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Pesquisa : D20.888.065.115.060 [Categoria DeCS]
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[PMID]:28982705
[Au] Autor:Zhang Y; Huang H
[Ad] Endereço:Department of Cell and Molecular Biology and.
[Ti] Título:SK Channels Regulate Resting Properties and Signaling Reliability of a Developing Fast-Spiking Neuron.
[So] Source:J Neurosci;37(44):10738-10747, 2017 Nov 01.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Reliable and precise signal transmission is essential in circuits of the auditory brainstem to encode timing with submillisecond accuracy. Globular bushy cells reliably and faithfully transfer spike signals to the principal neurons of the medial nucleus of the trapezoid body (MNTB) through the giant glutamatergic synapse, the calyx of Held. Thus, the MNTB works as a relay nucleus that preserves the temporal pattern of firing at high frequency. Using whole-cell patch-clamp recordings, we observed a K conductance mediated by small-conductance calcium-activated potassium (SK) channels in the MNTB neurons from rats of either sex. SK channels were activated by intracellular Ca sparks and mediated spontaneous transient outward currents in developing MNTB neurons. SK channels were also activated by Ca influx through voltage-gated Ca channels and synaptically activated NMDA receptors. Blocking SK channels with apamin depolarized the resting membrane potential, reduced resting conductance, and affected the responsiveness of MNTB neurons to signal inputs. Moreover, SK channels were activated by action potentials and affected the spike afterhyperpolarization. Blocking SK channels disrupted the one-to-one signal transmission from presynaptic calyces to postsynaptic MNTB neurons and induced extra postsynaptic action potentials in response to presynaptic firing. These data reveal that SK channels play crucial roles in regulating the resting properties and maintaining reliable signal transmission of MNTB neurons. Reliable and precise signal transmission is required in auditory brainstem circuits to localize the sound source. The calyx of Held synapse in the mammalian medial nucleus of the trapezoid body (MNTB) plays an important role in sound localization. We investigated the potassium channels that shape the reliability of signal transfer across the calyceal synapse and observed a potassium conductance mediated by small-conductance calcium-activated potassium (SK) channels in rat MNTB principal neurons. We found that SK channels are tonically activated and contribute to the resting membrane properties of MNTB neurons. Interestingly, SK channels are transiently activated by calcium sparks and calcium influx during action potentials and control the one-to-one signal transmission from presynaptic calyces to postsynaptic MNTB neurons.
[Mh] Termos MeSH primário: Potenciais da Membrana/fisiologia
Neurônios/fisiologia
Canais de Potássio Ativados por Cálcio de Condutância Baixa/fisiologia
Corpo Trapezoide/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Potenciais de Ação/fisiologia
Animais
Apamina/farmacologia
Tronco Encefálico/fisiologia
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Potenciais Pós-Sinápticos Excitadores/fisiologia
Feminino
Masculino
Potenciais da Membrana/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Técnicas de Cultura de Órgãos
Ratos
Ratos Wistar
Superfamília Shaker de Canais de Potássio/antagonistas & inibidores
Superfamília Shaker de Canais de Potássio/farmacologia
Canais de Potássio Ativados por Cálcio de Condutância Baixa/antagonistas & inibidores
Fatores de Tempo
Corpo Trapezoide/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Shaker Superfamily of Potassium Channels); 0 (Small-Conductance Calcium-Activated Potassium Channels); 24345-16-2 (Apamin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1243-17.2017


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[PMID]:28405682
[Au] Autor:Kim JY; An HJ; Kim WH; Park YY; Park KD; Park KK
[Ad] Endereço:Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu 705-718, Republic of Korea.
[Ti] Título:Apamin suppresses biliary fibrosis and activation of hepatic stellate cells.
[So] Source:Int J Mol Med;39(5):1188-1194, 2017 May.
