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Pesquisa : A08.186.854.697.500.500 [Categoria DeCS]
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[PMID]:28017670
[Au] Autor:Piao LH; Fujita T; Yu T; Kumamoto E
[Ad] Endereço:Department of Physiology, Saga Medical School, 5-1-1 Nabeshima, Saga 849-8501, Japan.
[Ti] Título:Presynaptic facilitation by tetracaine of glutamatergic spontaneous excitatory transmission in the rat spinal substantia gelatinosa - Involvement of TRPA1 channels.
[So] Source:Brain Res;1657:245-252, 2017 Feb 15.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The amide-type local anesthetic (LA) lidocaine activates transient receptor potential (TRP) ankyrin-1 (TRPA1) channels to facilitate spontaneous l-glutamate release onto spinal substantia gelatinosa (SG) neurons, which play a crucial role in regulating nociceptive transmission. In contrast, the ester-type LA procaine reduces the spontaneous release of l-glutamate in SG neurons. In order to determine whether TRPA1 activation by LAs is specific to amide-types, we examined the actions of tetracaine, another ester-type LA, and other amide-type LAs on glutamatergic spontaneous excitatory transmission in SG neurons by focusing on TRP activation. Whole-cell patch-clamp recordings were performed on SG neurons of adult rat spinal cord slices at a holding potential of -70mV. Bath-applied tetracaine increased spontaneous excitatory postsynaptic current (sEPSC) frequency in a concentration-dependent manner. Tetracaine activity was resistant to the voltage-gated Na -channel blocker tetrodotoxin, the TRP vanilloid-1 antagonist capsazepine, and the TRP melastatin-8 antagonist BCTC, but was inhibited by the non-selective TRP antagonist ruthenium red and the TRPA1 antagonist HC-030031. With respect to amide-type LAs, prilocaine had a tendency to increase sEPSC frequency, while ropivacaine and levobupivacaine reduced the frequency. In conclusion, tetracaine facilitated spontaneous l-glutamate release from nerve terminals by activating TRPA1 channels in the SG, resulting in an increase in the excitability of SG neurons. TRPA1 activation was not specific to amide-type or ester-type LAs. The facilitatory action of LAs may be involved in pain occurring after recovery from spinal anesthesia.
[Mh] Termos MeSH primário: Ácido Glutâmico/metabolismo
Neurotransmissores/farmacologia
Terminações Pré-Sinápticas/efeitos dos fármacos
Substância Gelatinosa/efeitos dos fármacos
Canais de Cátion TRPC/metabolismo
Tetracaína/farmacologia
[Mh] Termos MeSH secundário: Acetanilidas/farmacologia
Amidas/farmacologia
Anestésicos Locais/farmacologia
Animais
Bupivacaína/análogos & derivados
Bupivacaína/farmacologia
Capsaicina/análogos & derivados
Capsaicina/farmacologia
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Potenciais Pós-Sinápticos Excitadores/fisiologia
Masculino
Dor/metabolismo
Técnicas de Patch-Clamp
Terminações Pré-Sinápticas/metabolismo
Prilocaína/farmacologia
Purinas/farmacologia
Pirazinas/farmacologia
Piridinas/farmacologia
Ratos Sprague-Dawley
Rutênio Vermelho/farmacologia
Substância Gelatinosa/metabolismo
Canal de Cátion TRPA1
Tetrodotoxina/farmacologia
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(1,3-dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)-N-(4-isopropylphenyl)acetamide); 0 (Acetanilides); 0 (Amides); 0 (Anesthetics, Local); 0 (N-(4-tert-butylphenyl)-4-(3-chloropyridin-2-yl)tetrahydropyrazine-1(2H)-carboxamide); 0 (Neurotransmitter Agents); 0 (Purines); 0 (Pyrazines); 0 (Pyridines); 0 (TRPA1 Cation Channel); 0 (TRPC Cation Channels); 0 (Trpa1 protein, rat); 046O35D44R (Prilocaine); 0619F35CGV (Tetracaine); 11103-72-3 (Ruthenium Red); 3KX376GY7L (Glutamic Acid); 4368-28-9 (Tetrodotoxin); 7IO5LYA57N (ropivacaine); A5H73K9U3W (levobupivacaine); LFW48MY844 (capsazepine); S07O44R1ZM (Capsaicin); Y8335394RO (Bupivacaine)
[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:161227
[St] Status:MEDLINE


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[PMID]:28219864
[Au] Autor:Li LC; Zhang DY; Peng SC; Wu J; Jiang CY; Liu T
[Ad] Endereço:Department of Pain Clinic, First Affiliated Hospital of Nanchang University, Nanchang, 330006, China. E-mail: 19893395@qq.com.
