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[PMID]:29250981
[Au] Autor:Evangelista E; Lopez R; Dauvilliers Y
[Ad] Endereço:a Centre National de Référence Narcolepsie Hypersomnies, Unité des Troubles du Sommeil, Service de Neurologie , Hôpital Gui-de-Chauliac Montpellier , Montpellier , France.
[Ti] Título:Update on treatment for idiopathic hypersomnia.
[So] Source:Expert Opin Investig Drugs;27(2):187-192, 2018 Feb.
[Is] ISSN:1744-7658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Idiopathic hypersomnia (IH) is a poorly characterized orphan central disorder of hypersomnolence responsible for excessive daytime sleepiness (EDS), prolonged nighttime sleep and sleep inertia that often require long-term symptomatic stimulant medication. To date, no drug has currently the authorization for the treatment of IH patients worldwide. Areas covered: The authors reviewed data on pharmacological treatment of IH obtained from published literature (Medline/PubMed/Web of Science) and Clinicaltrial.gov database from 1997 to 2017. Most of data on treatment of IH derived from observational studies and case series with only three well-designed clinical trials available. Expert opinion: In two recent randomized, double-blind, placebo-controlled trials, modafinil improves EDS in IH. Most of other wakefulness-promoting agents labeled for narcolepsy have similar efficacy in cases series of IH patients. Pitolisant and sodium oxybate show promising results in two retrospective studies. The efficacy of γ-aminobutyric acid-A receptor antagonists on objective EDS needs to be clarified. All these medications are used off-label for the management of EDS in IH. Specific clinical instruments and objective tests are required in IH to better evaluate the severity of EDS and responsiveness to medications, but also prolonged sleep and sleep inertia, to optimize the whole management of IH patients.
[Mh] Termos MeSH primário: Estimulantes do Sistema Nervoso Central/uso terapêutico
Hipersonolência Idiopática/tratamento farmacológico
Promotores da Vigília/uso terapêutico
[Mh] Termos MeSH secundário: Aprovação de Drogas
Antagonistas de Receptores de GABA-A/uso terapêutico
Seres Humanos
Hipersonolência Idiopática/fisiopatologia
Uso Off-Label
Ensaios Clínicos Controlados Aleatórios como Assunto
Índice de Gravidade de Doença
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Central Nervous System Stimulants); 0 (GABA-A Receptor Antagonists); 0 (Wakefulness-Promoting Agents)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1080/13543784.2018.1417385


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[PMID]:28336066
[Au] Autor:Yamaura K; Kiyonaka S; Hamachi I
[Ad] Endereço:Graduate School of Engineering, Kyoto University, Katsura, Kyoto, Japan.
[Ti] Título:Construction of Protein-Based Biosensors Using Ligand-Directed Chemistry for Detecting Analyte Binding.
[So] Source:Methods Enzymol;589:253-280, 2017.
[Is] ISSN:1557-7988
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Protein-based fluorescent biosensors are powerful tools for quantitative detection of biomolecules or drugs with high sensitivity under physiological conditions. However, conventional methods for construction of biosensors require structural data with high resolution or amino acid sequence information in most cases, which hampers applicability of this method to structurally complicated receptor proteins. To sidestep such limitations, we recently developed a new method that employs ligand-directed chemistry coupled with a bimolecular fluorescence quenching and recovery system, which enabled the conversion of various kinds of membrane-bound receptors to "turn-on" type fluorescent sensors. Here, we describe a protocol for construction of "turn-on" type fluorescent biosensors based on the GABA receptor which permits quantitative analysis of the ligand affinity.