[Is] ISSN:1791-244X
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Cholestatic liver disease is characterized by the progressive destruction of biliary epithelial cells (BECs) followed by fibrosis, cirrhosis and liver failure. Activated hepatic stellate cells (HSCs) and portal fibroblasts are the major cellular effectors of enhanced collagen deposition in biliary fibrosis. Apamin, an 18 amino acid peptide neurotoxin found in apitoxin (bee venom), is known to block Ca2+-activated K+ channels and prevent carbon tetrachloride-induced liver fibrosis. In the present study, we aimed to ascertain whether apamin inhibits biliary fibrosis and the proliferation of HSCs. Cholestatic liver fibrosis was established in mouse models with 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) feeding. Cellular assays were performed on HSC-T6 cells (rat immortalized HSCs). DDC feeding led to increased hepatic damage and proinflammtory cytokine levels. Notably, apamin treatment resulted in decreased liver injury and proinflammatory cytokine levels. Moreover, apamin suppressed the deposition of collagen, proliferation of BECs and expression of fibrogenic genes in the DDC-fed mice. In HSCs, apamin suppressed activation of HSCs by inhibiting the Smad signaling pathway. These data suggest that apamin may be a potential therapeutic target in cholestatic liver disease.
[Mh] Termos MeSH primário: Apamina/farmacologia
Células Estreladas do Fígado/efeitos dos fármacos
Células Estreladas do Fígado/metabolismo
Cirrose Hepática Biliar/etiologia
Cirrose Hepática Biliar/metabolismo
[Mh] Termos MeSH secundário: Animais
Biópsia
Proliferação Celular/efeitos dos fármacos
Citocinas/metabolismo
Dieta
Modelos Animais de Doenças
Matriz Extracelular/metabolismo
Mediadores da Inflamação/metabolismo
Cirrose Hepática Biliar/patologia
Masculino
Camundongos
Transdução de Sinais/efeitos dos fármacos
Proteínas Smad/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammation Mediators); 0 (Smad Proteins); 24345-16-2 (Apamin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.3892/ijmm.2017.2922


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[PMID]:28302447
[Au] Autor:Tanaka S; Ono Y; Sakamoto K
[Ad] Endereço:Department of Pharmacology, Fukushima Medical University School of Medicine, 1 Hikarigaoka, Fukushima, Fukushima, 960-1295, Japan.
[Ti] Título:DCEBIO facilitates myogenic differentiation via intermediate conductance Ca activated K channel activation in C2C12 myoblasts.
[So] Source:J Pharmacol Sci;133(4):276-279, 2017 Apr.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Membrane hyperpolarization is suggested to be a trigger for skeletal muscle differentiation. We investigated whether DCEBIO, an opener of the small/intermediate conductance Ca activated K (SK /IK ) channels, increase myogenic differentiation in C2C12 skeletal myoblasts. DCEBIO significantly increased myotube formation, protein expression level of myosin heavy chain II, and mRNA expression level of myogenin in C2C12 myoblasts cultured in differentiation medium. DCEBIO induced myotube formation and hyperpolarization were reduced by the IK channel blocker TRAM-34, but not by the SK channel blocker apamin. These findings show that DCEBIO increases myogenic differentiation by activating IK channels.
[Mh] Termos MeSH primário: Benzimidazóis/farmacologia
Diferenciação Celular/efeitos dos fármacos
Mioblastos/citologia
Canais de Potássio Cálcio-Ativados/efeitos dos fármacos
[Mh] Termos MeSH secundário: Apamina/farmacologia
Células Cultivadas
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Fibras Musculares Esqueléticas/efeitos dos fármacos
Músculo Esquelético/citologia
Mioblastos/metabolismo
Miogenina/genética
Miogenina/metabolismo
Cadeias Pesadas de Miosina/genética
Cadeias Pesadas de Miosina/metabolismo
Canais de Potássio Cálcio-Ativados/antagonistas & inibidores
Pirazóis/farmacologia
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one); 0 (Benzimidazoles); 0 (Myogenin); 0 (Potassium Channels, Calcium-Activated); 0 (Pyrazoles); 0 (RNA, Messenger); 0 (TRAM 34); 24345-16-2 (Apamin); EC 3.6.4.1 (Myosin Heavy Chains)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE


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[PMID]:28223151
[Au] Autor:Ruamyod K; Watanapa WB; Shayakul C
[Ad] Endereço:Department of Physiology Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand. Electronic address: katesirin.ruy@mahidol.ac.th.
