh] Termos MeSH primário: Vias Aferentes/fisiologia
Cabelo
Mecanorreceptores/fisiologia
Nociceptores/fisiologia
Células Receptoras Sensoriais/fisiologia
Tato/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Potenciais de Ação/fisiologia
Animais
Antineoplásicos Hormonais/farmacologia
Peptídeo Relacionado com Gene de Calcitonina/genética
Peptídeo Relacionado com Gene de Calcitonina/metabolismo
Channelrhodopsins
Diterpenos/farmacologia
Feminino
Cabelo/fisiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Neurotoxinas/farmacologia
Pele/inervação
Canais de Cátion TRPV/genética
Canais de Cátion TRPV/metabolismo
Tamoxifeno/farmacologia
Gânglio Trigeminal/diagnóstico por imagem
Gânglio Trigeminal/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (Calca protein, mouse); 0 (Channelrhodopsins); 0 (Diterpenes); 0 (Neurotoxins); 0 (TRPV Cation Channels); 0 (TRPV1 protein, mouse); 094ZI81Y45 (Tamoxifen); 83652-28-2 (Calcitonin Gene-Related Peptide); A5O6P1UL4I (resiniferatoxin)
[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:170818
[St] Status:MEDLINE


  6 / 10602 MEDLINE  
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[PMID]:28734788
[Au] Autor:Taha O; Opitz T; Mueller M; Pitsch J; Becker A; Evert BO; Beck H; Jeub M
[Ad] Endereço:Department of Neurology, University of Bonn Medical Center, Sigmund Freud Straße 25, 53105 Bonn, Germany; Department of Epileptology, University of Bonn Medical Center, Sigmund Freud Straße 25, 53105 Bonn, Germany.
[Ti] Título:Neuropathic pain in experimental autoimmune neuritis is associated with altered electrophysiological properties of nociceptive DRG neurons.
[So] Source:Exp Neurol;297:25-35, 2017 Nov.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Guillain-Barré syndrome (GBS) is an acute, immune-mediated polyradiculoneuropathy characterized by rapidly progressive paresis and sensory disturbances. Moderate to severe and often intractable neuropathic pain is a common symptom of GBS, but its underlying mechanisms are unknown. Pathology of GBS is classically attributed to demyelination of large, myelinated peripheral fibers. However, there is increasing evidence that neuropathic pain in GBS is associated with impaired function of small, unmyelinated, nociceptive fibers. We therefore examined the functional properties of small DRG neurons, the somata of nociceptive fibers, in a rat model of GBS (experimental autoimmune neuritis=EAN). EAN rats developed behavioral signs of neuropathic pain. This was accompanied by a significant shortening of action potentials due to a more rapid repolarization and an increase in repetitive firing in a subgroup of capsaicin-responsive DRG neurons. Na current measurements revealed a significant increase of the fast TTX-sensitive current and a reduction of the persistent TTX-sensitive current component. These changes of Na currents may account for the significant decrease in AP duration leading to an overall increase in excitability and are therefore possibly directly linked to pathological pain behavior. Thus, like in other animal models of neuropathic and inflammatory pain, Na channels seem to be crucially involved in the pathology of GBS and may constitute promising targets for pain modulating pharmaceuticals.
[Mh] Termos MeSH primário: Gânglios Espinais/fisiopatologia
Neuralgia/fisiopatologia
Neurite Autoimune Experimental/fisiopatologia
Nociceptores/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Fenômenos Eletrofisiológicos/fisiologia
Gânglios Espinais/patologia
Masculino
Neuralgia/patologia
Neurite Autoimune Experimental/patologia
Nociceptores/patologia
Medição da Dor/métodos
Ratos
Ratos Endogâmicos Lew
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170724
[St] Status:MEDLINE


  7 / 10602 MEDLINE  
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[PMID]:28712652
[Au] Autor:Kaneko T; Macara AM; Li R; Hu Y; Iwasaki K; Dunnings Z; Firestone E; Horvatic S; Guntur A; Shafer OT; Yang CH; Zhou J; Ye B
[Ad] Endereço:Life Sciences Institute and Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
[Ti] Título:Serotonergic Modulation Enables Pathway-Specific Plasticity in a Developing Sensory Circuit in Drosophila.
[So] Source:Neuron;95(3):623-638.e4, 2017 Aug 02.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:How experiences during development cause long-lasting changes in sensory circuits and affect behavior in mature animals are poorly understood. Here we establish a novel system for mechanistic analysis of the plasticity of developing neural circuits by showing that sensory experience during development alters nociceptive behavior and circuit physiology in Drosophila larvae. Despite the convergence of nociceptive and mechanosensory inputs on common second-order neurons (SONs), developmental noxious input modifies transmission from nociceptors to their SONs, but not from mechanosensors to the same SONs, which suggests striking sensory pathway specificity. These SONs activate serotonergic neurons to inhibit nociceptor-to-SON transmission; stimulation of nociceptors during development sensitizes nociceptor presynapses to this feedback inhibition. Our results demonstrate that, unlike associative learning, which involves inputs from two sensory pathways, sensory pathway-specific plasticity in the Drosophila nociceptive circuit is in part established through feedback modulation. This study elucidates a novel mechanism that enables pathway-specific plasticity in sensory systems. VIDEO ABSTRACT.
[Mh] Termos MeSH primário: Vias Aferentes/fisiologia
Comportamento Animal/fisiologia
Rede Nervosa/crescimento & desenvolvimento
Plasticidade Neuronal/fisiologia
Nociceptores/metabolismo
Neurônios Serotoninérgicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Drosophila melanogaster
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE


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[PMID]:28642283
[Au] Autor:Melo-Carrillo A; Noseda R; Nir RR; Schain AJ; Stratton J; Strassman AM; Burstein R
[Ad] Endereço:Department of Anesthesia, Critical Care, and Pain Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215.
[Ti] Título:Selective Inhibition of Trigeminovascular Neurons by Fremanezumab: A Humanized Monoclonal Anti-CGRP Antibody.
[So] Source:J Neurosci;37(30):7149-7163, 2017 07 26.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A large body of evidence supports an important role for calcitonin gene-related peptide (CGRP) in migraine pathophysiology. This evidence gave rise to a global effort to develop a new generation of therapeutics that inhibit the interaction of CGRP with its receptor in migraineurs. Recently, a new class of such drugs, humanized anti-CGRP monoclonal antibodies (CGRP-mAbs), were found to be effective in reducing the frequency of migraine. The purpose of this study was to better understand how the CGRP-mAb fremanezumab (TEV-48125) modulates meningeal sensory pathways. To answer this question, we used single-unit recording to determine the effects of fremanezumab (30 mg/kg, IV) and its isotype control Ab on spontaneous and evoked activity in naive and cortical spreading depression (CSD)-sensitized trigeminovascular neurons in the spinal trigeminal nucleus of anesthetized male and female rats. The study demonstrates that, in both sexes, fremanezumab inhibited naive high-threshold (HT) neurons, but not wide-dynamic range trigeminovascular neurons, and that the inhibitory effects on the neurons were limited to their activation from the intracranial dura but not facial skin or cornea. In addition, when given sufficient time, fremanezumab prevents the activation and sensitization of HT neurons by CSD. Mechanistically, these findings suggest that HT neurons play a critical role in the initiation of the perception of headache and the development of cutaneous allodynia and central sensitization. Clinically, the findings may help to explain the therapeutic benefit of CGRP-mAb in reducing headaches of intracranial origin such as migraine with aura and why this therapeutic approach may not be effective for every migraine patient. Calcitonin gene-related peptide (CGRP) monoclonal antibodies (CGRP-mAbs) are capable of preventing migraine. However, their mechanism of action is unknown. In the current study, we show that, if given enough time, a CGRP-mAb can prevent the activation and sensitization of high-threshold (central) trigeminovascular neurons by cortical spreading depression, but not their activation from the skin or cornea, suggesting a potential explanation for selectivity to migraine headache, but not other pains, and a predominantly peripheral site of action.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/imunologia
Peptídeo Relacionado com Gene de Calcitonina/imunologia
Acoplamento Neurovascular/fisiologia
Nociceptores/fisiologia
Núcleo Espinal do Trigêmeo/fisiologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/administração & dosagem
Anticorpos Monoclonais/farmacologia
Depressão Alastrante da Atividade Elétrica Cortical/fisiologia
Feminino
Seres Humanos
Masculino
Acoplamento Neurovascular/efeitos dos fármacos
Nociceptores/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Núcleo Espinal do Trigêmeo/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (TEV-48125); 83652-28-2 (Calcitonin Gene-Related Peptide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0576-17.2017


