Base de dados : MEDLINE
Pesquisa : D27.505.519.625.300 [Categoria DeCS]
Referências encontradas : 690 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 69 ir para página                         

  1 / 690 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28874448
[Au] Autor:Bardóczi Z; Pál B; Koszeghy Á; Wilheim T; Watanabe M; Záborszky L; Liposits Z; Kalló I
[Ad] Endereço:Laboratory of Endocrine Neurobiology, Institute of Experimental Medicine, HAS, 1083, Budapest, Hungary.
[Ti] Título:Glycinergic Input to the Mouse Basal Forebrain Cholinergic Neurons.
[So] Source:J Neurosci;37(39):9534-9549, 2017 Sep 27.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The basal forebrain (BF) receives afferents from brainstem ascending pathways, which has been implicated first by Moruzzi and Magoun (1949) to induce forebrain activation and cortical arousal/waking behavior; however, it is very little known about how brainstem inhibitory inputs affect cholinergic functions. In the current study, glycine, a major inhibitory neurotransmitter of brainstem neurons, and gliotransmitter of local glial cells, was tested for potential interaction with BF cholinergic (BFC) neurons in male mice. In the BF, glycine receptor α subunit-immunoreactive (IR) sites were localized in choline acetyltransferase (ChAT)-IR neurons. The effect of glycine on BFC neurons was demonstrated by bicuculline-resistant, strychnine-sensitive spontaneous IPSCs (sIPSCs; 0.81 ± 0.25 × 10 Hz) recorded in whole-cell conditions. Potential neuronal as well as glial sources of glycine were indicated in the extracellular space of cholinergic neurons by glycine transporter type 1 (GLYT1)- and GLYT2-IR processes found in apposition to ChAT-IR cells. Ultrastructural analyses identified synapses of GLYT2-positive axon terminals on ChAT-IR neurons, as well as GLYT1-positive astroglial processes, which were localized in the vicinity of synapses of ChAT-IR neurons. The brainstem raphe magnus was determined to be a major source of glycinergic axons traced retrogradely from the BF. Our results indicate a direct effect of glycine on BFC neurons. Furthermore, the presence of high levels of plasma membrane glycine transporters in the vicinity of cholinergic neurons suggests a tight control of extracellular glycine in the BF. Basal forebrain cholinergic (BFC) neurons receive various activating inputs from specific brainstem areas and channel this information to the cortex via multiple projections. So far, very little is known about inhibitory brainstem afferents to the BF. The current study established glycine as a major regulator of BFC neurons by (1) identifying glycinergic neurons in the brainstem projecting to the BF, (2) showing glycine receptor α subunit-immunoreactive (IR) sites in choline acetyltransferase (ChAT)-IR neurons, (3) demonstrating glycine transporter type 2 (GLYT2)-positive axon terminals synapsing on ChAT-IR neurons, and (4) localizing GLYT1-positive astroglial processes in the vicinity of synapses of ChAT-IR neurons. The effect of glycine on BFC neurons was demonstrated by bicuculline-resistant, strychnine-sensitive spontaneous IPSCs recorded in whole-cell conditions.
[Mh] Termos MeSH primário: Neurônios Colinérgicos/metabolismo
Glicina/metabolismo
Prosencéfalo/metabolismo
[Mh] Termos MeSH secundário: Animais
Bicuculina/farmacologia
Colina O-Acetiltransferase/genética
Colina O-Acetiltransferase/metabolismo
Neurônios Colinérgicos/efeitos dos fármacos
Neurônios Colinérgicos/fisiologia
Feminino
Glicina/farmacologia
Glicinérgicos/farmacologia
Proteínas da Membrana Plasmática de Transporte de Glicina/genética
Proteínas da Membrana Plasmática de Transporte de Glicina/metabolismo
Potenciais Pós-Sinápticos Inibidores
Masculino
Camundongos
Neuroglia/metabolismo
Prosencéfalo/citologia
Estricnina/farmacologia
Sinapses/efeitos dos fármacos
Sinapses/metabolismo
Sinapses/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycine Agents); 0 (Glycine Plasma Membrane Transport Proteins); EC 2.3.1.6 (Choline O-Acetyltransferase); H9Y79VD43J (Strychnine); TE7660XO1C (Glycine); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171015
[Lr] Data última revisão:
171015
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3348-16.2017


  2 / 690 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28254751
[Au] Autor:Conceição EP; Madden CJ; Morrison SF
[Ad] Endereço:Department of Neurological Surgery, Oregon Health & Science University, Portland, Oregon santosda@ohsu.edu.