[Ti] Título:Testosterone rapidly increases Ca -activated K currents causing hyperpolarization in human coronary artery endothelial cells.
[So] Source:J Steroid Biochem Mol Biol;168:118-126, 2017 Apr.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Testosterone has endothelium-dependent vasodilatory effects on the coronary artery, with some reports suggesting endothelial ion channel involvement. This study employed the whole-cell patch clamp technique to investigate the effect of testosterone on ion channels in human coronary artery endothelial cells (HCAECs) and the mechanisms involved. We found that 0.03-3µM testosterone significantly induced a rapid, concentration-dependent increase in total HCAEC current (EC , 71.96±1.66nM; maximum increase, 59.13±8.37%; mean±SEM). The testosterone-enhanced currents consisted of small- and large-conductance Ca -activated K currents (SK and BK currents), but not Cl and nonselective cation currents. Either a non-permeant testosterone conjugate or the non-aromatizable androgen dihydrotestosterone (DHT) could increase HCAEC currents as well. The androgen receptor antagonist flutamide prevented this testosterone, testosterone conjugate, and DHT effect, while the estrogen receptor antagonist fulvestrant did not. Incubating HCAECs with pertussis toxin or protein kinase A inhibitor H-89 largely inhibited the testosterone effect, while pre-incubation with phospholipase C inhibitor U-73122, prostacyclin inhibitor indomethacin, nitric oxide synthase inhibitor L-NAME or cytochrome P450 inhibitor MS-PPOH, did not. Finally, testosterone application induced HCAEC hyperpolarization within minutes; this effect was prevented by SK and BK current inhibitors apamin and iberiotoxin. This is the first electrophysiological demonstration of androgen-induced K current increase, leading to hyperpolarization, in any endothelial cell, and the first report of SK as a testosterone target. Our data show that testosterone rapidly increased whole-cell HCAEC SK and BK currents via a surface androgen receptor, G protein, and protein kinase A. This mechanism may explain rapid testosterone-induced coronary vasodilation seen in vivo.
[Mh] Termos MeSH primário: Vasos Coronários/citologia
Células Endoteliais/metabolismo
Subunidades alfa Gi-Go de Proteínas de Ligação ao GTP/metabolismo
Canais de Potássio Cálcio-Ativados/metabolismo
Testosterona/sangue
[Mh] Termos MeSH secundário: Androgênios/química
Apamina/química
Linhagem Celular
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Células Endoteliais/efeitos dos fármacos
Epoprostenol/antagonistas & inibidores
Estrenos/química
Seres Humanos
Indometacina/química
NG-Nitroarginina Metil Éster/química
Óxido Nítrico Sintase/química
Pirrolidinonas/química
Receptores Androgênicos/metabolismo
Transdução de Sinais
Testosterona/química
Vasodilatação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androgens); 0 (Estrenes); 0 (Potassium Channels, Calcium-Activated); 0 (Pyrrolidinones); 0 (Receptors, Androgen); 112648-68-7 (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione); 24345-16-2 (Apamin); 3XMK78S47O (Testosterone); DCR9Z582X0 (Epoprostenol); EC 1.14.13.39 (Nitric Oxide Synthase); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 3.6.5.1 (GTP-Binding Protein alpha Subunits, Gi-Go); V55S2QJN2X (NG-Nitroarginine Methyl Ester); XXE1CET956 (Indomethacin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170704
[Lr] Data última revisão:
170704
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170223
[St] Status:MEDLINE


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[PMID]:28213506
[Au] Autor:Yin D; Hsieh YC; Tsai WC; Wu AZ; Jiang Z; Chan YH; Xu D; Yang N; Shen C; Chen Z; Lin SF; Chen PS; Everett TH
[Ad] Endereço:From the Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis (D.Y., Y.-C.H., W.-C.T., A.Z.-Y.W., Z.J., Y.-H.C., D.X., N.Y., Z.C., S.-F.L., P.-S.C., T.H.E.); Department of Cardiology (D.Y.) and Department of Gynecolo
[Ti] Título:Role of Apamin-Sensitive Calcium-Activated Small-Conductance Potassium Currents on the Mechanisms of Ventricular Fibrillation in Pacing-Induced Failing Rabbit Hearts.
