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  1 / 121 MEDLINE  
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[PMID]:29307525
[Au] Autor:Candenas L; Pinto FM; Cejudo-Román A; González-Ravina C; Fernández-Sánchez M; Pérez-Hernández N; Irazusta J; Subirán N
[Ad] Endereço:Instituto de Investigaciones Químicas (L.C., F.M.P., A.C.-R., N.P.), CSIC, Seville, Spain. Electronic address: luzcandenas@iiq.csic.es.
[Ti] Título:Veratridine-sensitive Na channels regulate human sperm fertilization capacity.
[So] Source:Life Sci;196:48-55, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: The sperm plasma membrane contains specific ion channels and transporters that initiate changes in Ca , Na , K and H ions in the sperm cytoplasm. Ion channels are key regulators of the sperm membrane potential, cytoplasmic Ca and intracellular pH (pH ), which leads to regulate motility, capacitation, acrosome reaction and other physiological processes crucial for successful fertilization. Expression of epithelial sodium channels (ENaC) and voltage-gated sodium channels (Na ) in human spermatozoa has been reported, but the role of Na fluxes sodium channels in the regulation of sperm cell function remains poorly understood. In this context, we aimed to analyze the physiological role of Na channels in human sperm. MAIN METHODS: Motility and hyperactivation analysis was conducted by CASA analysis. Flow cytometry and spectrophotometry approaches were carried out to measure Capacitation, Acrosome reaction, immunohistochemistry for Tyr-residues phosporylation, [Ca ] levels and membrane potential. KEY FINDINGS: Functional studies showed that veratridine, a voltage-gated sodium channel activator, increased sperm progressive motility without producing hyperactivation while the Na antagonist lidocaine did induce hyperactivated motility. Veratridine increased protein tyrosine phosphorylation, an event occurring during capacitation, and its effects were inhibited in the presence of lidocaine and tetrodotoxin. Veratridine had no effect on the acrosome reaction by itself, but was able to block the progesterone-induced acrosome reaction. Moreover, veratridine caused a membrane depolarization and modified the effect of progesterone on [Ca ] and sperm membrane potential. SIGNIFICANCE: Our results suggest that veratridine-sensitive Na channels are involved on human sperm fertility acquisition regulating motility, capacitation and the progesterone-induced acrosome reaction in human sperm.
[Mh] Termos MeSH primário: Fertilização/efeitos dos fármacos
Agonistas de Canais de Sódio/farmacologia
Canais de Sódio/efeitos dos fármacos
Espermatozoides/efeitos dos fármacos
Veratridina/farmacologia
[Mh] Termos MeSH secundário: Reação Acrossômica/efeitos dos fármacos
Adolescente
Adulto
Feminino
Seres Humanos
Imuno-Histoquímica
Técnicas In Vitro
Lidocaína/farmacologia
Masculino
Potenciais da Membrana/efeitos dos fármacos
Progesterona/antagonistas & inibidores
Progesterona/farmacologia
Receptores Androgênicos/efeitos dos fármacos
Sêmen/efeitos dos fármacos
Sódio/metabolismo
Bloqueadores dos Canais de Sódio/farmacologia
Capacitação Espermática/efeitos dos fármacos
Motilidade Espermática/efeitos dos fármacos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Androgen); 0 (Sodium Channel Agonists); 0 (Sodium Channel Blockers); 0 (Sodium Channels); 4G7DS2Q64Y (Progesterone); 71-62-5 (Veratridine); 98PI200987 (Lidocaine); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


  2 / 121 MEDLINE  
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[PMID]:28259560
[Au] Autor:Agharkar AS; Gonzales EB
[Ad] Endereço:Center for Neuroscience Discovery, Institute for Healthy Aging, University of North Texas Health Science Center, Fort Worth, TX, USA.
[Ti] Título:4-Chlorophenylguanidine is an ASIC3 agonist and positive allosteric modulator.
