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[PMID]:29247746
[Au] Autor:Sun X; Tang L; Winesett S; Chang W; Cheng SX
[Ad] Endereço:Department of Physiology and Pathophysiology, School of Basic Medicine, Qingdao University, Qingdao, China; Department of Pediatrics, University of Florida, Gainesville, FL, USA.
[Ti] Título:Calcimimetic R568 inhibits tetrodotoxin-sensitive colonic electrolyte secretion and reduces c-fos expression in myenteric neurons.
[So] Source:Life Sci;194:49-58, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Calcium-sensing receptor (CaSR) is expressed on neurons of both submucosal and myenteric plexuses of the enteric nervous system (ENS) and the CaSR agonist R568 inhibited Cl secretion in intestine. The purpose of this study was to localize the primary site of action of R568 in the ENS and to explore how CaSR regulates secretion through the ENS. MATERIALS AND METHODS: Two preparations of rat proximal and distal colon were used. The full-thickness preparation contained both the submucosal and myenteric plexuses, whereas for the "stripped" preparation the myenteric plexus with the muscle layers was removed. Both preparations were mounted onto Ussing chambers and Cl secretory responses were compared by measuring changes in short circuit current (I ). Two tissue-specific CaSR knockouts (i.e., neuron-specific vs. enterocyte-specific) were generated to compare the effect of R568 on expression of c-fos protein in myenteric neurons by immunocytochemistry. KEY FINDINGS: In full-thickness colons, tetrodotoxin (TTX) inhibited I , both in proximal and distal colons. A nearly identical inhibition was produced by R568. However, in stripped preparations, while the effect of TTX on I largely remained, the effect of R568 was nearly completely eliminated. In keeping with this, R568 reduced c-fos protein expression only in myenteric neurons of wild type mice and mutant mice that contained CaSR in neurons (i.e., Cre/Casr mice), but not in myenteric neurons of Cre/Casr mice in which neuronal cell CaSR was eliminated. SIGNIFICANCE: These results indicate that R568 exerts its anti-secretory effects predominantly via CaSR-mediated inhibition of neuronal activity in the myenteric plexus.
[Mh] Termos MeSH primário: Eletrólitos/metabolismo
Plexo Mientérico/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Fenetilaminas/farmacologia
Propilaminas/farmacologia
Proteínas Proto-Oncogênicas c-fos/metabolismo
Receptores de Detecção de Cálcio/metabolismo
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
[Mh] Termos MeSH secundário: Animais
Colo/efeitos dos fármacos
Colo/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Plexo Mientérico/citologia
Neurônios/metabolismo
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Electrolytes); 0 (N-(2-chlorophenylpropyl)-1-(3-methoxyphenyl)ethylamine); 0 (Phenethylamines); 0 (Propylamines); 0 (Proto-Oncogene Proteins c-fos); 0 (Receptors, Calcium-Sensing); 0 (Sodium Channel Blockers); 4368-28-9 (Tetrodotoxin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE


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[PMID]:29311444
[Au] Autor:Tsujimura K; Yoshimura H; Taguri T; Motomura H
[Ad] Endereço:Nagasaki Prefectural Institute of Environment and Public Health.
[Ti] Título:[Tetrodotoxin (TTX) Monitoring of Biological Specimens and Toxin Profile in a Food Poisoning Case Caused by the Scavenging Gastropod Nassarius (Alectrion) glans "Kinshibai"].
[So] Source:Shokuhin Eiseigaku Zasshi;58(6):253-259, 2017.
[Is] ISSN:1882-1006
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:In November 2015, a patient presented with symptoms of toxicity after eating whole boiled samples of the scavenging gastropod Nassarius (Alectrion) glans "Kinshibai" in Nagasaki. This food poisoning case was the third recorded in Japan. The case was investigated by evaluation of the toxin profile of the gastropod, and monitoring of tetrodotoxin (TTX) levels in serum and urine sampled from the affected individual. One gastropod contained a harmful dose of TTX (2.5 mg/ individual in food residue sample 2). In biological samples, maximum TTX concentrations were 42.8 ng/mL in serum on the day after onset of symptoms. TTX urinary excretion was calculated to be 2.4 mg. From the measured TTX concentrations, it was estimated that a lethal dose had been ingested in this case. Moreover, it was found by LC-QqQ-MS/MS analysis and mouse bioassay that the toxicity of "Kinshibai" was not solely due to TTX. The remaining toxicity was thought to be due to 11-oxoTTX. As in previous poisoning cases, it was concluded that ingestion of this gastropod poses a high risk of food poisoning.