[Ti] Título:[Rebound depolarization of substantia gelatinosa neurons and its modulatory mechanisms in rat spinal dorsal horn].
[So] Source:Nan Fang Yi Ke Da Xue Xue Bao;37(2):204-209, 2016 Feb 20.
[Is] ISSN:1673-4254
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To investigate the rebound depolarization of substantia gelatinosa (SG) neurons in rat spinal dorsal horn and explore its modulatory mechanisms to provide better insights into rebound depolarization-related diseases. METHODS: Parasagittal slices of the spinal cord were prepared from 3- to 5-week-old Sprague-Dawley rats. The electrophysiologic characteristics and responses to hyperpolarization stimulation were recorded using whole-cell patch-clamp technique. The effects of hyperpolarization-activated cyclic nucleotide gated cation (HCN) channel blockers and T-type calcium channel blockers on rebound depolarization of the neurons were studied. RESULTS: A total of 63 SG neurons were recorded. Among them, 23 neurons showed no rebound depolarization, 19 neurons showed rebound depolarization without spikes, and 21 neurons showed rebound depolarization with spikes. The action potential thresholds of the neurons without rebound depolarization were significantly higher than those of the neurons with rebound depolarization and spikes (-28.7∓1.6 mV vs -36.0∓2.0 mV, P<0.05). The two HCN channel blockers CsCl and ZD7288 significantly delayed the latency of rebound depolarization with spike from 45.9∓11.6 ms to 121.6∓51.3 ms (P<0.05) and from 36.2∓10.3 ms to 73.6∓13.6 ms (P<0.05), respectively. ZD7288 also significantly prolonged the latency of rebound depolarization without spike from 71.9∓35.1 ms to 267.0∓68.8 ms (P<0.05). The T-type calcium channel blockers NiCl2 and mibefradil strongly decreased the amplitude of rebound depolarization with spike from 19.9∓6.3 mV to 9.5∓4.5 mV (P<0.05) and from 26.1∓9.4 mV to 15.5∓5.0 mV (P<0.05), respectively. Mibefradil also significantly decreased the amplitude of rebound depolarization without spike from 14.3∓3.0 mV to 7.9∓2.0 mV (P<0.05). CONCLUSION: Nearly two-thirds of the SG neurons have rebound depolarizations modulated by HCN channel and T-type calcium channel.
[Mh] Termos MeSH primário: Neurônios/citologia
Corno Dorsal da Medula Espinal/citologia
Substância Gelatinosa/citologia
[Mh] Termos MeSH secundário: Potenciais de Ação
Animais
Bloqueadores dos Canais de Cálcio/farmacologia
Canais de Cálcio Tipo T
Polaridade Celular
Césio/farmacologia
Cloretos/farmacologia
Canais de Cátion Regulados por Nucleotídeos Cíclicos/antagonistas & inibidores
Técnicas de Patch-Clamp
Pirimidinas/farmacologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Calcium Channels, T-Type); 0 (Chlorides); 0 (Cyclic Nucleotide-Gated Cation Channels); 0 (Pyrimidines); 133059-99-1 (ICI D2788); 1KSV9V4Y4I (Cesium); GNR9HML8BA (cesium chloride)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE


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[PMID]:27573517
[Au] Autor:Kozuka Y; Kawamata M; Furue H; Ishida T; Tanaka S; Namiki A; Yamakage M
[Ad] Endereço:Department of Anesthesiology, Sapporo Medical University School of Medicine, Sapporo, Japan.
[Ti] Título:Changes in synaptic transmission of substantia gelatinosa neurons after spinal cord hemisection revealed by analysis using in vivo patch-clamp recording.
[So] Source:Mol Pain;12, 2016.