[So] Source:J Pharmacol Sci;133(3):184-186, 2017 Mar.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Acid-sensing ion channels (ASICs) are proton-sensitive sodium channels that open in response to lowered extracellular pH and are expressed in the central and peripheral nervous systems. The ASIC3 subtype is found primarily in the periphery where the channel mediates pain signals caused by ischemia and inflammation. Here, we provide identify 4-chlorophenylguanidine (4-CPG) as an ASIC3 positive allosteric modulator and newest member of the growing group of guanidine modulators of ASICs. Furthermore, the 4-CPG reversed the effects of ASIC3 desensitization. The molecule 4-CPG offers a novel chemical backbone for the design of new ASIC3 ligands to study ASIC3 in vivo.
[Mh] Termos MeSH primário: Canais Iônicos Sensíveis a Ácido/fisiologia
Guanidina/análogos & derivados
Agonistas de Canais de Sódio/farmacologia
[Mh] Termos MeSH secundário: Animais
Células CHO
Cricetulus
Guanidina/farmacologia
Concentração de Íons de Hidrogênio
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acid Sensing Ion Channels); 0 (Sodium Channel Agonists); 0 (chlorophenylguanidine); JU58VJ6Y3B (Guanidine)
[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:170306
[St] Status:MEDLINE


  3 / 121 MEDLINE  
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[PMID]:27556810
[Au] Autor:Lin Z; Santos S; Padilla K; Printzenhoff D; Castle NA
[Ad] Endereço:Neuroscience and Pain Research Unit, Pfizer Inc., Durham, North Carolina, United States of America.
[Ti] Título:Biophysical and Pharmacological Characterization of Nav1.9 Voltage Dependent Sodium Channels Stably Expressed in HEK-293 Cells.
[So] Source:PLoS One;11(8):e0161450, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The voltage dependent sodium channel Nav1.9, is expressed preferentially in peripheral sensory neurons and has been linked to human genetic pain disorders, which makes it target of interest for the development of new pain therapeutics. However, characterization of Nav1.9 pharmacology has been limited due in part to the historical difficulty of functionally expressing recombinant channels. Here we report the successful generation and characterization of human, mouse and rat Nav1.9 stably expressed in human HEK-293 cells. These cells exhibit slowly activating and inactivating inward sodium channel currents that have characteristics of native Nav1.9. Optimal functional expression was achieved by coexpression of Nav1.9 with ß1/ß2 subunits. While recombinantly expressed Nav1.9 was found to be sensitive to sodium channel inhibitors TC-N 1752 and tetracaine, potency was up to 100-fold less than reported for other Nav channel subtypes despite evidence to support an interaction with the canonical local anesthetic (LA) binding region on Domain 4 S6. Nav1.9 Domain 2 S6 pore domain contains a unique lysine residue (K799) which is predicted to be spatially near the local anesthetic interaction site. Mutation of this residue to the consensus asparagine (K799N) resulted in an increase in potency for tetracaine, but a decrease for TC-N 1752, suggesting that this residue can influence interaction of inhibitors with the Nav1.9 pore. In summary, we have shown that stable functional expression of Nav1.9 in the widely used HEK-293 cells is possible, which opens up opportunities to better understand channel properties and may potentially aid identification of novel Nav1.9 based pharmacotherapies.