[Mh] Termos MeSH primário: Doenças Transmitidas por Alimentos/diagnóstico
Doenças Transmitidas por Alimentos/etiologia
Gastrópodes
Tetrodotoxina/sangue
Tetrodotoxina/urina
[Mh] Termos MeSH secundário: Idoso
Animais
Bioensaio/métodos
Biomarcadores/sangue
Biomarcadores/urina
Cromatografia Líquida/métodos
Análise de Alimentos/métodos
Gastrópodes/química
Seres Humanos
Japão
Masculino
Camundongos
Monitorização Fisiológica/métodos
Risco
Espectrometria de Massas em Tandem/métodos
Tetrodotoxina/análise
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 4368-28-9 (Tetrodotoxin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.3358/shokueishi.58.253


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[PMID]:28452816
[Au] Autor:Santamaria CM; Zhan C; McAlvin JB; Zurakowski D; Kohane DS
[Ad] Endereço:From the *Laboratory for Biomaterials and Drug Delivery, Division of Critical Care Medicine, Department of Anesthesiology; †Division of Medicine Critical Care, Department of Medicine; and ‡Department of Anesthesiology, Perioperative, and Pain Medicine, Boston Children's Hospital, Boston, Massachusetts.
[Ti] Título:Tetrodotoxin, Epinephrine, and Chemical Permeation Enhancer Combinations in Peripheral Nerve Blockade.
[So] Source:Anesth Analg;124(6):1804-1812, 2017 06.
[Is] ISSN:1526-7598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Chemical permeation enhancers (CPEs) have the potential to improve nerve blockade by site 1 sodium channel blockers such as tetrodotoxin (TTX). Here, we investigated the efficacy and toxicity of CPE-enhanced nerve blockade across a range of TTX concentrations using 2 CPEs (sodium octyl sulfate and octyl trimethyl ammonium bromide). We also tested the hypothesis that CPEs could be used to reduce the concentrations of TTX and/or of a second adjuvant drug (in this case, epinephrine) needed to achieve prolonged local anesthesia METHODS:: Sprague-Dawley rats were injected at the sciatic nerve with combinations of TTX and CPEs, with and without epinephrine. Sensory and motor nerve blockade were assessed using a modified hot plate test and a weight-bearing test, respectively. Systemic and local toxicities of the different combinations were assessed. RESULTS: Addition of increasing concentrations of TTX to fixed concentrations of CPEs produced a marked concentration-dependent improvement in the rate of successful nerve blocks and in nerve block duration. CPEs did not affect systemic toxicity. At some concentrations, the addition of sodium octyl sulfate increased the duration of block from TTX plus epinephrine, and epinephrine increased that from TTX plus CPEs. The addition of epinephrine did not cause an increase in local toxicity, and it markedly reduced systemic toxicity. CONCLUSIONS: CPEs can prolong the duration of nerve blockade across a range of concentrations of TTX. CPEs could also be used to reduce the concentration of epinephrine needed to achieve a given degree of nerve block. CPEs may be useful in enhancing nerve blockade from site 1 sodium channel blockers.