[Mh] Termos MeSH primário: Técnicas Biossensoriais/métodos
Avaliação Pré-Clínica de Medicamentos/métodos
Receptores de GABA-A/metabolismo
[Mh] Termos MeSH secundário: Animais
Corantes Fluorescentes/análise
Corantes Fluorescentes/metabolismo
Agonistas de Receptores de GABA-A/farmacologia
Antagonistas de Receptores de GABA-A/farmacologia
Células HEK293
Seres Humanos
Ligantes
Microscopia de Fluorescência/métodos
Modelos Moleculares
Imagem Óptica/métodos
Receptores de GABA-A/análise
Espectrometria de Fluorescência/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fluorescent Dyes); 0 (GABA-A Receptor Agonists); 0 (GABA-A Receptor Antagonists); 0 (Ligands); 0 (Receptors, GABA-A)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE


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[PMID]:28288863
[Au] Autor:Callan SP; Apawu AK; Mathews TA; Bowen SE
[Ad] Endereço:Department of Psychology, Wayne State University, 5057 Woodward Ave, Detroit, MI, 48202, USA. Electronic address: sean.callan@wayne.edu.
[Ti] Título:Toluene's effects on activity and extracellular dopamine in the mouse are altered by GABA antagonism.
[So] Source:Neurosci Lett;647:67-71, 2017 Apr 24.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The abuse of inhalants like toluene continues to be widespread around the world, especially among children and teenagers. Despite its frequency of misuse, the dynamics between dopamine (DA) and gamma-aminobutyric acid (GABA) in response to toluene exposure remains unclear. To further decipher toluene's actions, we used a dynamic exposure system in combination with microdialysis to examine in vivo the effects of acutely inhaled toluene on DA release within the mouse caudate putamen (CPu). Results show that toluene inhalation produced increases in DA levels and locomotor activity. In mice that were pretreated with the GABA antagonist, bicuculline, there was no change in the locomotor response during toluene but activity was potentiated following toluene exposure. Bicuculline pretreatment increased extracellular DA levels during toluene exposure, suggesting that DA and GABA-releasing neuron interaction may play a role in the rewarding properties of toluene.
[Mh] Termos MeSH primário: Bicuculina/farmacologia
Dopamina/metabolismo
Espaço Extracelular/metabolismo
Antagonistas de Receptores de GABA-A/farmacologia
Exposição por Inalação/efeitos adversos
Tolueno/toxicidade
[Mh] Termos MeSH secundário: Administração por Inalação
Animais
Masculino
Camundongos
Microdiálise
Atividade Motora/efeitos dos fármacos
Putamen/efeitos dos fármacos
Putamen/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA-A Receptor Antagonists); 3FPU23BG52 (Toluene); VTD58H1Z2X (Dopamine); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170315
[St] Status:MEDLINE


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[PMID]:28153485
[Au] Autor:Mihalik B; Pálvölgyi A; Bogár F; Megyeri K; Ling I; Barkóczy J; Bartha F; Martinek TA; Gacsályi I; Antoni FA
[Ad] Endereço:Division of Preclinical Research, Egis Pharmaceuticals PLC, Hungary.
[Ti] Título:Loop-F of the α-subunit determines the pharmacologic profile of novel competitive inhibitors of GABA receptors.
[So] Source:Eur J Pharmacol;798:129-136, 2017 Mar 05.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The neurotransmitter γ-amino butyric acid (GABA) has a fundamental role in CNS function and ionotropic (GABA ) receptors that mediate many of the actions of GABA are important therapeutic targets. This study reports the mechanism of action of novel GABA antagonists based on a tricyclic oxazolo-2,3-benzodiazepine scaffold. These compounds are orthosteric antagonists of GABA on heteropentameric GABA receptors of αxß2γ2 configuration expressed in HEK293 cells. In silico modelling predicted that the test compounds docked in the GABA binding-pocket and would interact with amino-acid residues in the α- and ß-subunit interface that are known to be important for the binding of GABA. Intriguingly, optimal docking also required an interaction with the non-conserved amino-terminal segment of Loop-F of the α-subunit. Testing of a compound with altered regiochemistry of the oxazolone moiety supported the model with respect to the conserved GABA-interacting residues in vitro as well as in vivo. The prediction regarding loop-F was examined by replacing the amino-terminal variable segment of loop-F of the α5-subunit with the corresponding residues in the α1- and α2-subunits. When tested with the novel inhibitors, the receptors formed by the modified α5-subunits displayed the pharmacologic phenotype of the source of loop-F. In summary, these data show that the variable amino-terminal segment of loop-F of the α-subunit determines the pharmacologic selectivity of the novel tricyclic inhibitors of GABA receptors.