[Mh] Termos MeSH primário: Expressão Gênica
Canal de Sódio Disparado por Voltagem NAV1.9/genética
Canal de Sódio Disparado por Voltagem NAV1.9/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Anestésicos Locais/química
Anestésicos Locais/farmacologia
Animais
Sítios de Ligação
Células HEK293
Seres Humanos
Concentração Inibidora 50
Ativação do Canal Iônico/efeitos dos fármacos
Lisina/química
Lisina/metabolismo
Potenciais da Membrana/efeitos dos fármacos
Camundongos
Modelos Moleculares
Conformação Molecular
Canal de Sódio Disparado por Voltagem NAV1.9/química
Ligação Proteica
Ratos
Agonistas de Canais de Sódio/química
Agonistas de Canais de Sódio/farmacologia
Bloqueadores dos Canais de Sódio/química
Bloqueadores dos Canais de Sódio/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anesthetics, Local); 0 (NAV1.9 Voltage-Gated Sodium Channel); 0 (Sodium Channel Agonists); 0 (Sodium Channel Blockers); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160825
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0161450


  4 / 121 MEDLINE  
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[PMID]:26920689
[Au] Autor:Radu BM; Banciu A; Banciu DD; Radu M
[Ad] Endereço:Department of Neurological and Movement Sciences, Section of Anatomy and Histology, University of Verona, Verona, Italy; Department of Anatomy, Animal Physiology and Biophysics, Faculty of Biology, University of Bucharest, Bucharest, Romania.
[Ti] Título:Acid-Sensing Ion Channels as Potential Pharmacological Targets in Peripheral and Central Nervous System Diseases.
[So] Source:Adv Protein Chem Struct Biol;103:137-67, 2016.
[Is] ISSN:1876-1623
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Acid-sensing ion channels (ASICs) are widely expressed in the body and represent good sensors for detecting protons. The pH drop in the nervous system is equivalent to ischemia and acidosis, and ASICs are very good detectors in discriminating slight changes in acidity. ASICs are important pharmacological targets being involved in a variety of pathophysiological processes affecting both the peripheral nervous system (e.g., peripheral pain, diabetic neuropathy) and the central nervous system (e.g., stroke, epilepsy, migraine, anxiety, fear, depression, neurodegenerative diseases, etc.). This review discusses the role played by ASICs in different pathologies and the pharmacological agents acting on ASICs that might represent promising drugs. As the majority of above-mentioned pathologies involve not only neuronal dysfunctions but also microvascular alterations, in the next future, ASICs may be also considered as potential pharmacological targets at the vasculature level. Perspectives and limitations in the use of ASICs antagonists and modulators as pharmaceutical agents are also discussed.
[Mh] Termos MeSH primário: Canais Iônicos Sensíveis a Ácido/genética
Doenças do Sistema Nervoso Central/tratamento farmacológico
Neurônios/efeitos dos fármacos
Doenças do Sistema Nervoso Periférico/tratamento farmacológico
[Mh] Termos MeSH secundário: Bloqueadores do Canal Iônico Sensível a Ácido/uso terapêutico
Canais Iônicos Sensíveis a Ácido/efeitos dos fármacos
Doenças do Sistema Nervoso Central/classificação
Doenças do Sistema Nervoso Central/genética
Seres Humanos
Terapia de Alvo Molecular
Neurônios/patologia
Doenças do Sistema Nervoso Periférico/classificação
Doenças do Sistema Nervoso Periférico/genética
Agonistas de Canais de Sódio/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Acid Sensing Ion Channel Blockers); 0 (Acid Sensing Ion Channels); 0 (Sodium Channel Agonists)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160227
[Lr] Data última revisão:
160227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160228
[St] Status:MEDLINE


  5 / 121 MEDLINE  
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[PMID]:26637352
[Au] Autor:Du Y; Nomura Y; Zhorov BS; Dong K
[Ad] Endereço:From the Department of Entomology, Genetics and Neuroscience Programs, Michigan State University, East Lansing, Michigan 48824.
[Ti] Título:Evidence for Dual Binding Sites for 1,1,1-Trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) in Insect Sodium Channels.