[Mh] Termos MeSH primário: Agonistas Adrenérgicos/farmacologia
Ácidos Alcanossulfônicos/farmacologia
Anestésicos Locais/farmacologia
Epinefrina/farmacologia
Bloqueio Nervoso/métodos
Compostos de Amônio Quaternário/farmacologia
Nervo Isquiático/efeitos dos fármacos
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
[Mh] Termos MeSH secundário: Agonistas Adrenérgicos/toxicidade
Anestésicos Locais/toxicidade
Animais
Difusão
Relação Dose-Resposta a Droga
Epinefrina/toxicidade
Masculino
Atividade Motora/efeitos dos fármacos
Bloqueio Nervoso/efeitos adversos
Limiar da Dor/efeitos dos fármacos
Permeabilidade
Ratos Sprague-Dawley
Bloqueadores dos Canais de Sódio/toxicidade
Tetrodotoxina/toxicidade
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Adrenergic Agonists); 0 (Alkanesulfonic Acids); 0 (Anesthetics, Local); 0 (Quaternary Ammonium Compounds); 0 (Sodium Channel Blockers); 15461-38-8 (octyltrimethylammonium); 4368-28-9 (Tetrodotoxin); DU4821I15A (1-octanesulfonic acid); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1213/ANE.0000000000002072


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[PMID]:28938466
[Au] Autor:Chimerel C; Riccio C; Murison K; Gribble FM; Reimann F
[Ad] Endereço:Metabolic Research Laboratories and Medical Research Council (MRC) Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, University of Cambridge, Cambridge CB2 0QQ, United Kingdom.
[Ti] Título:Optogenetic Analysis of Depolarization-Dependent Glucagonlike Peptide-1 Release.
[So] Source:Endocrinology;158(10):3426-3434, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Incretin hormones play an important role in the regulation of food intake and glucose homeostasis. Glucagonlike peptide-1 (GLP-1)-secreting cells have been demonstrated to be electrically excitable and to fire action potentials (APs) with increased frequency in response to nutrient exposure. However, nutrients can also be metabolized or activate G-protein-coupled receptors, thus potentially stimulating GLP-1 secretion independent of their effects on the plasma membrane potential. Here we used channelrhodopsins to manipulate the membrane potential of GLUTag cells, a well-established model of GLP-1-secreting enteroendocrine L cells. Using channelrhodopsins with fast or slow on/off kinetics (CheTA and SSFO, respectively), we found that trains of light pulses could trigger APs and calcium elevation in GLUTag cells stably expressing either CheTA or SSFO. Tetrodotoxin reduced light-triggered AP frequency but did not impair calcium responses, whereas further addition of the calcium-channel blockers nifedipine and ω-conotoxin GVIA abolished both APs and calcium transients. Light pulse trains did not trigger GLP-1 secretion from CheTA-expressing cells under basal conditions but were an effective stimulus when cyclic adenosine monophosphate (cAMP) concentrations were elevated by forskolin plus 3-isobutyl 1-methylxanthine. In SSFO-expressing cells, light-stimulated GLP-1 release was observed at resting and elevated cAMP concentrations and was blocked by nifedipine plus ω-conotoxin GVIA but not tetrodotoxin. We conclude that cAMP elevation or cumulative membrane depolarization triggered by SSFO enhances the efficiency of light-triggered action potential firing, voltage-gated calcium entry, and GLP-1 secretion.
[Mh] Termos MeSH primário: Potenciais de Ação/efeitos dos fármacos
Bloqueadores dos Canais de Cálcio/farmacologia
Células Enteroendócrinas/efeitos dos fármacos
Peptídeo 1 Semelhante ao Glucagon/efeitos dos fármacos
Potenciais da Membrana/efeitos dos fármacos
[Mh] Termos MeSH secundário: 1-Metil-3-Isobutilxantina/farmacologia
Animais
Cálcio/metabolismo
Colforsina/farmacologia
Células Enteroendócrinas/metabolismo
Células Enteroendócrinas/secreção
Peptídeo 1 Semelhante ao Glucagon/secreção
Camundongos
Nifedipino/farmacologia
Optogenética
Técnicas de Patch-Clamp
Inibidores de Fosfodiesterase/farmacologia
Rodopsina
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
Vasodilatadores/farmacologia
ômega-Conotoxina GVIA/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Phosphodiesterase Inhibitors); 0 (Sodium Channel Blockers); 0 (Vasodilator Agents); 1F7A44V6OU (Colforsin); 4368-28-9 (Tetrodotoxin); 89750-14-1 (Glucagon-Like Peptide 1); 9009-81-8 (Rhodopsin); 92078-76-7 (omega-Conotoxin GVIA); I9ZF7L6G2L (Nifedipine); SY7Q814VUP (Calcium); TBT296U68M (1-Methyl-3-isobutylxanthine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00434


  5 / 12444 MEDLINE  
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Antunes, Edson
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[PMID]:28837636
[Au] Autor:Campos R; Mónica FZ; Rodrigues RL; Rojas-Moscoso JA; Moreno RA; Cogo JC; de Oliveira MA; Antunes E; De Nucci G
[Ad] Endereço:Faculty of Medical Sciences, Department of Pharmacology, University of Campinas (UNICAMP), Campinas, Brazil.