[So] Source:Circ Arrhythm Electrophysiol;10(2):e004434, 2017 02.
[Is] ISSN:1941-3084
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ventricular fibrillation (VF) during heart failure is characterized by stable reentrant spiral waves (rotors). Apamin-sensitive small-conductance calcium-activated potassium currents ( ) are heterogeneously upregulated in failing hearts. We hypothesized that influences the location and stability of rotors during VF. METHODS AND RESULTS: Optical mapping was performed on 9 rabbit hearts with pacing-induced heart failure. The epicardial right ventricular and left ventricular surfaces were simultaneously mapped in a Langendorff preparation. At baseline and after apamin (100 nmol/L) infusion, the action potential duration (APD ) was determined, and VF was induced. Areas with a >50% increase in the maximum action potential duration (ΔAPD) after apamin infusion were considered to have a high distribution. At baseline, the distribution density of phase singularities during VF in high distribution areas was higher than in other areas (0.0035±0.0011 versus 0.0014±0.0010 phase singularities/pixel; =0.004). In addition, high dominant frequencies also colocalized to high distribution areas (26.0 versus 17.9 Hz; =0.003). These correlations were eliminated during VF after apamin infusion, as the number of phase singularities (17.2 versus 11.0; =0.009) and dominant frequencies (22.1 versus 16.2 Hz; =0.022) were all significantly decreased. In addition, reentrant spiral waves became unstable after apamin infusion, and the duration of VF decreased. CONCLUSIONS: The current influences the mechanism of VF in failing hearts as phase singularities, high dominant frequencies, and reentrant spiral waves all correlated to areas of high . Apamin eliminated this relationship and reduced VF vulnerability.
[Mh] Termos MeSH primário: Apamina/farmacologia
Insuficiência Cardíaca/fisiopatologia
Canais de Potássio Ativados por Cálcio de Condutância Baixa/efeitos dos fármacos
Canais de Potássio Ativados por Cálcio de Condutância Baixa/metabolismo
Fibrilação Ventricular/prevenção & controle
Fibrilação Ventricular/fisiopatologia
[Mh] Termos MeSH secundário: Potenciais de Ação/fisiologia
Animais
Estimulação Cardíaca Artificial
Modelos Animais de Doenças
Feminino
Coelhos
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Small-Conductance Calcium-Activated Potassium Channels); 24345-16-2 (Apamin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170615
[Lr] Data última revisão:
170615
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170219
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCEP.116.004434


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[PMID]:28115487
[Au] Autor:Yorgason JT; Zeppenfeld DM; Williams JT
[Ad] Endereço:Vollum Institute, Oregon Health & Science University, Portland, Oregon 97239.
[Ti] Título:Cholinergic Interneurons Underlie Spontaneous Dopamine Release in Nucleus Accumbens.