[So] Source:J Biol Chem;291(9):4638-48, 2016 Feb 26.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:1,1,1-Trichloro-2,2-bis(p-chlorophenyl)ethane (DDT), the first organochlorine insecticide, and pyrethroid insecticides are sodium channel agonists. Although the use of DDT is banned in most of the world due to its detrimental impact on the ecosystem, indoor residual spraying of DDT is still recommended for malaria control in Africa. Development of resistance to DDT and pyrethroids is a serious global obstacle for managing disease vectors. Mapping DDT binding sites is necessary for understanding mechanisms of resistance and modulation of sodium channels by structurally different ligands. The pioneering model of the housefly sodium channel visualized the first receptor for pyrethroids, PyR1, in the II/III domain interface and suggested that DDT binds within PyR1. Previously, we proposed the second pyrethroid receptor, PyR2, at the I/II domain interface. However, whether DDT binds to both pyrethroid receptor sites remains unknown. Here, using computational docking of DDT into the Kv1.2-based mosquito sodium channel model, we predict that two DDT molecules can bind simultaneously within PyR1 and PyR2. The bulky trichloromethyl group of each DDT molecule fits snugly between four helices in the bent domain interface, whereas two p-chlorophenyl rings extend into two wings of the interface. Model-driven mutagenesis and electrophysiological analysis confirmed these propositions and revealed 10 previously unknown DDT-sensing residues within PyR1 and PyR2. Our study proposes a dual DDT-receptor model and provides a structural background for rational development of new insecticides.
[Mh] Termos MeSH primário: Aedes
DDT/metabolismo
Proteínas de Insetos/metabolismo
Inseticidas/metabolismo
Modelos Moleculares
Canal de Sódio Disparado por Voltagem NAV1.1/metabolismo
Agonistas de Canais de Sódio/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Substituição de Aminoácidos
Animais
Sítios de Ligação
DDT/química
Proteínas de Insetos/agonistas
Proteínas de Insetos/química
Inseticidas/química
Canal de Potássio Kv1.2/química
Canal de Potássio Kv1.2/metabolismo
Ligantes
Conformação Molecular
Simulação de Acoplamento Molecular
Dados de Sequência Molecular
Método de Monte Carlo
Mutação
Canal de Sódio Disparado por Voltagem NAV1.1/química
Estrutura Terciária de Proteína
Receptores de Neurotransmissores/química
Receptores de Neurotransmissores/metabolismo
Alinhamento de Sequência
Agonistas de Canais de Sódio/química
Homologia Estrutural de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Insect Proteins); 0 (Insecticides); 0 (Kv1.2 Potassium Channel); 0 (Ligands); 0 (NAV1.1 Voltage-Gated Sodium Channel); 0 (Receptors, Neurotransmitter); 0 (Sodium Channel Agonists); 0 (pyrethrin receptor); CIW5S16655 (DDT)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170226
[Lr] Data última revisão:
170226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151206
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M115.678672


  6 / 121 MEDLINE  
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[PMID]:26582234
[Au] Autor:Wang Y; O'Bryant Z; Wang H; Huang Y
[Ad] Endereço:School of Pharmacy, Anhui Medical University, Meishan Road, Hefei, 230032, Anhui, China.
[Ti] Título:Regulating Factors in Acid-Sensing Ion Channel 1a Function.
[So] Source:Neurochem Res;41(4):631-45, 2016 Apr.
[Is] ISSN:1573-6903
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In recent years, research of acid sensing ion channels (ASICs) has increased tremendously, especially studies focusing on ASIC1a, which plays a critical role in many important physiologic and pathological functions. This review will discuss factors regulating ASIC1a expression and activity in various conditions and will provide a theoretical basis for clinical development and application of ASIC1a modifiers.
[Mh] Termos MeSH primário: Canais Iônicos Sensíveis a Ácido/metabolismo
[Mh] Termos MeSH secundário: Bloqueadores do Canal Iônico Sensível a Ácido/farmacologia
Animais
Seres Humanos
Oxirredução
Transdução de Sinais
Agonistas de Canais de Sódio/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Acid Sensing Ion Channel Blockers); 0 (Acid Sensing Ion Channels); 0 (Sodium Channel Agonists)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151120
[St] Status:MEDLINE
[do] DOI:10.1007/s11064-015-1768-x


  7 / 121 MEDLINE  
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[PMID]:25947342
[Au] Autor:Gao S; Yu Y; Ma ZY; Sun H; Zhang YL; Wang XT; Wang C; Fan WM; Zheng QY; Ma CL
[Ad] Endereço:Department of Physiology, Binzhou Medical University, Yantai Campus, 346 Guanhai Road, Laishan District, Yantai, 264003, Shandong, China.