[Ti] Título:Glycinergic inhibition of BAT sympathetic premotor neurons in rostral raphe pallidus.
[So] Source:Am J Physiol Regul Integr Comp Physiol;312(6):R919-R926, 2017 06 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The rostral raphe pallidus (rRPa) contains sympathetic premotor neurons controlling thermogenesis in brown adipose tissue (BAT). We sought to determine whether a tonic activation of glycine receptors (Gly R) in the rRPa contributes to the inhibitory regulation of BAT sympathetic nerve activity (SNA) and of cardiovascular parameters in anesthetized rats. Nanoinjection of the Gly R antagonist, strychnine (STR), into the rRPa of intact rats increased BAT SNA (peak: +495%), BAT temperature (T , +1.1°C), expired CO , (+0.4%), core body temperature (T , +0.2°C), mean arterial pressure (MAP, +4 mmHg), and heart rate (HR, +57 beats/min). STR into rRPa in rats with a postdorsomedial hypothalamus transection produced similar increases in BAT thermogenic and cardiovascular parameters. Glycine nanoinjection into the rRPa evoked a potent inhibition of the cooling-evoked increases in BAT SNA (nadir: -74%), T (-0.2°C), T (-0.2°C), expired CO (-0.2%), MAP (-8 mmHg), and HR (-22 beats/min) but had no effect on the increases in these variables evoked by STR nanoinjection into rRPa. Nanoinjection of GABA into the rRPa inhibited the STR-evoked BAT SNA (nadir: -86%) and reduced the expired CO (-0.4%). Blockade of glutamate receptors in rRPa reduced the STR-evoked increases in BAT SNA (nadir: -61%), T (-0.5°C), expired CO (-0.3%), MAP (-9 mmHg), and HR (-33 beats/min). We conclude that a tonically active glycinergic input to the rRPa contributes to the inhibitory regulation of the discharge of BAT sympathetic premotor neurons and of BAT thermogenesis and energy expenditure.
[Mh] Termos MeSH primário: Tecido Adiposo Marrom/inervação
Sistema Cardiovascular/inervação
Glicina/metabolismo
Núcleos da Rafe do Mesencéfalo/metabolismo
Neurônios Motores/metabolismo
Inibição Neural
Receptores da Glicina/metabolismo
Sistema Nervoso Simpático/metabolismo
Termogênese
[Mh] Termos MeSH secundário: Potenciais de Ação
Animais
Pressão Arterial
Glicinérgicos/administração & dosagem
Frequência Cardíaca
Injeções
Masculino
Núcleos da Rafe do Mesencéfalo/efeitos dos fármacos
Neurônios Motores/efeitos dos fármacos
Inibição Neural/efeitos dos fármacos
Ratos Sprague-Dawley
Receptores da Glicina/antagonistas & inibidores
Sistema Nervoso Simpático/efeitos dos fármacos
Termogênese/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycine Agents); 0 (Receptors, Glycine); TE7660XO1C (Glycine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170304
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00551.2016


  3 / 690 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27984182
[Au] Autor:Smith BJ; Côté PD; Tremblay F
[Ad] Endereço:Department of Biology, Dalhousie University, 1355 Oxford St., PO Box 15000, Halifax, NS B3H 4R2, Canada. Electronic address: BN948751@dal.ca.
[Ti] Título:Contribution of Na 1.8 sodium channels to retinal function.
[So] Source:Neuroscience;340:279-290, 2017 Jan 06.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We examined the contribution of the sodium channel isoform Na 1.8 to retinal function using the specific blocker A803467. We found that A803467 has little influence on the electroretinogram (ERG) a- and b-waves, but significantly reduces the oscillatory potentials (OPs) to 40-60% of their original amplitude, with significant changes in implicit time in the rod-driven range. To date, only two cell types were found in mouse to express Na 1.8; the starburst amacrine cells (SBACs), and a subtype of retinal ganglion cells (RGCs). When we recorded light responses from ganglion cells using a multielectrode array we found significant and opposing changes in two physiological groups of RGCs. ON-sustained cells showed significant decreases while transient ON-OFF cells showed significant increases. The effects on ON-OFF transient cells but not ON-sustained cells disappeared in the presence of an inhibitory cocktail. We have previously shown that RGCs have only a minor contribution to the OPs (Smith et al., 2014), therefore suggesting that SBACs might be a significant contributor to this ERG component. Targeting SBACs with the cholinergic neurotoxin ethylcholine mustard aziridinium (AF64A) caused a reduction in the amplitude of the OPs similar to A803467. Our results, both using the ERG and MEA recordings from RGCs, suggest that Na 1.8 plays a role in modulating specific aspects of the retinal physiology and that SBACs are a fundamental cellular contributor to the OPs in mice, a clear demonstration of the dichotomy between ERG b-wave and OPs.