[So] Source:J Neurosci;37(8):2086-2096, 2017 Feb 22.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The release of dopamine from terminals in the NAc is regulated by a number of factors, including voltage-gated ion channels, D2-autoreceptors, and nAChRs. Cholinergic interneurons (CINs) drive dopamine release through activation of nAChRs on dopamine terminals. Using cyclic voltammetry in mouse brain slices, nAChR-dependent spontaneous dopamine transients and the mechanisms underlying the origin were examined in the NAc. Spontaneous events were infrequent (0.3 per minute), but the rate and amplitude were increased after blocking Kv channels with 4-aminopyridine. Although the firing frequency of CINs was increased by blocking glutamate reuptake with TBOA and the Sk blocker apamin, only 4-aminopyridine increased the frequency of dopamine transients. In contrast, inhibition of CIN firing with the µ/δ selective opioid [Met ]enkephalin (1 µm) decreased spontaneous dopamine transients. Cocaine increased the rate and amplitude of dopamine transients, suggesting that the activity of the dopamine transporter limits the detection of these events. In the presence of cocaine, the rate of spontaneous dopamine transients was further increased after blocking D2-autoreceptors. Blockade of muscarinic receptors had no effect on evoked dopamine release, suggesting that feedback inhibition of acetylcholine release was not involved. Thus, although spontaneous dopamine transients are reliant on nAChRs, the frequency was not strictly governed by the activity of CINs. The increase in frequency of spontaneous dopamine transients induced by cocaine was not due to an increase in cholinergic tone and is likely a product of an increase in detection resulting from decreased dopamine reuptake. The actions of dopamine in the NAc are thought to be responsible for endogenous reward and the reinforcing properties of drugs of abuse, such as psychostimulants. The present work examines the mechanisms underlying nAChR-induced spontaneous dopamine release. This study demonstrates that spontaneous dopamine release is (1) dependent of the activation of nicotinic receptors, (2) independent on the spontaneous activity of cholinergic interneurons, and (3) that cocaine increased the detection of dopamine transients by prolonging the presence and increasing the diffusion of dopamine in the extracellular space. The release of acetylcholine is therefore responsible for spontaneous dopamine transients, and cocaine augments dopamine tone without altering activity of cholinergic interneurons.
[Mh] Termos MeSH primário: Acetilcolina/metabolismo
Dopamina/metabolismo
Interneurônios/metabolismo
Núcleo Accumbens/citologia
[Mh] Termos MeSH secundário: 4-Aminopiridina/farmacologia
Acetilcolina/farmacologia
Potenciais de Ação/efeitos dos fármacos
Análise de Variância
Animais
Apamina/farmacologia
Ácido Aspártico/farmacologia
Cocaína/farmacologia
Inibidores da Captação de Dopamina/farmacologia
Estimulação Elétrica
Encefalina Metionina/farmacologia
Feminino
Técnicas In Vitro
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Técnicas de Patch-Clamp
Bloqueadores dos Canais de Potássio/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dopamine Uptake Inhibitors); 0 (Potassium Channel Blockers); 0 (benzyloxyaspartate); 24345-16-2 (Apamin); 30KYC7MIAI (Aspartic Acid); 58569-55-4 (Enkephalin, Methionine); BH3B64OKL9 (4-Aminopyridine); I5Y540LHVR (Cocaine); N9YNS0M02X (Acetylcholine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170125
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3064-16.2017


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[PMID]:28108814
[Au] Autor:Voos P; Yazar M; Lautenschläger R; Rauh O; Moroni A; Thiel G
[Ad] Endereço:Department of Biology, Plant Membrane Biophysics, Technische Universität Darmstadt, Schnittspahnstrasse 3, 64287, Darmstadt, Germany.
[Ti] Título:The small neurotoxin apamin blocks not only small conductance Ca activated K channels (SK type) but also the voltage dependent Kv1.3 channel.
[So] Source:Eur Biophys J;46(6):517-523, 2017 Sep.