  9 / 10602 MEDLINE  
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[PMID]:28640016
[Au] Autor:Sugiyama D; Kang S; Arpey N; Arunakul P; Usachev YM; Brennan TJ
[Ad] Endereço:From the Departments of Anesthesia (D.S., S.K., N.A., P.A., T.J.B.) and Pharmacology (Y.M.U., T.J.B.), Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa.
[Ti] Título:Hydrogen Peroxide Induces Muscle Nociception via Transient Receptor Potential Ankyrin 1 Receptors.
[So] Source:Anesthesiology;127(4):695-708, 2017 Oct.
[Is] ISSN:1528-1175
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: H2O2 has a variety of actions in skin wounds but has been rarely studied in deep muscle tissue. Based on response to the transient receptor potential ankyrin 1 antagonists after plantar incision, we hypothesized that H2O2 exerts nociceptive effects via the transient receptor potential ankyrin 1 in muscle. METHODS: Nociceptive behaviors in rats (n = 269) and mice (n = 16) were evaluated after various concentrations and volumes of H2O2 were injected into the gastrocnemius muscle or subcutaneous tissue. The effects of H2O2 on in vivo spinal dorsal horn neuronal activity and lumbar dorsal root ganglia neurons in vitro were evaluated from 26 rats and 6 mice. RESULTS: Intramuscular (mean ± SD: 1,436 ± 513 s) but not subcutaneous (40 ± 58 s) injection of H2O2 (100 mM, 0.6 ml) increased nociceptive time. Conditioned place aversion was evident after intramuscular (-143 ± 81 s) but not subcutaneous (-2 ± 111 s) injection of H2O2. These H2O2-induced behaviors were blocked by transient receptor potential ankyrin 1 antagonists. Intramuscular injection of H2O2 caused sustained in vivo activity of dorsal horn neurons, and H2O2 activated a subset of dorsal root ganglia neurons in vitro. Capsaicin nerve block decreased guarding after plantar incision and reduced nociceptive time after intramuscular H2O2. Nociceptive time after intramuscular H2O2 in transient receptor potential ankyrin 1 knockout mice was shorter (173 ± 156 s) compared with wild-type mice (931 ± 629 s). CONCLUSIONS: The greater response of muscle tissue to H2O2 may help explain why incision that includes deep muscle but not skin incision alone produces spontaneous activity in nociceptive pathways.
[Mh] Termos MeSH primário: Peróxido de Hidrogênio/farmacologia
Músculo Esquelético/efeitos dos fármacos
Nociceptividade/efeitos dos fármacos
Canais de Cátion TRPC/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anti-Infecciosos Locais/farmacologia
Modelos Animais de Doenças
Feminino
Gânglios Espinais/efeitos dos fármacos
Masculino
Nociceptores/efeitos dos fármacos
Células do Corno Posterior/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Canal de Cátion TRPA1
Canais de Cátion TRPC/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Infective Agents, Local); 0 (TRPA1 Cation Channel); 0 (TRPC Cation Channels); 0 (Trpa1 protein, rat); BBX060AN9V (Hydrogen Peroxide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1097/ALN.0000000000001756


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[PMID]:28622486
[Au] Autor:Ita ME; Zhang S; Holsgrove TP; Kartha S; Winkelstein BA
[Ti] Título:The Physiological Basis of Cervical Facet-Mediated Persistent Pain: Basic Science and Clinical Challenges.
[So] Source:J Orthop Sports Phys Ther;47(7):450-461, 2017 Jul.
[Is] ISSN:1938-1344
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Synopsis Chronic neck pain is a common condition and a primary clinical symptom of whiplash and other spinal injuries. Loading-induced neck injuries produce abnormal kinematics between the vertebrae, with the potential to injure facet joints and the afferent fibers that innervate the specific joint tissues, including the capsular ligament. Mechanoreceptive and nociceptive afferents that innervate the facet have their peripheral terminals in the capsule, cell bodies in the dorsal root ganglia, and terminal processes in the spinal cord. As such, biomechanical loading of these afferents can initiate nociceptive signaling in the peripheral and central nervous systems. Their activation depends on the local mechanical environment of the joint and encodes the neural processes that initiate pain and lead to its persistence. This commentary reviews the complex anatomical, biomechanical, and physiological consequences of facet-mediated whiplash injury and pain. The clinical presentation of facet-mediated pain is complex in its sensory and emotional components. Yet, human studies are limited in their ability to elucidate the physiological mechanisms by which abnormal facet loading leads to pain. Over the past decade, however, in vivo models of cervical facet injury that reproduce clinical pain symptoms have been developed and used to define the complicated and multifaceted electrophysiological, inflammatory, and nociceptive signaling cascades that are involved in the pathophysiology of whiplash facet pain. Integrating the whiplash-like mechanics in vivo and in vitro allows transmission of pathophysiological mechanisms across scales, with the hope of informing clinical management. Yet, despite these advances, many challenges remain. This commentary further describes and highlights such challenges. J Orthop Sports Phys Ther 2017;47(7):450-461. Epub 16 Jun 2017. doi:10.2519/jospt.2017.7255.
[Mh] Termos MeSH primário: Vértebras Cervicais/fisiopatologia
Lesões do Pescoço/fisiopatologia
Cervicalgia/fisiopatologia
Articulação Zigapofisária/lesões
[Mh] Termos MeSH secundário: Fenômenos Biomecânicos
Dor Crônica
Seres Humanos
Ligamentos Articulares/lesões
Ligamentos Articulares/inervação
Ligamentos Articulares/fisiopatologia
Nociceptores/fisiologia
Entorses e Distensões/fisiopatologia
Pesquisa Médica Translacional
Traumatismos em Chicotada/fisiopatologia
Articulação Zigapofisária/inervação
Articulação Zigapofisária/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.2519/jospt.2017.7255



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