[Mh] Termos MeSH primário: Canal de Sódio Disparado por Voltagem NAV1.8/metabolismo
Retina/metabolismo
Visão Ocular/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Potenciais de Ação/fisiologia
Compostos de Anilina/farmacologia
Animais
Aziridinas/farmacologia
Colina/análogos & derivados
Colina/farmacologia
Antagonistas Colinérgicos/farmacologia
Eletrorretinografia
Furanos/farmacologia
Glicinérgicos/farmacologia
Camundongos Endogâmicos C57BL
Microeletrodos
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Periodicidade
Estimulação Luminosa
Retina/efeitos dos fármacos
Bloqueadores dos Canais de Sódio/farmacologia
Estricnina/farmacologia
Técnicas de Cultura de Tecidos
Visão Ocular/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (A 803467); 0 (Aniline Compounds); 0 (Aziridines); 0 (Cholinergic Antagonists); 0 (Furans); 0 (Glycine Agents); 0 (NAV1.8 Voltage-Gated Sodium Channel); 0 (Scn10a protein, mouse); 0 (Sodium Channel Blockers); A668M9E227 (ethylcholine aziridinium); H9Y79VD43J (Strychnine); N91BDP6H0X (Choline)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161217
[St] Status:MEDLINE


  4 / 690 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27581450
[Au] Autor:Zhang B; Südhof TC
[Ad] Endereço:Department of Molecular and Cellular Physiology and Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305 zbo@stanford.edu.
[Ti] Título:Neuroligins Are Selectively Essential for NMDAR Signaling in Cerebellar Stellate Interneurons.
[So] Source:J Neurosci;36(35):9070-83, 2016 Aug 31.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Neuroligins are postsynaptic cell-adhesion molecules that contribute to synapse specification. However, many other postsynaptic cell-adhesion molecules are known and the relative contributions of neuroligins versus other such molecules in different types of synapses and neurons remains largely unknown. Here, we have studied the role of neuroligins in cerebellar stellate interneurons that participate in a well defined circuit that converges on Purkinje cells as the major output neurons of cerebellar cortex. By crossing triple conditional knock-out (cKO) mice targeting all three major neuroligins [neuroligin-1 to neuroligin-3 (NL123)] with parvalbumin-Cre (PV-Cre) transgenic mice, we deleted neuroligins from inhibitory cerebellar interneurons and Purkinje cells, allowing us to study the effects of neuroligin deletions on cerebellar stellate cell synapses by electrophysiology in acute slices. PV-Cre/NL123 cKO mice did not exhibit gross alterations of cerebellar structure or cerebellar interneuron morphology. Strikingly, electrophysiological recordings in stellate cells from these PV-Cre/NL123 cKO mice revealed a large decrease in NMDAR-mediated excitatory synaptic responses, which, in stellate cells, are largely extrasynaptic, without a change in AMPA-receptor-mediated responses. Parallel analyses in PV-Cre/NL1 mice that are single NL1 cKO mice uncovered the same phenotype, demonstrating that NL1 is responsible for recruiting extrasynaptic NMDARs. Moreover, we observed only a modest impairment in inhibitory synaptic responses in stellate cells lacking NL123 despite a nearly complete suppression of inhibitory synaptic transmission in Purkinje cells by the same genetic manipulation. Our results suggest that, unlike other types of neurons investigated, neuroligins are selectively essential in cerebellar stellate interneurons for enabling the function of extrasynaptic NMDARs. SIGNIFICANCE STATEMENT: Neuroligins are postsynaptic cell-adhesion molecules genetically linked to autism. However, the contributions of neuroligins to interneuron functions remain largely unknown. Here, we analyzed the role of neuroligins in cerebellar stellate interneurons. We deleted neuroligin-1, neuroligin-2, and neuroligin-3, the major cerebellar neuroligin isoforms, from stellate cells in triple NL123 conditional knock-out mice and analyzed synaptic responses by acute slice electrophysiology. We find that neuroligins are selectively essential for extrasynaptic NMDAR-mediated signaling, but dispensable for both AMPAR-mediated and inhibitory synaptic transmission. Our results reveal a critical and selective role for neuroligins in the regulation of NMDAR responses in cerebellar stellate interneurons.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular Neuronais/metabolismo