[Is] ISSN:1744-8069
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: After spinal cord injury, central neuropathic pain develops in the majority of spinal cord injury patients. Spinal hemisection in rats, which has been developed as an animal model of spinal cord injury in humans, results in hyperexcitation of spinal dorsal horn neurons soon after the hemisection and thereafter. The hyperexcitation is likely caused by permanent elimination of the descending pain systems. We examined the change in synaptic transmission of substantia gelatinosa neurons following acute spinal hemisection by using an in vivo whole-cell patch-clamp technique. RESULTS: An increased spontaneous action potential firings of substantia gelatinosa neurons was detected in hemisected rats compared with that in control animals. The frequencies and amplitudes of spontaneous excitatory postsynaptic currents and of evoked excitatory postsynaptic currentss in response to non-noxious and noxious stimuli were not different between hemisected and control animals. On the contrary, the amplitude and frequency of spontaneous inhibitory postsynaptic currents of substantia gelatinosa neurons in hemisected animals were significantly smaller and lower, respectively, than those in control animals (P < 0.01). Large amplitude and high-frequency spontaneous inhibitory postsynaptic currents, which could not be elicited by mechanical stimuli, were seen in 44% of substantia gelatinosa neurons in control animals but only in 17% of substantia gelatinosa neurons in hemisected animals. In control animals, such large amplitude spontaneous inhibitory postsynaptic currents were suppressed by spinal application of tetrodotoxin (1 µM). Cervical application of lidocaine (2%, 10 µl) also inhibited such large amplitude of inhibitory postsynaptic currents. The proportion of multi-receptive substantia gelatinosa neurons, which exhibit action potential firing in response to non-noxious and noxious stimuli, was much larger in hemisected animals than in control animals. CONCLUSIONS: These suggest that substantia gelatinosa neurons receive tonic inhibition by spinal inhibitory interneurons which generate persistent action potentials. Spinal hemisection results in hyperexcitation of substantia gelatinosa neurons at least in part by eliminating the tonic descending control of spinal inhibitory interneurons from supraspinal levels.
[Mh] Termos MeSH primário: Neurônios/fisiologia
Traumatismos da Medula Espinal/patologia
Substância Gelatinosa/patologia
Transmissão Sináptica/fisiologia
[Mh] Termos MeSH secundário: Anestésicos Intravenosos/farmacologia
Animais
Bicuculina/farmacologia
Modelos Animais de Doenças
Estimulação Elétrica
Lateralidade Funcional
Hiperalgesia/etiologia
Hiperalgesia/fisiopatologia
Masculino
Neurônios/classificação
Neurônios/efeitos dos fármacos
Neurotransmissores/farmacologia
Técnicas de Patch-Clamp
Estimulação Física
Ratos
Ratos Sprague-Dawley
Traumatismos da Medula Espinal/complicações
Estricnina/farmacologia
Transmissão Sináptica/efeitos dos fármacos
Tetrodotoxina/farmacologia
Uretana/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anesthetics, Intravenous); 0 (Neurotransmitter Agents); 3IN71E75Z5 (Urethane); 4368-28-9 (Tetrodotoxin); H9Y79VD43J (Strychnine); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160831
[St] Status:MEDLINE


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[PMID]:27462070
[Au] Autor:Kay CW; Ursu D; Sher E; King AE
[Ad] Endereço:School of Biomedical Sciences, University of Leeds, Leeds, LS2 9JT, United Kingdom.
[Ti] Título:The role of Cx36 and Cx43 in 4-aminopyridine-induced rhythmic activity in the spinal nociceptive dorsal horn: an electrophysiological study in vitro.
[So] Source:Physiol Rep;4(14), 2016 07.
[Is] ISSN:2051-817X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Connexin (Cx) proteins and gap junctions support the formation of neuronal and glial syncytia that are linked to different forms of rhythmic firing and oscillatory activity in the CNS. In this study, quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to profile developmental expression of two specific Cx proteins, namely glial Cx43 and neuronal Cx36, in postnatal lumbar spinal cord aged 4, 7, and 14 days. Extracellular electrophysiology was used to determine the contribution of Cx36 and Cx43 to a previously described form of 4-aminopyridine (4-AP)-induced 4-12 Hz rhythmic activity within substantia gelatinosa (SG) of rat neonatal dorsal horn (DH) in vitro. The involvement of Cx36 and Cx43 was probed pharmacologically using quinine, a specific uncoupler of Cx36 and the mimetic peptide blocker Gap 26 which targets Cx43. After establishment of 4-12 Hz rhythmic activity by 4-AP (25 µmol/L), coapplication of quinine (250 µmol/L) reduced 4-AP-induced 4-12 Hz rhythmic activity (P < 0.05). Preincubation of spinal cord slices with Gap 26 (100 µmol/L), compromised the level of 4-AP-induced 4-12 Hz rhythmic activity in comparison with control slices preincubated in ACSF alone (P < 0.05). Conversely, the nonselective gap junction "opener" trimethylamine (TMA) enhanced 4-12 Hz rhythmic behavior (P < 0.05), further supporting a role for Cx proteins and gap junctions. These data have defined a physiological role for Cx36 and Cx43 in rhythmic firing in SG, a key nociceptive processing area of DH. The significance of these data in the context of pain and Cx proteins as a future analgesic drug target requires further study.