[Mh] Termos MeSH primário: Benzodiazepinas/química
Benzodiazepinas/farmacologia
Antagonistas de Receptores de GABA-A/química
Antagonistas de Receptores de GABA-A/farmacologia
Subunidades Proteicas/metabolismo
Receptores de GABA-A/química
Receptores de GABA-A/metabolismo
[Mh] Termos MeSH secundário: Benzodiazepinas/metabolismo
Ligação Competitiva
Simulação por Computador
Antagonistas de Receptores de GABA-A/metabolismo
Células HEK293
Seres Humanos
Simulação de Acoplamento Molecular
Oxazóis/química
Conformação Proteica
Subunidades Proteicas/química
Relação Estrutura-Atividade
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA-A Receptor Antagonists); 0 (Oxazoles); 0 (Protein Subunits); 0 (Receptors, GABA-A); 12794-10-4 (Benzodiazepines); 56-12-2 (gamma-Aminobutyric Acid)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE


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[PMID]:28111254
[Au] Autor:Salari AA; Amani M
[Ad] Endereço:Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Salari Institute of Cognitive and Behavioral Disorders, Alborz, Iran.
[Ti] Título:Neonatal blockade of GABA-A receptors alters behavioral and physiological phenotypes in adult mice.
[So] Source:Int J Dev Neurosci;57:62-71, 2017 Apr.
[Is] ISSN:1873-474X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Gamma-aminobutyric acid (GABA) plays an inhibitory role in the mature brain, and has a complex and bidirectional effect in different parts of the immature brain which affects proliferation, migration and differentiation of neurons during development. There is also increasing evidence suggesting that activation or blockade of the GABA-A receptors during early life can induce brain and behavioral abnormalities in adulthood. We investigated whether neonatal blockade of the GABA-A receptors by bicuculline can alter anxiety- and depression-like behaviors, body weight, food intake, corticosterone and testosterone levels in adult mice (postnatal days 80-95). To this end, neonatal mice were treated with either DMSO or bicuculline (70, 150 and 300µg/kg) during postnatal days 7, 9 and 11. When grown to adulthood, mice were exposed to behavioral tests to measure anxiety- (elevated plus-maze and light-dark box) and depression-like behaviors (tail suspension test and forced swim test). Stress-induced serum corticosterone and testosterone levels, body weight and food intake were also evaluated. Neonatal bicuculline exposure at dose of 300µg/kg decreased anxiety-like behavior, stress-induced corticosterone levels and increased testosterone levels, body weight and food intake, without significantly influencing depression-like behavior in adult male mice. However, no significant changes in these parameters were observed in adult females. These findings suggest that neonatal blockade of GABA-A receptors affects anxiety-like behavior, physiological and hormonal parameters in a sex-dependent manner in mice. Taken together, these data corroborate the concept that GABA-A receptors during early life have an important role in programming neurobehavioral phenotypes in adulthood.