Córtex Cerebral/citologia
Interneurônios/fisiologia
Receptores de N-Metil-D-Aspartato/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Proteínas de Bactérias/genética
Proteínas de Bactérias/metabolismo
Moléculas de Adesão Celular Neuronais/genética
Fármacos atuantes sobre Aminoácidos Excitatórios/farmacologia
Feminino
Antagonistas GABAérgicos/farmacologia
Glicinérgicos/farmacologia
Interneurônios/efeitos dos fármacos
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Masculino
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Camundongos
Camundongos Transgênicos
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Parvalbuminas/genética
Parvalbuminas/metabolismo
Técnicas de Patch-Clamp
Picrotoxina/farmacologia
Células de Purkinje/efeitos dos fármacos
Células de Purkinje/fisiologia
Transdução de Sinais/genética
Transdução de Sinais/fisiologia
Estatísticas não Paramétricas
Estricnina/farmacologia
Potenciais Sinápticos/efeitos dos fármacos
Potenciais Sinápticos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Cell Adhesion Molecules, Neuronal); 0 (Excitatory Amino Acid Agents); 0 (GABA Antagonists); 0 (Glycine Agents); 0 (Luminescent Proteins); 0 (Membrane Proteins); 0 (Nerve Tissue Proteins); 0 (Parvalbumins); 0 (Receptors, N-Methyl-D-Aspartate); 0 (neuroligin 1); 0 (neuroligin 2); 0 (neuroligin 3); 0 (yellow fluorescent protein, Bacteria); 124-87-8 (Picrotoxin); H9Y79VD43J (Strychnine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160902
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1356-16.2016


  5 / 690 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27440241
[Au] Autor:McMenamin CA; Anselmi L; Travagli RA; Browning KN
[Ad] Endereço:Department of Neural and Behavioral Sciences, Penn State College of Medicine, Hershey, Pennsylvania.
[Ti] Título:Developmental regulation of inhibitory synaptic currents in the dorsal motor nucleus of the vagus in the rat.
[So] Source:J Neurophysiol;116(4):1705-1714, 2016 Oct 01.
[Is] ISSN:1522-1598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prior immunohistochemical studies have demonstrated that at early postnatal time points, central vagal neurons receive both glycinergic and GABAergic inhibitory inputs. Functional studies have demonstrated, however, that adult vagal efferent motoneurons receive only inhibitory GABAergic synaptic inputs, suggesting loss of glycinergic inhibitory neurotransmission during postnatal development. The purpose of the present study was to test the hypothesis that the loss of glycinergic inhibitory synapses occurs in the immediate postnatal period. Whole cell patch-clamp recordings were made from dorsal motor nucleus of the vagus (DMV) neurons from postnatal days 1-30, and the effects of the GABA receptor antagonist bicuculline (1-10 µM) and the glycine receptor antagonist strychnine (1 µM) on miniature inhibitory postsynaptic current (mIPSC) properties were examined. While the baseline frequency of mIPSCs was not altered by maturation, perfusion with bicuculline either abolished mIPSCs altogether or decreased mIPSC frequency and decay constant in the majority of neurons at all time points. In contrast, while strychnine had no effect on mIPSC frequency, its actions to increase current decay time declined during postnatal maturation. These data suggest that in early postnatal development, DMV neurons receive both GABAergic and glycinergic synaptic inputs. Glycinergic neurotransmission appears to decline by the second postnatal week, and adult neurons receive principally GABAergic inhibitory inputs. Disruption of this developmental switch from GABA-glycine to purely GABAergic transmission in response to early life events may, therefore, lead to adverse consequences in vagal efferent control of visceral functions.