[Mh] Termos MeSH primário: Conexina 43/fisiologia
Conexinas/fisiologia
Corno Dorsal da Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: 4-Aminopiridina/farmacologia
Animais
Conexina 43/genética
Conexinas/genética
Junções Comunicantes/efeitos dos fármacos
Junções Comunicantes/fisiologia
Regulação da Expressão Gênica no Desenvolvimento/fisiologia
Vértebras Lombares
Masculino
Bloqueadores dos Canais de Potássio/farmacologia
Ratos Wistar
Corno Dorsal da Medula Espinal/efeitos dos fármacos
Substância Gelatinosa/efeitos dos fármacos
Substância Gelatinosa/metabolismo
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Connexin 43); 0 (Connexins); 0 (Potassium Channel Blockers); 0 (connexin 36); 0 (connexin 43 protein, rat); BH3B64OKL9 (4-Aminopyridine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170309
[Lr] Data última revisão:
170309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160728
[St] Status:MEDLINE


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[PMID]:27383702
[Au] Autor:Demirkaya K; Akgün ÖM; Senel B; Öncel Torun Z; Seyrek M; Lacivita E; Leopoldo M; Dogrul A
[Ad] Endereço:- Gulhane Medical Academy, Department of Restorative Dentistry and Endodontics, Ankara, Turkey.
[Ti] Título:Selective 5-HT7 receptor agonists LP 44 and LP 211 elicit an analgesic effect on formalin-induced orofacial pain in mice.
[So] Source:J Appl Oral Sci;24(3):218-22, 2016 May-Jun.
[Is] ISSN:1678-7765
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To investigate the antinociceptive effects of pharmacological activation of 5-HT7 receptors on orofacial pain in mice. MATERIAL AND METHODS: Nociception was evaluated by using an orofacial formalin test in male Balb-C mice. Selective 5-HT7 receptor agonists, LP 44 and LP 211 (1, 5, and 10 mg/kg), were given intraperitoneally 30 min prior to a formalin injection. A bolus of 10 µl of 4% subcutaneous formalin was injected into the upper lip of mice and facial grooming behaviors were monitored. The behavioral responses consisted of two distinct periods, the early phase corresponding to acute pain (Phase I: 0-12 min) and the late phase (Phase II: 12-30 min). RESULTS: LP 44 and LP 211 (1, 5, and 10 mg/kg) produced an analgesic effect with reductions in face rubbing time in both Phase I and Phase II of the formalin test. CONCLUSION: Our results suggest that 5-HT7 receptor agonists may be promising analgesic drugs in the treatment of orofacial pain.
[Mh] Termos MeSH primário: Analgésicos/uso terapêutico
Dor Facial/tratamento farmacológico
Piperazinas/uso terapêutico
Receptores de Serotonina
Agonistas de Receptores de Serotonina/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Dor Facial/induzido quimicamente
Formaldeído
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Reprodutibilidade dos Testes
Substância Gelatinosa/efeitos dos fármacos
Fatores de Tempo
Resultado do Tratamento
Nervo Trigêmeo/efeitos dos fármacos
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (N-(4-cyanophenylmethyl)-4-(2-diphenyl)-1-piperazinehexanamide); 0 (Piperazines); 0 (Receptors, Serotonin); 0 (Serotonin Receptor Agonists); 0 (serotonin 7 receptor); 1HG84L3525 (Formaldehyde)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:160708
[St] Status:MEDLINE


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[PMID]:27088014
[Au] Autor:Ropero Peláez FJ; Taniguchi S
[Ad] Endereço:Center of Mathematics, Computation and Cognition, Universidade Federal do ABC, 09210-180 Santo André, SP, Brazil.
[Ti] Título:The Gate Theory of Pain Revisited: Modeling Different Pain Conditions with a Parsimonious Neurocomputational Model.
[So] Source:Neural Plast;2016:4131395, 2016.