[Is] ISSN:1432-1017
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Apamin is frequently used as a specific blocker of small-conductance Ca -activated (SK type) K channels. Here we show that the small neurotoxin is not as specific as anticipated. It is also a high-affinity inhibitor with an IC of 13 nM of the Kv1.3 channel; it blocks the latter with potency similar to the Kv1.3 blocker PAP-1. Since SK type channels and Kv1.3 channels are frequently coexpressed in different tissues such as cells of the immune system, apamin must be used with caution as a pharmacological tool.
[Mh] Termos MeSH primário: Apamina/toxicidade
Canal de Potássio Kv1.3/antagonistas & inibidores
Neurotoxinas/toxicidade
Bloqueadores dos Canais de Potássio/toxicidade
Canais de Potássio Cálcio-Ativados/antagonistas & inibidores
[Mh] Termos MeSH secundário: Fenômenos Eletrofisiológicos/efeitos dos fármacos
Células HEK293
Seres Humanos
Concentração Inibidora 50
Canal de Potássio Kv1.3/metabolismo
Proteínas Associadas a Pancreatite
Canais de Potássio Cálcio-Ativados/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Kv1.3 Potassium Channel); 0 (Neurotoxins); 0 (Pancreatitis-Associated Proteins); 0 (Potassium Channel Blockers); 0 (Potassium Channels, Calcium-Activated); 0 (REG3A protein, human); 24345-16-2 (Apamin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170122
[St] Status:MEDLINE
[do] DOI:10.1007/s00249-016-1196-0


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[PMID]:27844406
[Au] Autor:Li N; He X; Li Z; Liu Y; Wang P
[Ad] Endereço:Department of Urology, Fourth Affiliated Hospital, China Medical University, 4 Chongshan East Road, Shenyang, Liaoning, China.
[Ti] Título:Partial bladder outlet obstruction is associated with decreased expression and function of the small-conductance Ca -activated K channel in guinea pig detrusor smooth muscle.
[So] Source:Int Urol Nephrol;49(1):17-26, 2017 Jan.
[Is] ISSN:1573-2584
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Partial bladder outlet obstruction (PBOO) usually induces overactive bladder (OAB) associated with detrusor overactivity (DO) which is related to the increased contractility of detrusor smooth muscle (DSM). The pharmacological activation of small-conductance Ca -activated K (SK) channels dramatically attenuates DSM contractility. However, the role of SK channels in the PBOO DSM is less clear. Here, we tested the hypothesis that PBOO is associated with decreased expression and function of SK channels in DSM and that the activation of SK channels is a potential target to regulate DO. METHODS: Two weeks after surgically inducing PBOO in female guinea pigs, cystometry indicated that DO was achieved. Using this animal model, we conducted quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and isometric tension recordings. RESULTS: The qRT-PCR experiments indicated that PBOO DSM had reduced SK channel mRNA expression. Isometric tension recordings showed a decreased inhibitory effect of NS309 on spontaneous phasic and electrical field stimulation-induced contractions via the activation of SK channels in PBOO DSM. CONCLUSIONS: This study presents the novel finding that PBOO is associated with attenuated DSM SK channel expression and function, which results in increased DSM contractility and contributes to DO. Therefore, SK channels could be a therapeutic target to control OAB.