[Ti] Título:Tetrodotoxin-insensitive electrical field stimulation-induced contractions on Crotalus durissus terrificus corpus cavernosum.
[So] Source:PLoS One;12(8):e0183766, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Reptiles are the first amniotes to develop an intromitent penis, however until now the mechanisms involved in the electrical field stimulation-induced contraction on corpora cavernosa isolated from Crotalus durissus terrificus were not investigated. Crotalus and rabbit corpora cavernosa were mounted in 10 mL organ baths for isometric tension recording. Electrical field stimulation (EFS)-induced contractions were performed in presence/absence of phentolamine (10 µM), guanethidine (30 µM), tetrodotoxin (1 µM and 1mM), A-803467 (10 µM), 3-iodo-L-Tyrosine (1 mM), salsolinol (3 µM) and a modified Krebs solution (equimolar substitution of NaCl by N-methyl-D-glucamine). Immuno-histochemistry for tyrosine hydroxylase was also performed. Electrical field stimulation (EFS; 8 Hz and 16 Hz) caused contractions in both Crotalus and rabbit corpora cavernosa. The contractions were abolished by previous incubation with either phentolamine or guanethidine. Tetrodotoxin (1 µM) also abolished the EFS-induced contractions of rabbit CC, but did not affect EFS-induced contractions of Crotalus CC. Addition of A-803467 (10 µM) did not change the EFS-induced contractions of Crotalus CC but abolished rabbit CC contractions. 3-iodo-L-Tyrosine and salsolinol had no effect on EFS-induced contractions of Crotalus CC and Rabbit CC. Replacement of NaCl by N- Methyl-D-glucamine (NMDG) abolished EFS-induced contractions of rabbit CC, but did not affect Crotalus CC. The presence of tyrosine hydroxylase was identified in endothelial cells only of Crotalus CC. Since the EFS-induced contractions of Crotalus CC is dependent on catecholamine release, insensitive to TTX, insensitive to A803467 and to NaCl replacement, it indicates that the source of cathecolamine is unlikely to be from adrenergic terminals. The finding that tyrosine hydroxylase is present in endothelial cells suggests that these cells can modulate Crotalus CC tone.
[Mh] Termos MeSH primário: Crotalus/fisiologia
Estimulação Elétrica
Pênis/efeitos dos fármacos
Tetrodotoxina/farmacologia
[Mh] Termos MeSH secundário: Compostos de Anilina/farmacologia
Animais
Callithrix
Furanos/farmacologia
Imuno-Histoquímica
Masculino
Contração Muscular/efeitos dos fármacos
Pênis/fisiologia
Coelhos
Receptores Adrenérgicos/fisiologia
Canais de Sódio/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (A 803467); 0 (Aniline Compounds); 0 (Furans); 0 (Receptors, Adrenergic); 0 (Sodium Channels); 4368-28-9 (Tetrodotoxin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183766


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[PMID]:28739252
[Au] Autor:Szulczyk B; Nurowska E
[Ad] Endereço:Department of Drug Technology and Pharmaceutical Biotechnology, The Medical University of Warsaw, Banacha 1, 02-097, Poland. Electronic address: bartlomiej.szulczyk@wum.edu.pl.
[Ti] Título:Valproic acid inhibits TTX-resistant sodium currents in prefrontal cortex pyramidal neurons.