[Ti] Título:NMDAR-Mediated Hippocampal Neuronal Death is Exacerbated by Activities of ASIC1a.
[So] Source:Neurotox Res;28(2):122-37, 2015 Aug.
[Is] ISSN:1476-3524
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NMDARs and ASIC1a both exist in central synapses and mediate important physiological and pathological conditions, but the functional relationship between them is unclear. Here we report several novel findings that may shed light on the functional relationship between these two ion channels in the excitatory postsynaptic membrane of mouse hippocampus. Firstly, NMDAR activation induced by either NMDA or OGD led to increased [Ca(2+)](i)and greater apoptotic and necrotic cell deaths in cultured hippocampal neurons; these cell deaths were prevented by application of NMDAR antagonists. Secondly, ASIC1a activation induced by pH 6.0 extracellular solution (ECS) showed similar increases in apoptotic and necrotic cell deaths; these cell deaths were prevented by ASIC1a antagonists, and also by NMDAR antagonists. Since increased [Ca(2+)](i)leads to increased cell deaths and since NMDAR exhibits much greater calcium permeability than ASIC1a, these data suggest that ASIC1a-induced neuronal death is mediated through activation of NMDARs. Thirdly, treatment of hippocampal cultures with both NMDA and acidic ECS induced greater degrees of cell deaths than either NMDA or acidic ECS treatment alone. These results suggest that ASIC1a activation up-regulates NMDAR function. Additional data supporting the functional relationship between ASIC1a and NMDAR are found in our electrophysiology experiments in hippocampal slices, where stimulation of ASIC1a induced a marked increase in NMDAR EPSC amplitude, and inhibition of ASIC1a resulted in a decrease in NMDAR EPSC amplitude. In summary, we present evidence that ASIC1a activity facilitates NMDAR function and exacerbates NMDAR-mediated neuronal death in pathological conditions. These findings are invaluable to the search for novel therapeutic targets in the treatment of brain ischemia.
[Mh] Termos MeSH primário: Canais Iônicos Sensíveis a Ácido/metabolismo
Morte Celular/fisiologia
Hipocampo/fisiopatologia
Neurônios/fisiologia
Receptores de N-Metil-D-Aspartato/metabolismo
[Mh] Termos MeSH secundário: Bloqueadores do Canal Iônico Sensível a Ácido/farmacologia
Animais
Cálcio/metabolismo
Caspase 3/metabolismo
Morte Celular/efeitos dos fármacos
Hipóxia Celular/efeitos dos fármacos
Hipóxia Celular/fisiologia
Células Cultivadas
Antagonistas de Aminoácidos Excitatórios/farmacologia
Glucose/deficiência
Hipocampo/efeitos dos fármacos
Concentração de Íons de Hidrogênio
Camundongos Endogâmicos C57BL
N-Metilaspartato/metabolismo
Neurônios/efeitos dos fármacos
Receptores de N-Metil-D-Aspartato/agonistas
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
Agonistas de Canais de Sódio/farmacologia
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Accn2 protein, mouse); 0 (Acid Sensing Ion Channel Blockers); 0 (Acid Sensing Ion Channels); 0 (Excitatory Amino Acid Antagonists); 0 (Receptors, N-Methyl-D-Aspartate); 0 (Sodium Channel Agonists); 6384-92-5 (N-Methylaspartate); EC 3.4.22.- (Casp3 protein, mouse); EC 3.4.22.- (Caspase 3); IY9XDZ35W2 (Glucose); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150508
[St] Status:MEDLINE
[do] DOI:10.1007/s12640-015-9530-3


  8 / 121 MEDLINE  
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[PMID]:25812545
[Au] Autor:Clara A; Rauch S; Überbacher CA; Felgenhauer N; Drüge G
[Ad] Endereço:Abteilung für Anästhesie und Intensivmedizin, Krankenhaus "F. Tappeiner" Meran, 39012, Meran, Italien, andreas.clara@asbmeran-o.it.