[Mh] Termos MeSH primário: Músculo Liso/metabolismo
Canais de Potássio Ativados por Cálcio de Condutância Baixa/genética
Canais de Potássio Ativados por Cálcio de Condutância Baixa/metabolismo
Bexiga Urinária Hiperativa/metabolismo
Bexiga Urinária/metabolismo
[Mh] Termos MeSH secundário: Animais
Apamina/farmacologia
Modelos Animais de Doenças
Feminino
Expressão Gênica
Cobaias
Indóis/farmacologia
Contração Isométrica/efeitos dos fármacos
Músculo Liso/efeitos dos fármacos
Músculo Liso/fisiopatologia
Oximas/farmacologia
Pirazóis/farmacologia
RNA Mensageiro/metabolismo
Bexiga Urinária/efeitos dos fármacos
Bexiga Urinária/fisiopatologia
Obstrução do Colo da Bexiga Urinária/complicações
Bexiga Urinária Hiperativa/etiologia
Bexiga Urinária Hiperativa/fisiopatologia
Urodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (6,7-dichloro-1H-indole-2,3-dione 3-oxime); 0 (Indoles); 0 (Oximes); 0 (Pyrazoles); 0 (RNA, Messenger); 0 (Small-Conductance Calcium-Activated Potassium Channels); 0 (TRAM 34); 24345-16-2 (Apamin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161116
[St] Status:MEDLINE
[do] DOI:10.1007/s11255-016-1455-0


  9 / 1443 MEDLINE  
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[PMID]:27825825
[Au] Autor:Mourre C; Manrique C; Camon J; Aidi-Knani S; Deltheil T; Turle-Lorenzo N; Guiraudie-Capraz G; Amalric M
[Ad] Endereço:Aix Marseille Univ, CNRS, LNC, FR3C, Marseille, France.
[Ti] Título:Changes in SK channel expression in the basal ganglia after partial nigrostriatal dopamine lesions in rats: Functional consequences.
[So] Source:Neuropharmacology;113(Pt A):519-532, 2017 Feb.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Parkinson's disease (PD) is a progressive neurodegenerative disease originating from the loss of dopamine (DA) neurons in the substantia nigra pars compacta (SNC). The small-conductance calcium-activated potassium (SK) channels play an essential role in the regulation of midbrain DA neuron activity patterns, as well as excitability of other types of neurons of the basal ganglia. We therefore questioned whether the SK channel expression in the basal ganglia is modified in parkinsonian rats and how this could impact behavioral performance in a reaction time task. We used a rat model of early PD in which the progressive nigrostriatal DA degeneration was produced by bilateral infusions of 6-hydroxydopamine (6-OHDA) into the striatum. In situ hybridization of SK2 and SK3 mRNA and binding of iodinated apamin (SK2/SK3 blocker) were performed at 1, 8 or 21 days postsurgery in sham and 6-OHDA lesion groups. A significant decrease of SK3 channel expression was found in the SNC of lesioned animals at the three time points, with no change of SK2 channel expression. Interestingly, an upregulation of SK2 mRNA and apamin binding was found in the subthalamic nucleus (STN) at 21 days postlesion. These results were confirmed using quantitative real time polymerase chain reaction (qRT-PCR) approach. Functionally, the local infusion of apamin into the STN of parkinsonian rats enhanced the akinetic deficits produced by nigrostriatal DA lesions in a reaction time task while apamin infusion into the SNC had an opposite effect. These effects disappear when the positive modulator of SK channels (CyPPA) is co-administered with apamin. These findings suggest that an upregulation of SK2 channels in the STN may underlie the physiological adjustment to increased subthalamic excitability following partial DA denervation.
[Mh] Termos MeSH primário: Gânglios da Base/metabolismo
Corpo Estriado/metabolismo
Dopamina/metabolismo
Transtornos Parkinsonianos/metabolismo
Canais de Potássio Ativados por Cálcio de Condutância Baixa/biossíntese
Substância Negra/metabolismo
[Mh] Termos MeSH secundário: Animais
Apamina/toxicidade
Gânglios da Base/efeitos dos fármacos
Corpo Estriado/efeitos dos fármacos
Expressão Gênica
Masculino
Oxidopamina/toxicidade
Transtornos Parkinsonianos/genética
Ratos
Ratos Wistar
Tempo de Reação/efeitos dos fármacos
Tempo de Reação/fisiologia
Canais de Potássio Ativados por Cálcio de Condutância Baixa/genética
Substância Negra/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Small-Conductance Calcium-Activated Potassium Channels); 24345-16-2 (Apamin); 8HW4YBZ748 (Oxidopamine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161110
[St] Status:MEDLINE


  10 / 1443 MEDLINE  
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[PMID]:27767209
[Au] Autor:Garden DL; Rinaldi A; Nolan MF
[Ad] Endereço:Centre for Integrative Physiology, University of Edinburgh, Edinburgh, EH8 9XD, UK.