[So] Source:Biochem Biophys Res Commun;491(2):291-295, 2017 Sep 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Valproic acid is frequently prescribed and used to treat epilepsy, bipolar disorder and other conditions. However, the mechanism of action of valproic acid has not been fully elucidated. The aim of this study was to assess the influence of valproic acid (200 µM) on TTX-resistant sodium currents in mPFC pyramidal neurons. Valproic acid inhibited the maximal amplitude and did not change the activation parameters of TTX-resistant sodium currents. Moreover, valproic acid (2 µM and 200 µM) shifted the TTX-resistant sodium channel inactivation curve towards hyperpolarisation. In the presence of valproic acid, TTX-resistant sodium currents recovered from inactivation more slowly. Valproic acid did not influence the use-dependent blockade of TTX-resistant sodium currents. This study suggests that a potential new mechanism of the antiepileptic action of valproic acid is, among others, inhibition of TTX-resistant sodium currents.
[Mh] Termos MeSH primário: Anticonvulsivantes/farmacologia
Células Piramidais/efeitos dos fármacos
Bloqueadores dos Canais de Sódio/farmacologia
Canais de Sódio/metabolismo
Tetrodotoxina/farmacologia
Ácido Valproico/farmacologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Potenciais de Ação/fisiologia
Animais
Técnicas de Cultura de Células
Microtomia
Técnicas de Patch-Clamp
Córtex Pré-Frontal/citologia
Córtex Pré-Frontal/efeitos dos fármacos
Córtex Pré-Frontal/metabolismo
Cultura Primária de Células
Células Piramidais/citologia
Células Piramidais/metabolismo
Ratos
Sódio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticonvulsants); 0 (Sodium Channel Blockers); 0 (Sodium Channels); 4368-28-9 (Tetrodotoxin); 614OI1Z5WI (Valproic Acid); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


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[PMID]:28587910
[Au] Autor:Rambla-Alegre M; Reverté L; Del Río V; de la Iglesia P; Palacios O; Flores C; Caixach J; Campbell K; Elliott CT; Izquierdo-Muñoz A; Campàs M; Diogène J
[Ad] Endereço:IRTA, Ctra, Poble Nou, km 5.5, 43540 Sant Carles de la Ràpita, Tarragona, Spain. Electronic address: maria.rambla@irta.es.
[Ti] Título:Evaluation of tetrodotoxins in puffer fish caught along the Mediterranean coast of Spain. Toxin profile of Lagocephalus sceleratus.
[So] Source:Environ Res;158:1-6, 2017 10.
[Is] ISSN:1096-0953
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Although consumption of Tetraodontidae species is prohibited in the EU, intoxications are still reported. The evaluation of tetrodotoxins (TTXs) by mass spectrometry (LC-MS/MS and LC-HRMS) and a screening immunoassay (mELISA) in tetraodontid fishes caught along the Western Mediterranean Sea revealed high concentrations of TTXs in Lagocephalus sceleratus while no TTXs were identified in L. lagocephalus and Sphoeroides pachygaster individuals. The high TTXs content found in the L. sceleratus analysed herein demonstrate the occurrence of highly toxic puffer fish in the Western Mediterranean Sea. Being L. sceleratus a recent invasive species in the Mediterranean, surveillance, risk assessment and risk management measures are necessary. The strategy used within this research work could be a valuable tool for future food safety monitoring.
[Mh] Termos MeSH primário: Tetraodontiformes/metabolismo
Tetrodotoxina/análise
[Mh] Termos MeSH secundário: Animais
Cromatografia Líquida
Ensaio de Imunoadsorção Enzimática
Feminino
Espécies Introduzidas
Masculino
Espectrometria de Massas
Mar Mediterrâneo
Espanha
Especificidade da Espécie
Espectrometria de Massas em Tandem
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
4368-28-9 (Tetrodotoxin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE


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[PMID]:28546155
[Au] Autor:Xu Y; Cardell LO
[Ad] Endereço:Division of Ear, Nose, and Throat Diseases, Department of Clinical Sciences, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden; and yuan.xu@ki.se.
[Ti] Título:Long-term nicotine exposure dampens LPS-induced nerve-mediated airway hyperreactivity in murine airways.
[So] Source:Am J Physiol Lung Cell Mol Physiol;313(3):L516-L523, 2017 Sep 01.