[Mh] Termos MeSH primário: Potenciais Pós-Sinápticos Inibidores/fisiologia
Bulbo/crescimento & desenvolvimento
Bulbo/metabolismo
Potenciais Pós-Sinápticos em Miniatura/fisiologia
Neurônios/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Bicuculina/farmacologia
Antagonistas de Receptores de GABA-A/farmacologia
Glicinérgicos/farmacologia
Imuno-Histoquímica
Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos
Bulbo/citologia
Potenciais Pós-Sinápticos em Miniatura/efeitos dos fármacos
Neurônios/citologia
Neurônios/efeitos dos fármacos
Técnicas de Patch-Clamp
Ratos Sprague-Dawley
Receptores de GABA-A/metabolismo
Receptores da Glicina/antagonistas & inibidores
Receptores da Glicina/metabolismo
Estricnina/farmacologia
Técnicas de Cultura de Tecidos
Nervo Vago/citologia
Nervo Vago/crescimento & desenvolvimento
Nervo Vago/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA-A Receptor Antagonists); 0 (Glycine Agents); 0 (Receptors, GABA-A); 0 (Receptors, Glycine); H9Y79VD43J (Strychnine); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171001
[Lr] Data última revisão:
171001
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160722
[St] Status:MEDLINE
[do] DOI:10.1152/jn.00249.2016


  6 / 690 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27218870
[Au] Autor:Watson CJ
[Ad] Endereço:Department of Anesthesiology, University of Michigan, Ann Arbor, MI, USA.
[Ti] Título:Insular balance of glutamatergic and GABAergic signaling modulates pain processing.
[So] Source:Pain;157(10):2194-207, 2016 Oct.
[Is] ISSN:1872-6623
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuroimaging studies of patients with chronic pain have shown that neurotransmitter abnormalities, including increases in glutamate and decreases in GABA, could be responsible for the cortical hyperactivity and hyperalgesia/allodynia observed in some pain conditions. These finding are particularly evident in the insula, a brain region known to play a role in both the sensory-discriminative and the affective-motivational aspects of pain processing. However, clinical studies are not entirely able to determine the directionality of these findings, nor whether they are causal or epiphenomenon. Thus, a set of animal studies was performed to determine whether alterations in glutamate and GABA are the result of injury, the cause of augmented pain processing, or both. Compared with controls, the excitatory neurotransmitters glutamate and aspartate are significantly higher in the rat insula after chronic constriction injury of the sciatic nerve (CCI). The CCI also produced significant increases in allodynia (mechanical and cold), thermal hyperalgesia, and nociceptive aversiveness. Unilateral microinjection of ionotropic glutamate receptor antagonists restored these nociceptive behaviors to preinjury values. Increasing endogenous levels of GABA or enhancing signaling at inhibitory glycinergic receptors had similar effects as the glutamate receptor antagonists. In naive rats, increasing endogenous levels of glutamate, decreasing endogenous levels of GABA, or blocking strychnine-sensitive glycine receptors in the insula significantly increased thermal hyperalgesia and mechanical allodynia. These data support the hypothesis that an altered balance of excitatory and inhibitory neurotransmitters in brain regions such as the insula occurs in chronic pain states and leads to augmented central pain processing and increased pain sensitivity.
[Mh] Termos MeSH primário: Córtex Cerebral/metabolismo
Córtex Cerebral/patologia
Glutamatos/metabolismo
Ciática/patologia
Ácido gama-Aminobutírico/metabolismo
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Aprendizagem da Esquiva/efeitos dos fármacos
Modelos Animais de Doenças
Fármacos atuantes sobre Aminoácidos Excitatórios/farmacologia
GABAérgicos/farmacologia
Glicina/metabolismo
Glicinérgicos/farmacologia
Hiperalgesia/etiologia
Masculino
Microdiálise
Microinjeções
Medição da Dor
Limiar da Dor/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Ciática/metabolismo
Ciática/fisiopatologia
Estricnina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Excitatory Amino Acid Agents); 0 (GABA Agents); 0 (Glutamates); 0 (Glycine Agents); 56-12-2 (gamma-Aminobutyric Acid); H9Y79VD43J (Strychnine); TE7660XO1C (Glycine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160525
[St] Status:MEDLINE
[do] DOI:10.1097/j.pain.0000000000000615


  7 / 690 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27216901
[Au] Autor:Gopalakrishna G; Ithman MH; Lauriello J
[Ad] Endereço:Department of Psychiatry, University of Missouri-Columbia, One Hospital Drive, Columbia, MO 65212, USA. Electronic address: gopalakrishnag@health.missouri.edu.
[Ti] Título:Update on New and Emerging Treatments for Schizophrenia.
[So] Source:Psychiatr Clin North Am;39(2):217-38, 2016 06.