[Is] ISSN:1687-5443
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The gate control theory of pain proposed by Melzack and Wall in 1965 is revisited through two mechanisms of neuronal regulation: NMDA synaptic plasticity and intrinsic plasticity. The Melzack and Wall circuit was slightly modified by using strictly excitatory nociceptive afferents (in the original arrangement, nociceptive afferents were considered excitatory when they project to central transmission neurons and inhibitory when projecting to substantia gelatinosa). The results of our neurocomputational model are consistent with biological ones in that nociceptive signals are blocked on their way to the brain every time a tactile stimulus is given at the same locus where the pain was produced. In the computational model, the whole set of parameters, independently of their initialization, always converge to the correct values to allow the correct computation of the circuit. To test the model, other painful conditions were analyzed: phantom limb pain, wind-up and wind-down pain, breakthrough pain, and demyelinating syndromes like Guillain-Barré and multiple sclerosis.
[Mh] Termos MeSH primário: Modelos Neurológicos
Plasticidade Neuronal/fisiologia
Neurônios/fisiologia
Dor/fisiopatologia
Transmissão Sináptica/fisiologia
[Mh] Termos MeSH secundário: Simulação por Computador
Seres Humanos
Vias Neurais/fisiopatologia
Substância Gelatinosa/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161231
[Lr] Data última revisão:
161231
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160419
[St] Status:MEDLINE
[do] DOI:10.1155/2016/4131395


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[PMID]:27080947
[Au] Autor:Yin H; Bhattarai JP; Oh SM; Park SJ; Ahn DK; Han SK
[Ad] Endereço:* Department of Oral Physiology, School of Dentistry and Institute of Oral Bioscience, Chonbuk National University, Jeonju 561-756, Republic of Korea.
[Ti] Título:Baicalin Activates Glycine and γ-Aminobutyric Acid Receptors on Substantia Gelatinosa Neurons of the Trigeminal Subsnucleus Caudalis in Juvenile Mice.
[So] Source:Am J Chin Med;44(2):389-400, 2016.
[Is] ISSN:0192-415X
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) receives nociceptive afferent inputs from thin-myelinated A[Formula: see text] fibers and unmyelinated C fibers and has been shown to be involved in the processing of orofacial nociceptive information. Scutellaria baicalensis Georgi (Huang-Qin, SbG), one of the 50 fundamental herbs of Chinese herbology, has been used historically as anti-inflammatory and antineoplastic medicine. Baicalin, one of the major compounds of SbG, has been reported to have neuroprotective, anti-inflammatory and analgesic effects. However, the receptor type activated by baicalin and its precise action mechanism on the SG neurons of Vc have not yet been studied. The whole-cell patch clamp technique was performed to examine the ion channels activated by baicalin on the SG neurons of Vc. In high Cl[Formula: see text] pipette solution, the baicalin (300[Formula: see text][Formula: see text]M) induced repeatable inward currents ([Formula: see text][Formula: see text]pA, [Formula: see text]) without desensitization on all the SG neurons tested. Further, the inward currents showed a concentration (0.1-3[Formula: see text]mM) dependent pattern. The inward current was sustained in the presence of tetrodotoxin (0.5[Formula: see text][Formula: see text]M), a voltage sensitive Na[Formula: see text] channel blocker. In addition, baicalin-induced inward currents were reduced in the presence of picrotoxin (50[Formula: see text][Formula: see text]M), a GABAA receptor antagonist, flumazenil (100[Formula: see text][Formula: see text]M), a benzodiazepine-sensitive GABAA receptor antagonist, and strychnine (2[Formula: see text][Formula: see text]M), a glycine receptor antagonist, respectively. These results indicate that baicalin has inhibitory effects on the SG neurons of the Vc, which are due to the activation of GABAA and/or the glycine receptor. Our results suggest that baicalin may be a potential target for orofacial pain modulation.