[Is] ISSN:1522-1504
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nicotine is a major component of cigarette smoke. It causes addiction and is used clinically to aid smoke cessation. The aim of the present study is to investigate the effect of nicotine on lipopolysaccharide (LPS)-induced airway hyperreactivity (AHR) and to explore the potential involvement of neuronal mechanisms behind nicotine's effects in murine models in vivo and in vitro. BALB/c mice were exposed to nicotine in vivo via subcutaneous Alzet osmotic minipumps containing nicotine tartate salt solution (24 mg·kg ·day ) for 28 days. LPS (0.1 mg/ml, 20 µl) was administered intranasally for 3 consecutive days during the end of this period. Lung functions were measured with flexiVent. For the in vitro experiments, mice tracheae were organcultured with either nicotine (10 µM) or vehicle (DMSO, 0.1%) for 4 days. Contractile responses of the tracheal segments were measured in myographs following electric field stimulation (EFS; increasing frequencies of 0.2 to 12.8 Hz) before and after incubation with 10 µg/ml LPS for 1 h. Results showed that LPS induced AHR to methacholine in vivo and increased contractile responses to EFS in vitro. Interestingly, long-term nicotine exposure markedly dampened this LPS-induced AHR both in vitro and in vivo. Tetrodotoxin (TTX) inhibited LPS-induced AHR but did not further inhibit nicotine-suppressed AHR in vivo. In conclusion, long-term nicotine exposure dampened LPS-induced AHR. The effect of nicotine was mimicked by TTX, suggesting the involvement of neuronal mechanisms. This information might be used for evaluating the long-term effects of nicotine and further exploring of how tobacco products interact with bacterial airway infections.
[Mh] Termos MeSH primário: Hiper-Reatividade Brônquica/patologia
Pulmão/patologia
Tecido Nervoso/efeitos dos fármacos
Nicotina/farmacologia
[Mh] Termos MeSH secundário: Animais
Líquido da Lavagem Broncoalveolar
Colágeno/metabolismo
Estimulação Elétrica
Feminino
Inflamação/patologia
Lipopolissacarídeos
Pulmão/efeitos dos fármacos
Cloreto de Metacolina/farmacologia
Camundongos
Camundongos Endogâmicos BALB C
Técnicas de Cultura de Órgãos
Mecânica Respiratória/efeitos dos fármacos
Tetrodotoxina/toxicidade
Fatores de Tempo
Receptor 4 Toll-Like/metabolismo
Traqueia/efeitos dos fármacos
Traqueia/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipopolysaccharides); 0 (Toll-Like Receptor 4); 0W5ETF9M2K (Methacholine Chloride); 4368-28-9 (Tetrodotoxin); 6M3C89ZY6R (Nicotine); 9007-34-5 (Collagen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.1152/ajplung.00222.2016


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[PMID]:28510137
[Au] Autor:Dick OE; Krylov BV; Nozdrachev AD
[Ad] Endereço:Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg, 199034, Russia. glazov.holo@mail.ioffe.ru.
[Ti] Título:Possible mechanism of bursting suppression in nociceptive neurons.
[So] Source:Dokl Biochem Biophys;473(1):137-140, 2017 Mar.
[Is] ISSN:1608-3091
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Ab] Resumo:The use of the mathematical model of rat nociceptive neuron membrane allowed us to predict a new mechanism of suppression of ectopic bursting discharges, which arise in neurons of dorsal root ganglia and are one of the causes of neuropathic pain. The treatment with comenic acid leads to switching off the ectopic bursting discharges due to a decrease in the effective charge transferring via the activation gating structure of the slow sodium channels (Na 1.8a). Comenic acid is a drug substance of a new non-opioid analgesic [1] Thus, this analgesic not only reduces the frequency of rhythmic discharges of nociceptive neuron membrane [2] but also it suppresses its ectopic bursting discharges.