[Mh] Termos MeSH primário: Ansiedade/metabolismo
Comportamento Animal/fisiologia
Depressão/metabolismo
Receptores de GABA-A/metabolismo
[Mh] Termos MeSH secundário: Adaptação Ocular/efeitos dos fármacos
Adaptação Ocular/fisiologia
Fatores Etários
Animais
Animais Recém-Nascidos
Ansiedade/induzido quimicamente
Comportamento Animal/efeitos dos fármacos
Bicuculina/efeitos adversos
Peso Corporal/efeitos dos fármacos
Corticosterona/sangue
Depressão/induzido quimicamente
Modelos Animais de Doenças
Ingestão de Alimentos/efeitos dos fármacos
Feminino
Antagonistas de Receptores de GABA-A/efeitos adversos
Elevação dos Membros Posteriores
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Aprendizagem em Labirinto/fisiologia
Camundongos
Fatores Sexuais
Natação/psicologia
Testosterona/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA-A Receptor Antagonists); 0 (Receptors, GABA-A); 3XMK78S47O (Testosterone); W980KJ009P (Corticosterone); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170330
[Lr] Data última revisão:
170330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170124
[St] Status:MEDLINE


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[PMID]:28099880
[Au] Autor:Shojaei A; Anaraki AK; Mirnajafi-Zadeh J; Atapour N
[Ad] Endereço:Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
[Ti] Título:Modifications of inhibitory transmission onto pyramidal neurons by postnatal exposure to MK-801: Effects of enriched environment.
[So] Source:Int J Dev Neurosci;57:56-61, 2017 Apr.
[Is] ISSN:1873-474X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Early enriched environment (EE) prevents several deficits associated with postnatal MK-801 [N-Methyl-d-Aspartate (NMDA) receptor antagonist] treatment such as cognitive and locomotor deficits. We sought physiological correlates to such changes by looking at inhibitory synaptic inputs onto pyramidal cells in a prefrontal cortex slice preparation. Pharmacologically isolated γ-amino-butyric acid (GABA ) receptor-mediated currents were measured using whole-cell patch clamp recordings. Wistar rats were raised in standard or EE from birth up to the time of experiments and were injected with saline or MK-801 (1mg/kg) on postnatal days (P) 6-10. We recorded miniature inhibitory post-synaptic currents (mIPSCs) of pyramidal cells in layer II/III of prefrontal cortex and measured their frequency, amplitude and kinetics. In control animals, the amplitude and frequency of mIPSCs increased strikingly during development from P21 to P28. MK-801 accelerated the development of mIPSCs frequency but caused a significant decrease in the amplitude of mIPSCs on P28 suggesting a significant reduction of inhibition onto pyramidal cells. EE per se led to a significant increase in both frequency and amplitude of mIPSCs, but its application to MK-801-treated rats resulted in moderate rescue of GABAergic transmission on P28. We conclude that postnatal MK-801 leads to reduced inhibitory transmission onto pyramidal cells of prefrontal cortex at adolescence which may underlie behavioural and morphological differences detected in vivo in rats. EE presentation from birth rather prevents GABAergic alterations associated with postnatal MK-801 treatment at adolescence.
[Mh] Termos MeSH primário: Maleato de Dizocilpina/farmacologia
Meio Ambiente
Antagonistas de Aminoácidos Excitatórios/farmacologia
Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos
Córtex Pré-Frontal/citologia
Células Piramidais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Animais Recém-Nascidos
Bicuculina/farmacologia
Estimulação Elétrica
Feminino
Antagonistas de Receptores de GABA-A/farmacologia
Técnicas In Vitro
Masculino
Técnicas de Patch-Clamp
Gravidez
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Excitatory Amino Acid Antagonists); 0 (GABA-A Receptor Antagonists); 6LR8C1B66Q (Dizocilpine Maleate); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170330
[Lr] Data última revisão:
170330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE


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[PMID]:28034711
[Au] Autor:Bavis RW; Li KY; DeAngelis KJ; March RJ; Wallace JA; Logan S; Putnam RW
[Ad] Endereço:Department of Biology, Bates College, Lewiston, ME, USA. Electronic address: rbavis@bates.edu.
[Ti] Título:Ventilatory and chemoreceptor responses to hypercapnia in neonatal rats chronically exposed to moderate hyperoxia.
[So] Source:Respir Physiol Neurobiol;237:22-34, 2017 Mar.