[Mh] Termos MeSH primário: Flavonoides/farmacologia
Neurônios/metabolismo
Receptores de GABA/metabolismo
Receptores da Glicina/metabolismo
Substância Gelatinosa/citologia
Núcleo Inferior Caudal do Nervo Trigêmeo/citologia
[Mh] Termos MeSH secundário: Envelhecimento
Animais
Anti-Inflamatórios/farmacologia
Antineoplásicos Fitogênicos/farmacologia
Relação Dose-Resposta a Droga
Dor Facial/tratamento farmacológico
Feminino
Flavonoides/isolamento & purificação
Flavonoides/uso terapêutico
Masculino
Camundongos
Fármacos Neuroprotetores
Fitoterapia
Scutellaria baicalensis/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antineoplastic Agents, Phytogenic); 0 (Flavonoids); 0 (Neuroprotective Agents); 0 (Receptors, GABA); 0 (Receptors, Glycine); 347Q89U4M5 (baicalin)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160416
[St] Status:MEDLINE
[do] DOI:10.1142/S0192415X16500221


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[PMID]:26948545
[Au] Autor:Chen Y; Derkach VA; Smith PA
[Ad] Endereço:Department of Pharmacology and Neurosciences and Mental Health Institute, University of Alberta, Edmonton, AB T6G 2H7, Canada.
[Ti] Título:Loss of Ca(2+)-permeable AMPA receptors in synapses of tonic firing substantia gelatinosa neurons in the chronic constriction injury model of neuropathic pain.
[So] Source:Exp Neurol;279:168-177, 2016 May.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Synapses transmitting nociceptive information in the spinal dorsal horn undergo enduring changes following peripheral nerve injury. Indeed, such injury alters the expression of the GluA2 subunit of glutamatergic AMPA receptors (AMPARs) in the substantia gelatinosa and this predicts altered channel conductance and calcium permeability, leading to an altered function of excitatory synapses. We therefore investigated the functional properties of synaptic AMPA receptors in rat substantia gelatinosa neurons following 10-20d chronic constriction injury (CCI) of the sciatic nerve; a model of neuropathic pain. We measured their single-channel conductance and sensitivity to a blocker of calcium permeable AMPA receptors (CP-AMPARs), IEM1460 (50µM). In putative inhibitory, tonic firing neurons, CCI reduced the average single-channel conductance of synaptic AMPAR from 14.4±3.5pS (n=12) to 9.2±1.0pS (n=10, p<0.05). IEM1460 also more effectively antagonized evoked, spontaneous and miniature EPSCs in tonic neurons from sham operated animals than in those from animals that had been subjected to CCI. By contrast, CCI did not change the effectiveness of IEM1460 in delay firing neurons although average single channel conductance was increased from 7.6±1.2pS (n=11) to 12.2±1.5pS (n=10, p<0.01). CCI thus elicits plastic changes in a specific set of glutamatergic synapses of substantia gelatinosa due to subunit recomposition and loss of GluA2-lacking CP-AMPAR. These insights reveal a molecular mechanism of nerve injury acting at synapses of inhibitory neurons to reduce their drive and therefore inhibitory tone in the spinal cord, therefore contributing to the central sensitization associated with neuropathic pain.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Constrição Patológica/metabolismo
Neuralgia/metabolismo
Neurônios/metabolismo
Receptores de AMPA/metabolismo
Substância Gelatinosa/metabolismo
Sinapses/metabolismo
[Mh] Termos MeSH secundário: Adamantano/análogos & derivados
Adamantano/farmacologia
Animais
Antagonistas de Aminoácidos Excitatórios/farmacologia
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Masculino
Ratos
Receptores de AMPA/antagonistas & inibidores
Medula Espinal/efeitos dos fármacos
Medula Espinal/metabolismo
Sinapses/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Excitatory Amino Acid Antagonists); 0 (IEM 1460); 0 (Receptors, AMPA); PJY633525U (Adamantane); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160308
[St] Status:MEDLINE


  9 / 563 MEDLINE  
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[PMID]:26826332
[Au] Autor:Peng HZ; Ma LX; Lv MH; Hu T; Liu T
[Ad] Endereço:Department of Anesthesiology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, China.
[Ti] Título:Minocycline enhances inhibitory transmission to substantia gelatinosa neurons of the rat spinal dorsal horn.