[Ti] Título:Active integration of glutamatergic input to the inferior olive generates bidirectional postsynaptic potentials.
[So] Source:J Physiol;595(4):1239-1251, 2017 Feb 15.
[Is] ISSN:1469-7793
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:KEY POINTS: We establish experimental preparations for optogenetic investigation of glutamatergic input to the inferior olive. Neurones in the principal olivary nucleus receive monosynaptic extra-somatic glutamatergic input from the neocortex. Glutamatergic inputs to neurones in the inferior olive generate bidirectional postsynaptic potentials (PSPs), with a fast excitatory component followed by a slower inhibitory component. Small conductance calcium-activated potassium (SK) channels are required for the slow inhibitory component of glutamatergic PSPs and oppose temporal summation of inputs at intervals ≤ 20 ms. Active integration of synaptic input within the inferior olive may play a central role in control of olivo-cerebellar climbing fibre signals. ABSTRACT: The inferior olive plays a critical role in motor coordination and learning by integrating diverse afferent signals to generate climbing fibre inputs to the cerebellar cortex. While it is well established that climbing fibre signals are important for motor coordination, the mechanisms by which neurones in the inferior olive integrate synaptic inputs and the roles of particular ion channels are unclear. Here, we test the hypothesis that neurones in the inferior olive actively integrate glutamatergic synaptic inputs. We demonstrate that optogenetically activated long-range synaptic inputs to the inferior olive, including projections from the motor cortex, generate rapid excitatory potentials followed by slower inhibitory potentials. Synaptic projections from the motor cortex preferentially target the principal olivary nucleus. We show that inhibitory and excitatory components of the bidirectional synaptic potentials are dependent upon AMPA (GluA) receptors, are GABA independent, and originate from the same presynaptic axons. Consistent with models that predict active integration of synaptic inputs by inferior olive neurones, we find that the inhibitory component is reduced by blocking large conductance calcium-activated potassium channels with iberiotoxin, and is abolished by blocking small conductance calcium-activated potassium channels with apamin. Summation of excitatory components of synaptic responses to inputs at intervals ≤ 20 ms is increased by apamin, suggesting a role for the inhibitory component of glutamatergic responses in temporal integration. Our results indicate that neurones in the inferior olive implement novel rules for synaptic integration and suggest new principles for the contribution of inferior olive neurones to coordinated motor behaviours.
[Mh] Termos MeSH primário: Núcleo Olivar/metabolismo
Receptores de AMPA/metabolismo
Potenciais Sinápticos
[Mh] Termos MeSH secundário: Animais
Apamina/farmacologia
Ácido Glutâmico/metabolismo
Canais de Potássio Ativados por Cálcio de Condutância Alta/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Córtex Motor/citologia
Córtex Motor/metabolismo
Córtex Motor/fisiologia
Neurônios/metabolismo
Neurônios/fisiologia
Núcleo Olivar/citologia
Núcleo Olivar/fisiologia
Peptídeos/farmacologia
Bloqueadores dos Canais de Potássio/farmacologia
Canais de Potássio Ativados por Cálcio de Condutância Baixa/metabolismo
Sinapses/metabolismo
Sinapses/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Large-Conductance Calcium-Activated Potassium Channels); 0 (Peptides); 0 (Potassium Channel Blockers); 0 (Receptors, AMPA); 0 (Small-Conductance Calcium-Activated Potassium Channels); 24345-16-2 (Apamin); 3KX376GY7L (Glutamic Acid); 773HER9B6T (iberiotoxin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161022
[St] Status:MEDLINE
[do] DOI:10.1113/JP273424



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