[Is] ISSN:1558-3147
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although there has been more than 50 years of development, there remains a great need for better antipsychotic medications. This article looks at the recent advances in treatment of schizophrenia. New hypotheses have been suggested that may replace or complement the dopamine hypotheses. The article explores the different novel drugs that impact some of the key neurotransmitter systems currently. Phosphodiesterase 10A inhibitors and α-7 neuronal nicotinic acetylcholine receptor modulators constitute the majority. The marketing of these medications eventually may result in change about how schizophrenia is treated.
[Mh] Termos MeSH primário: Antipsicóticos/uso terapêutico
Aprovação de Drogas
Esquizofrenia/tratamento farmacológico
[Mh] Termos MeSH secundário: Fármacos atuantes sobre Aminoácidos Excitatórios/uso terapêutico
Glicinérgicos/uso terapêutico
Seres Humanos
Minociclina/uso terapêutico
Agonistas Nicotínicos/uso terapêutico
Inibidores de Fosfodiesterase/uso terapêutico
Piperazinas/uso terapêutico
Piperidinas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (Excitatory Amino Acid Agents); 0 (Glycine Agents); 0 (Nicotinic Agonists); 0 (Phosphodiesterase Inhibitors); 0 (Piperazines); 0 (Piperidines); AQ316B4F8C (blonanserin); FYY3R43WGO (Minocycline)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160525
[St] Status:MEDLINE


  8 / 690 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:27200412
[Au] Autor:Marchenko V; Koizumi H; Mosher B; Koshiya N; Tariq MF; Bezdudnaya TG; Zhang R; Molkov YI; Rybak IA; Smith JC
[Ad] Endereço:Department of Neurobiology and Anatomy, Drexel University College of Medicine , Philadelphia, Pennsylvania 19129.
[Ti] Título:Perturbations of Respiratory Rhythm and Pattern by Disrupting Synaptic Inhibition within Pre-Bötzinger and Bötzinger Complexes.
[So] Source:eNeuro;3(2), 2016 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The pre-Bötzinger (pre-BötC) and Bötzinger (BötC) complexes are the brainstem compartments containing interneurons considered to be critically involved in generating respiratory rhythm and motor pattern in mammals. Current models postulate that both generation of the rhythm and coordination of the inspiratory-expiratory pattern involve inhibitory synaptic interactions within and between these regions. Both regions contain glycinergic and GABAergic neurons, and rhythmically active neurons in these regions receive appropriately coordinated phasic inhibition necessary for generation of the normal three-phase respiratory pattern. However, recent experiments attempting to disrupt glycinergic and GABAergic postsynaptic inhibition in the pre-BötC and BötC in adult rats in vivo have questioned the critical role of synaptic inhibition in these regions, as well as the importance of the BötC, which contradicts previous physiological and pharmacological studies. To further evaluate the roles of synaptic inhibition and the BötC, we bilaterally microinjected the GABAA receptor antagonist gabazine and glycinergic receptor antagonist strychnine into the pre-BötC or BötC in anesthetized adult rats in vivo and in perfused in situ brainstem-spinal cord preparations from juvenile rats. Muscimol was microinjected to suppress neuronal activity in the pre-BötC or BötC. In both preparations, disrupting inhibition within pre-BötC or BötC caused major site-specific perturbations of the rhythm and disrupted the three-phase motor pattern, in some experiments terminating rhythmic motor output. Suppressing BötC activity also potently disturbed the rhythm and motor pattern. We conclude that inhibitory circuit interactions within and between the pre-BötC and BötC critically regulate rhythmogenesis and are required for normal respiratory motor pattern generation.
[Mh] Termos MeSH primário: Inibição Neural/fisiologia
Transtornos Respiratórios/fisiopatologia
Centro Respiratório/fisiologia
Taxa Respiratória/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Potenciais de Ação/fisiologia
Animais
Nervos Cranianos/fisiologia
Modelos Animais de Doenças
Antagonistas GABAérgicos/farmacologia
Agonistas de Receptores de GABA-A/farmacologia
Ácido Glutâmico/toxicidade
Glicinérgicos/farmacologia
Masculino
Muscimol/farmacologia
Rede Nervosa/efeitos dos fármacos
Rede Nervosa/fisiologia
Inibição Neural/efeitos dos fármacos
Piridazinas/farmacologia
Ratos
Ratos Sprague-Dawley
Transtornos Respiratórios/etiologia
Centro Respiratório/efeitos dos fármacos
Taxa Respiratória/efeitos dos fármacos
Medula Espinal/fisiologia
Estricnina/farmacologia
Vagotomia/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (GABA Antagonists); 0 (GABA-A Receptor Agonists); 0 (Glycine Agents); 0 (Pyridazines); 2763-96-4 (Muscimol); 3KX376GY7L (Glutamic Acid); 99460MG420 (gabazine); H9Y79VD43J (Strychnine)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160521
[St] Status:MEDLINE


  9 / 690 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27098031
[Au] Autor:Roux I; Wu JS; McIntosh JM; Glowatzki E
[Ad] Endereço:Department of Otolaryngology - Head and Neck Surgery, The Center for Hearing and Balance and the Center for Sensory Biology, The Johns Hopkins University School of Medicine, Baltimore, Maryland; iroux2@jhmi.edu.