[So] Source:Neuroscience;319:183-93, 2016 Apr 05.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Minocycline, a second-generation tetracycline, is well known for its antibiotic, anti-inflammatory, and antinociceptive effects. Modulation of synaptic transmission is one of the analgesic mechanisms of minocycline. Although it has been reported that minocycline may suppress excitatory glutamatergic synaptic transmission, it remains unclear whether it could affect inhibitory synaptic transmission, which also plays a key role in modulating pain signaling. To examine the effect of minocycline on synaptic transmission in rat spinal substantia gelatinosa (SG) neurons, we recorded spontaneous inhibitory postsynaptic currents (sIPSCs) using whole-cell patch-clamp recording at a holding potential of 0 mV. Bath application of minocycline significantly increased the frequency but not the amplitude of sIPSCs in a reversible and concentration-dependent manner with an EC50 of 85. The enhancement of inhibitory synaptic transmission produced by minocycline was not affected by the glutamate receptor antagonists CNQX and D-APV or by the voltage-gated sodium channel blocker tetrodotoxin (TTX). Moreover, the potency of minocycline for facilitating sIPSC frequency was the same in both glycinergic and GABAergic sIPSCs without changing their decay phases. However, the facilitatory effect of minocycline on sIPSCs was eliminated in a Ca(2+)-free Krebs solution or by co-administration with calcium channel blockers. In summary, our data demonstrate that baseline inhibitory synaptic transmission in SG neurons is markedly enhanced by minocycline. This may function to decrease the excitability of SG neurons, thus leading to a modulation of nociceptive transmission.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos
Minociclina/farmacologia
Substância Gelatinosa/efeitos dos fármacos
Transmissão Sináptica/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Masculino
Técnicas de Patch-Clamp
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); FYY3R43WGO (Minocycline)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160131
[St] Status:MEDLINE


  10 / 563 MEDLINE  
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[PMID]:26777279
[Au] Autor:Yang K
[Ad] Endereço:Electrophysiology Laboratory, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212001, China; Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA; Department of Basic Medical Sciences, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu 212013, China. Electronic address: yangk@ujs.edu.cn.
[Ti] Título:Regulation of excitability in tonic firing substantia gelatinosa neurons of the spinal cord by small-conductance Ca(2+)-activated K(+) channels.
[So] Source:Neuropharmacology;105:15-24, 2016 Jun.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The excitability of substantia gelatinosa (SG) neurons in the spinal dorsal horn determines the processing of nociceptive information from the periphery to the central nervous system. Small conductance Ca(2+)-activated K(+) (SK) channels on neurons supply strong negative feedback control on neuronal excitability by affecting afterhyperpolarization (AHP). However, the role of SK channels in regulating tonic-firing SG neuron excitability remains elusive. In the present study, whole-cell recordings were conducted in SG neurons from acute spinal cord slices of adult rats. The SK channel opener 1-ethyl-2-benzimidazolinone (1-EBIO) attenuated spike discharges and increased AHP amplitudes; this effect was mimicked by a high Ca(2+) external solution. Systemic administration of 1-EBIO attenuated the thermal-induced nociception behavior. Conversely, the inhibition of SK channels with apamin, a specific SK channel inhibitor, increased neuronal excitability and decreased the AHP amplitudes; this effect was mimicked by a Ca(2+)-free external solution. Apamin increased excitatory synaptic transmission by increasing the amplitudes of evoked excitatory postsynaptic potentials (eEPSPs). This facilitation depended on N-methyl-d-aspartate (NMDA) receptors, extracellular Mg(2+) and intracellular Ca(2+). Voltage-gated Ca(2+) channels (VGCCs) were also involved in the apamin-induced effects. Strikingly, 1-EBIO action on decreasing excitability persisted in the presence of apamin, indicating that 1-EBIO manipulates SK channels via a pathway rather than via apamin-sensitive SK channels. The data reveal a previously uncharacterized mechanism for manipulating SG neuronal excitability by Ca(2+) conductances via both apamin-sensitive and apamin-insensitive pathways. Because SG neurons in the dorsal horn are involved in regulating nociception, manipulating neuronal excitability via SK channels indicates a potential therapeutic target.
[Mh] Termos MeSH primário: Potenciais de Ação
Neurônios/fisiologia
Nociceptividade/fisiologia
Canais de Potássio Ativados por Cálcio de Condutância Baixa/fisiologia
Substância Gelatinosa/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Apamina/administração & dosagem
Benzimidazóis/administração & dosagem
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Masculino
Nociceptividade/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Receptores de N-Metil-D-Aspartato/fisiologia
Canais de Potássio Ativados por Cálcio de Condutância Baixa/agonistas
Canais de Potássio Ativados por Cálcio de Condutância Baixa/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzimidazoles); 0 (Receptors, N-Methyl-D-Aspartate); 0 (Small-Conductance Calcium-Activated Potassium Channels); 24345-16-2 (Apamin); M82W79SS4W (1-ethyl-2-benzimidazolinone)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160119
[St] Status:MEDLINE



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