[Ti] Título:[High-dose magnesium sulfate in the treatment of aconite poisoning].
[Ti] Título:Hochdosiertes Magnesiumsulfat bei Aconitumintoxikation..
[So] Source:Anaesthesist;64(5):381-4, 2015 May.
[Is] ISSN:1432-055X
[Cp] País de publicação:Germany
[La] Idioma:ger
[Ab] Resumo:This article reports the case of a 62-year-old male patient who ingested the roots of Monkshood (Aconitum napellus) and white hellebore (Veratrum album) dissolved in alcohol with a suicidal intention and suffered cardiotoxic and neurotoxic symptoms. After contacting the Poison Information Centre ventricular arrhythmia was treated with high-dose magnesium sulphate as the only antiarrhythmic agent and subsequently a stable sinus rhythm could be established after approximately 3 h. Aconitum napellus is considered the most poisonous plant in Europe and it is found in gardens, the Alps and the Highlands. Poisoning is mainly caused by the alkaloid aconite that leads to persistent opening and activation of voltage-dependent sodium channels resulting in severe cardiac and neurological toxicity. As no specific antidote is known so far, poisoning is associated with a high mortality. The therapy with high-dose magnesium sulphate is based on in vitro and animal experiments as well as limited clinical case reports.
[Mh] Termos MeSH primário: Aconitum/envenenamento
Antiarrítmicos/uso terapêutico
Sulfato de Magnésio/uso terapêutico
Veratrum/envenenamento
[Mh] Termos MeSH secundário: Alcaloides/envenenamento
Antiarrítmicos/administração & dosagem
Arritmias Cardíacas/induzido quimicamente
Arritmias Cardíacas/tratamento farmacológico
Eletrocardiografia
Cardiopatias/induzido quimicamente
Cardiopatias/tratamento farmacológico
Seres Humanos
Sulfato de Magnésio/administração & dosagem
Masculino
Meia-Idade
Síndromes Neurotóxicas/tratamento farmacológico
Agonistas de Canais de Sódio/envenenamento
Canais de Sódio/efeitos dos fármacos
Tentativa de Suicídio
Taquicardia/induzido quimicamente
Taquicardia/tratamento farmacológico
[Pt] Tipo de publicação:CASE REPORTS; ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkaloids); 0 (Anti-Arrhythmia Agents); 0 (Sodium Channel Agonists); 0 (Sodium Channels); 7487-88-9 (Magnesium Sulfate)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170916
[Lr] Data última revisão:
170916
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150328
[St] Status:MEDLINE
[do] DOI:10.1007/s00101-015-0013-y


  9 / 121 MEDLINE  
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[PMID]:25645866
[Au] Autor:Yamada M; Saitoh A; Ohashi M; Suzuki S; Oka J; Yamada M
[Ad] Endereço:Department of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashimachi, Kodaira, Tokyo, 187-8553, Japan.
[Ti] Título:Induction of c-Fos immunoreactivity in the amygdala of mice expressing anxiety-like behavior after local perfusion of veratrine in the prelimbic medial prefrontal cortex.
[So] Source:J Neural Transm (Vienna);122(8):1203-7, 2015 Aug.