[Mh] Termos MeSH primário: Modelos Neurológicos
Nociceptores/citologia
[Mh] Termos MeSH secundário: Ácidos Carboxílicos/farmacologia
Ativação do Canal Iônico/efeitos dos fármacos
Canal de Sódio Disparado por Voltagem NAV1.8/química
Canal de Sódio Disparado por Voltagem NAV1.8/metabolismo
Nociceptores/efeitos dos fármacos
Nociceptores/metabolismo
Pironas/farmacologia
Tetrodotoxina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carboxylic Acids); 0 (NAV1.8 Voltage-Gated Sodium Channel); 0 (Pyrones); 0 (comenic acid); 4368-28-9 (Tetrodotoxin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE
[do] DOI:10.1134/S1607672917020120


  10 / 12444 MEDLINE  
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[PMID]:28416443
[Au] Autor:Copeland CS; Wall TM; Sims RE; Neale SA; Nisenbaum E; Parri HR; Salt TE
[Ad] Endereço:Institute of Ophthalmology, University College London, 11-43 Bath Street, London, EC1V 9EL, UK; St George's, University of London, Cranmer Terrace, London, SW17 0RE, UK. Electronic address: carolinecopeland@gmail.com.
[Ti] Título:Astrocytes modulate thalamic sensory processing via mGlu2 receptor activation.
[So] Source:Neuropharmacology;121:100-110, 2017 Jul 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Astrocytes possess many of the same signalling molecules as neurons. However, the role of astrocytes in information processing, if any, is unknown. Using electrophysiological and imaging methods, we report the first evidence that astrocytes modulate neuronal sensory inhibition in the rodent thalamus. We found that mGlu2 receptor activity reduces inhibitory transmission from the thalamic reticular nucleus to the somatosensory ventrobasal thalamus (VB): mIPSC frequencies in VB slices were reduced by the Group II mGlu receptor agonist LY354740, an effect potentiated by mGlu2 positive allosteric modulator (PAM) LY487379 co-application (30 nM LY354740: 10.0 ± 1.6% reduction; 30 nM LY354740 & 30 µM LY487379: 34.6 ± 5.2% reduction). We then showed activation of mGlu2 receptors on astrocytes: astrocytic intracellular calcium levels were elevated by the Group II agonist, which were further potentiated upon mGlu2 PAM co-application (300 nM LY354740: ratio amplitude 0.016 ± 0.002; 300 nM LY354740 & 30 µM LY487379: ratio amplitude 0.035 ± 0.003). We then demonstrated mGlu2-dependent astrocytic disinhibition of VB neurons in vivo: VB neuronal responses to vibrissae stimulation trains were disinhibited by the Group II agonist and the mGlu2 PAM (LY354740: 156 ± 12% of control; LY487379: 144 ± 10% of control). Presence of the glial inhibitor fluorocitrate abolished the mGlu2 PAM effect (91 ± 5% of control), suggesting the mGlu2 component to the Group II effect can be attributed to activation of mGlu2 receptors localised on astrocytic processes within the VB. Gating of thalamocortical function via astrocyte activation represents a novel sensory processing mechanism. As this thalamocortical circuitry is important in discriminative processes, this demonstrates the importance of astrocytes in synaptic processes underlying attention and cognition.
[Mh] Termos MeSH primário: Astrócitos/fisiologia
Células Receptoras Sensoriais/fisiologia
Tálamo/citologia
Vibrissas/fisiologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Astrócitos/efeitos dos fármacos
Cálcio/metabolismo
Citratos/farmacologia
Relação Dose-Resposta a Droga
Inibidores Enzimáticos/farmacologia
Fármacos atuantes sobre Aminoácidos Excitatórios/farmacologia
Técnicas In Vitro
Iontoforese
Masculino
N-Metilaspartato/farmacologia
Ratos
Ratos Sprague-Dawley
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
Valina/análogos & derivados
Valina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Citrates); 0 (Enzyme Inhibitors); 0 (Excitatory Amino Acid Agents); 0 (Sodium Channel Blockers); 357-89-1 (fluorocitrate); 4368-28-9 (Tetrodotoxin); 6384-92-5 (N-Methylaspartate); 76326-31-3 (2-amino-5-phosphopentanoic acid); HG18B9YRS7 (Valine); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE



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