[Is] ISSN:1878-1519
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Rats reared in hyperoxia hypoventilate in normoxia and exhibit progressive blunting of the hypoxic ventilatory response, changes which are at least partially attributed to abnormal carotid body development. Since the carotid body also responds to changes in arterial CO /pH, we tested the hypothesis that developmental hyperoxia would attenuate the hypercapnic ventilatory response (HCVR) of neonatal rats by blunting peripheral and/or central chemoreceptor responses to hypercapnic challenges. Rats were reared in 21% O (Control) or 60% O (Hyperoxia) until studied at 4, 6-7, or 13-14days of age. Hyperoxia rats had significantly reduced single-unit carotid chemoafferent responses to 15% CO at all ages; CO sensitivity recovered within 7days after return to room air. Hypercapnic responses of CO -sensitive neurons of the caudal nucleus tractus solitarius (cNTS) were unaffected by chronic hyperoxia, but there was evidence for a small decrease in neuronal excitability. There was also evidence for augmented excitatory synaptic input to cNTS neurons within brainstem slices. Steady-state ventilatory responses to 4% and 8% CO were unaffected by developmental hyperoxia in all three age groups, but ventilation increased more slowly during the normocapnia-to-hypercapnia transition in 4-day-old Hyperoxia rats. We conclude that developmental hyperoxia impairs carotid body chemosensitivity to hypercapnia, and this may compromise protective ventilatory reflexes during dynamic respiratory challenges in newborn rats. Impaired carotid body function has less of an impact on the HCVR in older rats, potentially reflecting compensatory plasticity within the CNS.
[Mh] Termos MeSH primário: Corpo Carotídeo/patologia
Células Quimiorreceptoras/fisiologia
Hipercapnia/fisiopatologia
Hiperóxia/fisiopatologia
Ventilação Pulmonar/fisiologia
[Mh] Termos MeSH secundário: 6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Potenciais de Ação/fisiologia
Fatores Etários
Animais
Animais Recém-Nascidos
Bicuculina/farmacologia
Dióxido de Carbono/farmacologia
Corpo Carotídeo/crescimento & desenvolvimento
Antagonistas de Aminoácidos Excitatórios/farmacologia
Antagonistas de Receptores de GABA-A/farmacologia
Hiperóxia/patologia
Neurônios/efeitos dos fármacos
Técnicas de Patch-Clamp
Ratos
Ratos Sprague-Dawley
Potenciais Sinápticos/efeitos dos fármacos
Potenciais Sinápticos/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Excitatory Amino Acid Antagonists); 0 (GABA-A Receptor Antagonists); 142M471B3J (Carbon Dioxide); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161231
[St] Status:MEDLINE


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[PMID]:27923876
[Au] Autor:Hossein-Javaheri N; Wilkie MP; Lado WE; Buck LT
[Ad] Endereço:Department of Cell and Systems Biology, University of Toronto, 25 Harbord St, Toronto, ON, Canada M5S 3G5.
[Ti] Título:Stellate and pyramidal neurons in goldfish telencephalon respond differently to anoxia and GABA receptor inhibition.
[So] Source:J Exp Biol;220(Pt 4):695-704, 2017 Feb 15.
[Is] ISSN:1477-9145
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:With oxygen deprivation, the mammalian brain undergoes hyper-activity and neuronal death while this does not occur in the anoxia-tolerant goldfish ( ). Anoxic survival of the goldfish may rely on neuromodulatory mechanisms to suppress neuronal hyper-excitability. As γ-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the brain, we decided to investigate its potential role in suppressing the electrical activity of goldfish telencephalic neurons. Utilizing whole-cell patch-clamp recording, we recorded the electrical activities of both excitatory (pyramidal) and inhibitory (stellate) neurons. With anoxia, membrane potential ( ) depolarized in both cell types from -72.2 mV to -57.7 mV and from -64.5 mV to -46.8 mV in pyramidal and stellate neurons, respectively. While pyramidal cells remained mostly quiescent, action potential frequency (AP ) of the stellate neurons increased 68-fold. Furthermore, the GABA receptor reversal potential ( - ) was determined using the gramicidin perforated-patch-clamp method and found to be depolarizing in pyramidal (-53.8 mV) and stellate neurons (-42.1 mV). Although GABA was depolarizing, pyramidal neurons remained quiescent as was below the action potential threshold (-36 mV pyramidal and -38 mV stellate neurons). Inhibition of GABA receptors with gabazine reversed the anoxia-mediated response. While GABA receptor inhibition alone did not affect the anoxic response, co-antagonism of GABA and GABA receptors (gabazine and CGP-55848) led to the generation of seizure-like activities in both neuron types. We conclude that with anoxia, depolarizes towards which increases AP in stellate neurons and decreases AP in pyramidal neurons, and that GABA plays an important role in the anoxia tolerance of goldfish brain.
[Mh] Termos MeSH primário: Potenciais de Ação
Proteínas de Peixes/metabolismo
Carpa Dourada/fisiologia
Oxigênio/metabolismo
Células Piramidais/metabolismo
Receptores de GABA-A/metabolismo
Receptores de GABA-B/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Anaerobiose
Animais
Antagonistas de Receptores de GABA-A/farmacologia
Antagonistas de Receptores de GABA-B/farmacologia
Seres Humanos
Hipóxia/metabolismo
Técnicas de Patch-Clamp
Células Piramidais/citologia
Células Piramidais/efeitos dos fármacos
Telencéfalo/citologia
Telencéfalo/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fish Proteins); 0 (GABA-A Receptor Antagonists); 0 (GABA-B Receptor Antagonists); 0 (Receptors, GABA-A); 0 (Receptors, GABA-B); S88TT14065 (Oxygen)
[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:161208
[St] Status:MEDLINE
[do] DOI:10.1242/jeb.146605


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[PMID]:27918706
[Au] Autor:Vargas RA
[Ad] Endereço:Departamento de Ciencias Fisiológicas, Facultad de Medicina, Pontificia Universidad Javeriana , Bogotá, Colombia .
[Ti] Título:Effects of GABA, Neural Regulation, and Intrinsic Cardiac Factors on Heart Rate Variability in Zebrafish Larvae.
[So] Source:Zebrafish;14(2):106-117, 2017 Apr.
[Is] ISSN:1557-8542
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heart rate (HR) is a periodic activity that is variable over time due to intrinsic cardiac factors and extrinsic neural control, largely by the autonomic nervous system. Heart rate variability (HRV) is analyzed by measuring consecutive beat-to-beat intervals. This variability can contain information about the factors regulating cardiac activity under normal and pathological conditions, but the information obtained from such analyses is not yet fully understood. In this article, HRV in zebrafish larvae was evaluated under normal conditions and under the effect of substances that modify intrinsic cardiac activity and cardiac activity modulated by the nervous system. We found that the factors affecting intrinsic activity have negative chronotropic and arrhythmogenic effects at this stage of development, whereas neural modulatory factors have a lesser impact. The results suggest that cardiac activity largely depends on the intrinsic properties of the heart tissue in the early stages of development and, to a lesser extent, in the maturing nervous system. We also report, for the first time, the influence of the neurotransmitter gamma amino butyric acid on HRV. The results demonstrate the larval zebrafish model as a useful tool in the study of intrinsic cardiac activity and its role in heart diseases.
[Mh] Termos MeSH primário: Cafeína/farmacologia
Etanol/farmacologia
Frequência Cardíaca/efeitos dos fármacos
Coração/efeitos dos fármacos
Coração/inervação
Ácido gama-Aminobutírico/metabolismo
[Mh] Termos MeSH secundário: Acetilcolina/farmacologia
Animais
Bicuculina/farmacologia
Depressores do Sistema Nervoso Central/farmacologia
Estimulantes do Sistema Nervoso Central/farmacologia
Agonistas Colinérgicos/farmacologia
Dopamina/farmacologia
Dopaminérgicos/farmacologia
Agonistas de Receptores de GABA-A/farmacologia
Antagonistas de Receptores de GABA-A/farmacologia
Regulação da Expressão Gênica no Desenvolvimento
Larva
Lidocaína/farmacologia
Cloreto de Metacolina/farmacologia
Agonistas Muscarínicos/farmacologia
Muscimol/farmacologia
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Central Nervous System Depressants); 0 (Central Nervous System Stimulants); 0 (Cholinergic Agonists); 0 (Dopamine Agents); 0 (GABA-A Receptor Agonists); 0 (GABA-A Receptor Antagonists); 0 (Muscarinic Agonists); 0W5ETF9M2K (Methacholine Chloride); 2763-96-4 (Muscimol); 3G6A5W338E (Caffeine); 3K9958V90M (Ethanol); 56-12-2 (gamma-Aminobutyric Acid); 98PI200987 (Lidocaine); N9YNS0M02X (Acetylcholine); VTD58H1Z2X (Dopamine); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161206
[St] Status:MEDLINE
[do] DOI:10.1089/zeb.2016.1365


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[PMID]:27865151
[Au] Autor:Holtyn AF; Tiruveedhula VV; Stephen MR; Cook JM; Weerts EM
[Ad] Endereço:Johns Hopkins University School of Medicine, Division of Behavioral Biology, 5510 Nathan Shock Dr, Baltimore, MD 21224, USA.
[Ti] Título:Effects of the benzodiazepine GABA α1-preferring antagonist 3-isopropoxy-ß-carboline hydrochloride (3-ISOPBC) on alcohol seeking and self-administration in baboons.
[So] Source:Drug Alcohol Depend;170:25-31, 2017 Jan 01.
[Is] ISSN:1879-0046
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The major inhibitory neurotransmitter, gamma-aminobutyric acid (GABA), modulates many of the behavioral effects of alcohol, including sedation, tolerance, and withdrawal. The α1 subunit of the benzodiazepine GABA receptor is the most widely expressed alpha subunit in the brain, and has been implicated in the reinforcing- and abuse-related effects of alcohol. The aim of the present study was to examine whether treatment with a benzodiazepine GABA α1-preferring ligand, 3-isopropoxy-ß-carboline hydrochloride (3-ISOPBC), selectively decreases alcohol seeking and consumption. METHODS: Eight baboons self-administered alcohol (4% w/v; n=5; alcohol group) or a non-alcoholic beverage (n=3; control group) in Component 3 of a chained schedule of reinforcement. Responses in Component 2 provided indices of motivation to drink (seeking). Doses of 3-ISOPBC (5.0-30.0mg/kg) and vehicle were administered before drinking sessions under both acute and chronic (5day) conditions. RESULTS: Chronic, and not acute, administration of 3-ISOPBC significantly decreased self-administration responses, g/kg alcohol consumed, and the number of drinks in and duration of the first drinking bout in the alcohol group. In the control group, chronic administration of 3-ISOPBC did not significantly decrease any of these measures at any of the doses. CONCLUSIONS: The GABA α1-preferring ligand 3-ISOPBC may have therapeutic potential in the treatment of alcohol use disorder due to its ability to selectively reduce alcohol use.
[Mh] Termos MeSH primário: Consumo de Bebidas Alcoólicas/tratamento farmacológico
Benzodiazepinas/farmacologia
Comportamento de Procura de Droga/efeitos dos fármacos
Etanol/administração & dosagem
Antagonistas de Receptores de GABA-A/farmacologia
Reforço (Psicologia)
Autoadministração
[Mh] Termos MeSH secundário: Animais
Benzodiazepinas/uso terapêutico
Antagonistas de Receptores de GABA-A/uso terapêutico
Masculino
Motivação/efeitos dos fármacos
Papio
Resultado do Tratamento
Ácido gama-Aminobutírico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA-A Receptor Antagonists); 12794-10-4 (Benzodiazepines); 3K9958V90M (Ethanol); 56-12-2 (gamma-Aminobutyric Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161120
[St] Status:MEDLINE



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