[Is] ISSN:1435-1463
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:Local perfusion of the sodium channel activator veratrine in mouse prelimbic medial prefrontal cortex (PL) induced c-Fos immunoreactivity in the sub-regions of amygdala. Co-perfusion of the NMDA receptor antagonist MK-801 diminished the c-Fos expression. Significant correlations were observed between c-Fos immunoreactivity and behavioral measures in the open-field test. The PL stimulation activates a neural network projecting to the amygdala via NMDA receptor-mediated glutamatergic neurotransmission. Anxiety-like behavior induced after the PL stimulation may be partly mediated through the activation of amygdala.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/metabolismo
Ansiedade/metabolismo
Córtex Pré-Frontal/metabolismo
Proteínas Proto-Oncogênicas c-fos/metabolismo
[Mh] Termos MeSH secundário: 6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Tonsila do Cerebelo/efeitos dos fármacos
Animais
Ansiedade/tratamento farmacológico
Maleato de Dizocilpina/farmacologia
Antagonistas de Aminoácidos Excitatórios/farmacologia
Imuno-Histoquímica
Masculino
Camundongos Endogâmicos C57BL
Atividade Motora/efeitos dos fármacos
Atividade Motora/fisiologia
Vias Neurais/efeitos dos fármacos
Vias Neurais/metabolismo
Fotomicrografia
Córtex Pré-Frontal/efeitos dos fármacos
Agonistas de Canais de Sódio/administração & dosagem
Veratrina/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Excitatory Amino Acid Antagonists); 0 (Proto-Oncogene Proteins c-fos); 0 (Sodium Channel Agonists); 6LR8C1B66Q (Dizocilpine Maleate); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); ERQ7M6C50B (Veratrine)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150204
[St] Status:MEDLINE
[do] DOI:10.1007/s00702-015-1373-9


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[PMID]:25023314
[Au] Autor:Molnar P; Hickman JJ
[Ad] Endereço:Faculty of Natural Sciences, University of West Hungary, Károlyi Gáspár tér 4, Szombathely, H-9700, Hungary, pmolnar@pminfonet.com.
[Ti] Título:Modeling of action potential generation in NG108-15 cells.
[So] Source:Methods Mol Biol;1183:253-61, 2014.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In order to explore the possibility of identifying toxins based on their effect on the shape of action potentials, we created a computer model of the action potential generation in NG108-15 cells (a neuroblastoma/glioma hybrid cell line). To generate the experimental data for model validation, voltage-dependent sodium, potassium and high-threshold calcium currents, as well as action potentials, were recorded from NG108-15 cells with conventional whole-cell patch-clamp methods. Based on the classic Hodgkin-Huxley formalism and the linear thermodynamic description of the rate constants, ion-channel parameters were estimated using an automatic fitting method. Utilizing the established parameters, action potentials were generated using the Hodgkin-Huxley formalism and were fitted to the recorded action potentials. To demonstrate the applicability of the method for toxin detection and discrimination, the effect of tetrodotoxin (a sodium channel blocker) and tefluthrin (a pyrethroid that is a sodium channel opener) were studied. The two toxins affected the shape of the action potentials differently, and their respective effects were identified based on the predicted changes in the fitted parameters.
[Mh] Termos MeSH primário: Potenciais de Ação
Simulação por Computador
Modelos Neurológicos
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Técnicas de Cultura de Células/métodos
Linhagem Celular Tumoral
Ciclopropanos/análise
Ciclopropanos/farmacologia
Hidrocarbonetos Fluorados/análise
Hidrocarbonetos Fluorados/farmacologia
Canais Iônicos/metabolismo
Técnicas de Patch-Clamp/métodos
Agonistas de Canais de Sódio/análise
Agonistas de Canais de Sódio/farmacologia
Bloqueadores dos Canais de Sódio/análise
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
Termodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Cyclopropanes); 0 (Hydrocarbons, Fluorinated); 0 (Ion Channels); 0 (Sodium Channel Agonists); 0 (Sodium Channel Blockers); 2HE8P42H2J (2,3,5,6-tetrafluoro-4-methylbenzyl (Z)-(1RS)-cis-3-(2-chloro-3,3,3-trifluoroprop-1-enyl)-2,2-dimethylcyclopropanecarboxylate); 4368-28-9 (Tetrodotoxin)
[Em] Mês de entrada:1502
[Cu] Atualização por classe:140715
[Lr] Data última revisão:
140715
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140716
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-1096-0_16



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