[Ti] Título:Assessment of the expression and role of the α1-nAChR subunit in efferent cholinergic function during the development of the mammalian cochlea.
[So] Source:J Neurophysiol;116(2):479-92, 2016 Aug 01.
[Is] ISSN:1522-1598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hair cell (HC) activity in the mammalian cochlea is modulated by cholinergic efferent inputs from the brainstem. These inhibitory inputs are mediated by calcium-permeable nicotinic acetylcholine receptors (nAChRs) containing α9- and α10-subunits and by subsequent activation of calcium-dependent potassium channels. Intriguingly, mRNAs of α1- and γ-nAChRs, subunits of the "muscle-type" nAChR have also been found in developing HCs (Cai T, Jen HI, Kang H, Klisch TJ, Zoghbi HY, Groves AK. J Neurosci 35: 5870-5883, 2015; Scheffer D, Sage C, Plazas PV, Huang M, Wedemeyer C, Zhang DS, Chen ZY, Elgoyhen AB, Corey DP, Pingault V. J Neurochem 103: 2651-2664, 2007; Sinkkonen ST, Chai R, Jan TA, Hartman BH, Laske RD, Gahlen F, Sinkkonen W, Cheng AG, Oshima K, Heller S. Sci Rep 1: 26, 2011) prompting proposals that another type of nAChR is present and may be critical during early synaptic development. Mouse genetics, histochemistry, pharmacology, and whole cell recording approaches were combined to test the role of α1-nAChR subunit in HC efferent synapse formation and cholinergic function. The onset of α1-mRNA expression in mouse HCs was found to coincide with the onset of the ACh response and efferent synaptic function. However, in mouse inner hair cells (IHCs) no response to the muscle-type nAChR agonists (±)-anatoxin A, (±)-epibatidine, (-)-nicotine, or 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP) was detected, arguing against the presence of an independent functional α1-containing muscle-type nAChR in IHCs. In α1-deficient mice, no obvious change of IHC efferent innervation was detected at embryonic day 18, contrary to the hyperinnervation observed at the neuromuscular junction. Additionally, ACh response and efferent synaptic activity were detectable in α1-deficient IHCs, suggesting that α1 is not necessary for assembly and membrane targeting of nAChRs or for efferent synapse formation in IHCs.
[Mh] Termos MeSH primário: Cóclea
Regulação da Expressão Gênica no Desenvolvimento/fisiologia
Células Ciliadas Auditivas Internas/fisiologia
Receptores Nicotínicos/metabolismo
[Mh] Termos MeSH secundário: Acetilcolina/farmacologia
Fatores Etários
Animais
Animais Recém-Nascidos
Colina O-Acetiltransferase/genética
Colina O-Acetiltransferase/metabolismo
Colinérgicos/farmacologia
Cóclea/embriologia
Cóclea/crescimento & desenvolvimento
Cóclea/metabolismo
Embrião de Mamíferos
Glicinérgicos/farmacologia
Células Ciliadas Auditivas Internas/efeitos dos fármacos
Potenciais da Membrana/efeitos dos fármacos
Potenciais da Membrana/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Técnicas de Patch-Clamp
Potássio/farmacologia
Receptores Nicotínicos/genética
Canais de Potássio Ativados por Cálcio de Condutância Baixa/genética
Canais de Potássio Ativados por Cálcio de Condutância Baixa/metabolismo
Estricnina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CHRNA1 protein, mouse); 0 (Cholinergic Agents); 0 (Glycine Agents); 0 (Kcnn2 protein, mouse); 0 (Receptors, Nicotinic); 0 (Small-Conductance Calcium-Activated Potassium Channels); EC 2.3.1.6 (Choline O-Acetyltransferase); H9Y79VD43J (Strychnine); N9YNS0M02X (Acetylcholine); RWP5GA015D (Potassium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160422
[St] Status:MEDLINE
[do] DOI:10.1152/jn.01038.2015


  10 / 690 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:27067428
[Au] Autor:Wang X; Ma Z; Fu Z; Gao S; Yang L; Jin Y; Sun H; Wang C; Fan W; Chen L; Zheng QY; Bi G; Ma CL
[Ad] Endereço:Department of Physiology, Binzhou Medical University, Yantai, Shandong, China "Brain stroke" Key Lab of Shandong Health Administration Institute, Binzhou Medical University, Yantai, Shandong, China Department of Internal Neurology, Affiliated Hospital of Binzhou Medical University, Binzhou, Shandong
[Ti] Título:Hydroxysafflor Yellow A Protects Neurons From Excitotoxic Death through Inhibition of NMDARs.
[So] Source:ASN Neuro;8(2), 2016 Mar-Apr.
[Is] ISSN:1759-0914
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Excessive glutamate release causes overactivation of N-methyld-aspartate receptors (NMDARs), leading to excitatory neuronal damage in cerebral ischemia. Hydroxysafflor yellow A (HSYA), a compound extracted from Carthamus tinctorius L., has been reported to exert a neuroprotective effect in many pathological conditions, including brain ischemia. However, the underlying mechanism of HSYA's effect on neurons remains elusive. In the present study, we conducted experiments using patch-clamp recording of mouse hippocampal slices. In addition, we performed Ca(2+) imaging, Western blots, as well as mitochondrial-targeted circularly permuted yellow fluorescent protein transfection into cultured hippocampal neurons in order to decipher the physiological mechanism underlying HSYA's neuroprotective effect.Through the electrophysiology experiments, we found that HSYA inhibited NMDAR-mediated excitatory postsynaptic currents without affecting α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor and γ-aminobutyric acid A-type receptor-mediated currents. This inhibitory effect of HSYA on NMDARs was concentration dependent. HSYA did not show any preferential inhibition of either N-methyld-aspartate receptor subtype 2A- or N-methyld-aspartate receptor subtype 2B- subunit-containing NMDARs. Additionally, HSYA exhibits a facilitatory effect on paired NMDAR-mediated excitatory postsynaptic currents. Furthermore, HSYA reduced the magnitude of NMDAR-mediated membrane depolarization currents evoked by oxygen-glucose deprivation, and suppressed oxygen-glucose deprivation-induced and NMDAR-dependent ischemic long-term potentiation, which is believed to cause severe reperfusion damage after ischemia. Through the molecular biology experiments, we found that HSYA inhibited the NMDA-induced and NMDAR-mediated intracellular Ca(2+)concentration increase in hippocampal cultures, reduced apoptotic and necrotic cell deaths, and prevented mitochondrial damage. Together, our data demonstrate for the first time that HSYA protects hippocampal neurons from excitotoxic damage through the inhibition of NMDARs. This novel finding indicates that HSYA may be a promising pharmacological candidate for the treatment of brain ischemia.
[Mh] Termos MeSH primário: Chalcona/análogos & derivados
Neurônios/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Quinonas/farmacologia
Receptores de N-Metil-D-Aspartato/metabolismo
[Mh] Termos MeSH secundário: 6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Animais
Animais Recém-Nascidos
Região CA1 Hipocampal/citologia
Cálcio/metabolismo
Morte Celular/efeitos dos fármacos
Células Cultivadas
Estimulantes do Sistema Nervoso Central/farmacologia
Chalcona/farmacologia
Fármacos atuantes sobre Aminoácidos Excitatórios/farmacologia
Antagonistas de Aminoácidos Excitatórios/farmacologia
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Glucose/deficiência
Glicinérgicos/farmacologia
Hipóxia
Técnicas In Vitro
Potenciais da Membrana/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Picrotoxina/farmacologia
Estricnina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Central Nervous System Stimulants); 0 (Excitatory Amino Acid Agents); 0 (Excitatory Amino Acid Antagonists); 0 (Glycine Agents); 0 (Neuroprotective Agents); 0 (Quinones); 0 (Receptors, N-Methyl-D-Aspartate); 124-87-8 (Picrotoxin); 146087-19-6 (hydroxysafflor yellow A); 5S5A2Q39HX (Chalcone); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); H9Y79VD43J (Strychnine); IY9XDZ35W2 (Glucose); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160413
[St] Status:MEDLINE



página 1 de 69 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde