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[PMID]:29288665
[Au] Autor:Peoples JN; Taylor DG; Katchman AN; Ebert SN
[Ad] Endereço:Burnett School of Biomedical Sciences, Division of Metabolic and Cardiovascular Sciences, College of Medicine, University of Central Florida, 6900 Lake Nona Blvd, Orlando, FL 32827, United States.
[Ti] Título:Intact calcium signaling in adrenergic-deficient embryonic mouse hearts.
[So] Source:Biochem Biophys Res Commun;495(4):2547-2552, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mouse embryos that lack the ability to produce the adrenergic hormones, norepinephrine (NE) and epinephrine (EPI), due to disruption of the dopamine beta-hydroxylase (Dbh ) gene inevitably perish from heart failure during mid-gestation. Since adrenergic stimulation is well-known to enhance calcium signaling in developing as well as adult myocardium, and impairments in calcium signaling are typically associated with heart failure, we hypothesized that adrenergic-deficient embryonic hearts would display deficiencies in cardiac calcium signaling relative to adrenergic-competent controls at a developmental stage immediately preceding the onset of heart failure, which first appears beginning or shortly after mouse embryonic day 10.5 (E10.5). To test this hypothesis, we used ratiometric fluorescent calcium imaging techniques to measure cytosolic calcium transients, [Ca ] in isolated E10.5 mouse hearts. Our results show that spontaneous [Ca ] oscillations were intact and robustly responded to a variety of stimuli including extracellular calcium (5 mM), caffeine (5 mM), and NE (100 nM) in a manner that was indistinguishable from controls. Further, we show similar patterns of distribution (via immunofluorescent histochemical staining) and activity (via patch-clamp recording techniques) for the major voltage-gated plasma membrane calcium channel responsible for the L-type calcium current, I , in adrenergic-deficient and control embryonic cardiac cells. These results demonstrate that despite the absence of vital adrenergic hormones that consistently leads to embryonic lethality in vivo, intracellular and extracellular calcium signaling remain essentially intact and functional in embryonic mouse hearts through E10.5. These findings suggest that adrenergic stimulation is not required for the development of intracellular calcium oscillations or extracellular calcium signaling through I and that aberrant calcium signaling does not likely contribute to the onset of heart failure in this model.
[Mh] Termos MeSH primário: Adrenérgicos/metabolismo
Sinalização do Cálcio/fisiologia
Cálcio/metabolismo
Epinefrina/metabolismo
Coração/embriologia
Miocárdio/metabolismo
Norepinefrina/metabolismo
[Mh] Termos MeSH secundário: Animais
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenergic Agents); SY7Q814VUP (Calcium); X4W3ENH1CV (Norepinephrine); YKH834O4BH (Epinephrine)
[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:171231
[St] Status:MEDLINE


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[PMID]:28476642
[Au] Autor:Braz BY; Belforte JE; Murer MG; Galiñanes GL
[Ad] Endereço:Universidad de Buenos Aires, Facultad de Medicina, Departamento de Ciencias Fisiológicas, Grupo de Neurociencia de Sistemas, Buenos Aires, Argentina; Universidad de Buenos Aires, CONICET, Instituto de Fisiología y Biofísica (IFIBIO) Houssay, Buenos Aires, Argentina. Electronic address: barbybraz@gma
[Ti] Título:Properties of the corticostriatal long term depression induced by medial prefrontal cortex high frequency stimulation in vivo.
[So] Source:Neuropharmacology;121:278-286, 2017 Jul 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Repetitive stimulation of cognitive forebrain circuits at frequencies capable of inducing corticostriatal long term plasticity is increasingly being used with therapeutic purposes in patients with neuropsychiatric disorders. However, corticostriatal plasticity is rarely studied in the intact brain. Our aim was to study the mechanisms of corticostriatal long term depression (LTD) induced by high frequency stimulation (HFS) of the medial prefrontal cortex in vivo. Our main finding is that the LTD induced in the dorsomedial striatum by medial prefrontal cortex HFS in vivo (prefrontostriatal LTD) is not affected by manipulations that block or reduce the LTD induced in the dorsolateral striatum by motor cortex HFS in brain slices, including pharmacological dopamine receptor and CB1 receptor blockade, chronic nigrostriatal dopamine depletion, CB1 receptor genetic deletion and selective striatal cholinergic interneuron (SCIN) ablation. Conversely, like in the hippocampus and other brain areas, prefrontostriatal LTD is NMDA receptor dependent. Thus, we describe a novel form of corticostriatal LTD that operates in brain circuits involved in reward and cognition and could be relevant for understanding the therapeutic effects of deep brain stimulation.
[Mh] Termos MeSH primário: Corpo Estriado/citologia
Corpo Estriado/fisiologia
Depressão Sináptica de Longo Prazo/fisiologia
Neurônios/fisiologia
Córtex Pré-Frontal/fisiologia
[Mh] Termos MeSH secundário: Adrenérgicos/toxicidade
Animais
Animais Recém-Nascidos
Benzazepinas/farmacologia
Colina O-Acetiltransferase/genética
Colina O-Acetiltransferase/metabolismo
Corpo Estriado/lesões
Maleato de Dizocilpina/farmacologia
Antagonistas de Dopamina/farmacologia
Antagonistas de Aminoácidos Excitatórios/farmacologia
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/genética
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/metabolismo
Depressão Sináptica de Longo Prazo/efeitos dos fármacos
Depressão Sináptica de Longo Prazo/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Vias Neurais/fisiologia
Neurônios/efeitos dos fármacos
Oxidopamina/toxicidade
Piperidinas/farmacologia
Pirazóis/farmacologia
Receptor CB1 de Canabinoide/antagonistas & inibidores
Receptor CB1 de Canabinoide/genética
Receptor CB1 de Canabinoide/metabolismo
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agents); 0 (Benzazepines); 0 (Dopamine Antagonists); 0 (Excitatory Amino Acid Antagonists); 0 (Heparin-binding EGF-like Growth Factor); 0 (Piperidines); 0 (Pyrazoles); 0 (Receptor, Cannabinoid, CB1); 0 (SCH 23390); 3I4FA44MAI (AM 251); 6LR8C1B66Q (Dizocilpine Maleate); 8HW4YBZ748 (Oxidopamine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 2.3.1.6 (Choline O-Acetyltransferase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE


  3 / 1834 MEDLINE  
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[PMID]:28431876
[Au] Autor:Oliveira LM; Tuppy M; Moreira TS; Takakura AC
[Ad] Endereço:Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, 05508-000 São Paulo, SP, Brazil.
[Ti] Título:Role of the locus coeruleus catecholaminergic neurons in the chemosensory control of breathing in a Parkinson's disease model.
[So] Source:Exp Neurol;293:172-180, 2017 Jul.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A previous study has demonstrated that in the 6-hydroxydopamine (6-OHDA)-model of Parkinson's disease (PD) there is a reduction in the number of Phox2b neurons in the retrotrapezoid nucleus (RTN) and a decrease in the respiratory response to hypercapnia 40days after PD-induction. The functional deficiency is restored 60days after 6-OHDA injection and here we tested the hypothesis that the locus coeruleus (LC) could be a candidate to restore the breathing deficiency. Minute Ventilation (V ) in response to hypercapnia (7% CO ) was assessed one day before, and then 40 and 60days after bilateral 6-OHDA (24µg/µL) or vehicle injections into the LC in control or PD-induced male Wistar rats. Bilateral injections of 6-OHDA decreased catecholaminergic neurons by 86% and 83% in the substantia nigra pars compacta (SNpc) and LC, respectively. As already described, in animals with lesions to the SNpc (N=6/group), the reduction in the ventilatory response to hypercapnia was restored 60days after PD (1257±81 vs. vehicle: 1185±49mL/kg/min). However, in animals with PD and lesion in the LC, the ventilation was blunted (674±39mL/kg/min). In another group of PD rats, we observed a reduction in the number of hypercapnia-induced-fos cells in the RTN region (40days: 38±3 and 60days: 8.5±0.9 vs. vehicle 78±3 cells) and an increase in the LC (40days: 46±4 and 60days: 94±22 vs. vehicle 1±1 cells). Our data suggest that LC catecholaminergic neurons can be a candidate structure mediating chemoreceptor function in a model of PD.
[Mh] Termos MeSH primário: Catecolaminas/metabolismo
Locus Cerúleo/patologia
Neurônios/metabolismo
Doença de Parkinson Secundária/complicações
Doença de Parkinson Secundária/patologia
Ventilação Pulmonar/fisiologia
Respiração
[Mh] Termos MeSH secundário: Adrenérgicos/toxicidade
Animais
Dióxido de Carbono/farmacologia
Contagem de Células
Modelos Animais de Doenças
Hipercapnia/patologia
Hipercapnia/fisiopatologia
Locus Cerúleo/efeitos dos fármacos
Masculino
Neurônios/efeitos dos fármacos
Proteínas Oncogênicas v-fos/metabolismo
Oxidopamina/toxicidade
Doença de Parkinson Secundária/induzido quimicamente
Pletismografia
Ventilação Pulmonar/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Respiração/efeitos dos fármacos
Fatores de Tempo
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agents); 0 (Catecholamines); 0 (Oncogene Proteins v-fos); 142M471B3J (Carbon Dioxide); 8HW4YBZ748 (Oxidopamine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
[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:170423
[St] Status:MEDLINE


  4 / 1834 MEDLINE  
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[PMID]:28376279
[Au] Autor:Ay M; Luo J; Langley M; Jin H; Anantharam V; Kanthasamy A; Kanthasamy AG
[Ad] Endereço:Department of Biomedical Sciences, Parkinson's Disorder Research Laboratory, Iowa Center for Advanced Neurotoxicology, Iowa State University, Ames, Iowa, USA.
[Ti] Título:Molecular mechanisms underlying protective effects of quercetin against mitochondrial dysfunction and progressive dopaminergic neurodegeneration in cell culture and MitoPark transgenic mouse models of Parkinson's Disease.
[So] Source:J Neurochem;141(5):766-782, 2017 Jun.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Quercetin, one of the major flavonoids in plants, has been recently reported to have neuroprotective effects against neurodegenerative processes. However, since the molecular signaling mechanisms governing these effects are not well clarified, we evaluated quercetin's effect on the neuroprotective signaling events in dopaminergic neuronal models and further tested its efficacy in the MitoPark transgenic mouse model of Parkinson's disease (PD). Western blot analysis revealed that quercetin significantly induced the activation of two major cell survival kinases, protein kinase D1 (PKD1) and Akt in MN9D dopaminergic neuronal cells. Furthermore, pharmacological inhibition or siRNA knockdown of PKD1 blocked the activation of Akt, suggesting that PKD1 acts as an upstream regulator of Akt in quercetin-mediated neuroprotective signaling. Quercetin also enhanced cAMP response-element binding protein phosphorylation and expression of the cAMP response-element binding protein target gene brain-derived neurotrophic factor. Results from qRT-PCR, Western blot analysis, mtDNA content analysis, and MitoTracker assay experiments revealed that quercetin augmented mitochondrial biogenesis. Quercetin also increased mitochondrial bioenergetics capacity and protected MN9D cells against 6-hydroxydopamine-induced neurotoxicity. To further evaluate the neuroprotective efficacy of quercetin against the mitochondrial dysfunction underlying PD, we used the progressive dopaminergic neurodegenerative MitoPark transgenic mouse model of PD. Oral administration of quercetin significantly reversed behavioral deficits, striatal dopamine depletion, and TH neuronal cell loss in MitoPark mice. Together, our findings demonstrate that quercetin activates the PKD1-Akt cell survival signaling axis and suggest that further exploration of quercetin as a promising neuroprotective agent for treating PD may offer clinical benefits.
[Mh] Termos MeSH primário: Dopamina/metabolismo
Doenças Mitocondriais/tratamento farmacológico
Doenças Mitocondriais/etiologia
Degeneração Neural/tratamento farmacológico
Degeneração Neural/etiologia
Doença de Parkinson/complicações
Quercetina/uso terapêutico
[Mh] Termos MeSH secundário: Adrenérgicos/toxicidade
Animais
Antioxidantes/uso terapêutico
Linhagem Celular Transformada
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Proteínas de Ligação a DNA/genética
Comportamento Exploratório/efeitos dos fármacos
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Doenças Mitocondriais/complicações
Doenças Mitocondriais/genética
Proteínas Mitocondriais/genética
Oxidopamina/toxicidade
Consumo de Oxigênio/efeitos dos fármacos
Consumo de Oxigênio/genética
Doença de Parkinson/genética
Fosforilação/efeitos dos fármacos
Fosforilação/genética
Canais de Cátion TRPP/metabolismo
Fatores de Transcrição/genética
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agents); 0 (Antioxidants); 0 (DNA-Binding Proteins); 0 (Mitochondrial Proteins); 0 (TRPP Cation Channels); 0 (Transcription Factors); 0 (mitochondrial transcription factor A); 0 (polycystic kidney disease 1 protein); 8HW4YBZ748 (Oxidopamine); 9IKM0I5T1E (Quercetin); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170405
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.14033


  5 / 1834 MEDLINE  
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[PMID]:28294337
[Au] Autor:Cruces-Sande A; Méndez-Álvarez E; Soto-Otero R
[Ad] Endereço:Laboratory of Neurochemistry, Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Santiago de Compostela, Santiago de Compostela, Spain.
[Ti] Título:Copper increases the ability of 6-hydroxydopamine to generate oxidative stress and the ability of ascorbate and glutathione to potentiate this effect: potential implications in Parkinson's disease.
[So] Source:J Neurochem;141(5):738-749, 2017 Jun.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Copper is an essential metal for the function of many proteins related to important cellular reactions and also involved in the synaptic transmission. Although there are several mechanisms involved in copper homeostasis, a dysregulation in this process can result in serious neurological consequences, including degeneration of dopaminergic neurons. 6-Hydroxydopamine is a dopaminergic neurotoxin mainly used in experimental models of Parkinson's disease, whose neurotoxicity has been related to its ability to generate free radicals. In this study, we examined the effects induced by copper on 6-OHDA autoxidation. Our data show that both Cu and Cu caused an increase in OH production by 6-OHDA autoxidation, which was accompanied by an increase in the rate of both p-quinone formation and H O accumulation. The presence of ascorbate greatly enhanced this process by establishing a redox cycle which regenerates 6-OHDA from its p-quinone. However, the presence of glutathione did not change significantly the copper-induced effects. We observed that copper is able to potentiate the ability of 6-OHDA to cause both lipid peroxidation and protein oxidation, with the latter including a reduction in free-thiol content and an increase in carbonyl content. Ascorbate also increases the lipid peroxidation induced by the action of copper and 6-OHDA. Glutathione protects against the copper-induced lipid peroxidation, but does not reduce its potential to oxidize free thiols. These results clearly demonstrate the potential of copper to increase the capacity of 6-OHDA to generate oxidative stress and the ability of ascorbate to enhance this potential, which may contribute to the destruction of dopaminergic neurons.
[Mh] Termos MeSH primário: Adrenérgicos/farmacologia
Antioxidantes/farmacologia
Ácido Ascórbico/farmacologia
Cobre/farmacologia
Glutationa/farmacocinética
Estresse Oxidativo/efeitos dos fármacos
Oxidopamina/farmacologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/ultraestrutura
Sinergismo Farmacológico
Peróxido de Hidrogênio/metabolismo
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Oxirredução
Consumo de Oxigênio/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Estatísticas não Paramétricas
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agents); 0 (Antioxidants); 789U1901C5 (Copper); 8HW4YBZ748 (Oxidopamine); BBX060AN9V (Hydrogen Peroxide); GAN16C9B8O (Glutathione); PQ6CK8PD0R (Ascorbic Acid)
[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:170316
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.14019


  6 / 1834 MEDLINE  
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[PMID]:28256089
[Au] Autor:F Hernández L; Castela I; Ruiz-DeDiego I; Obeso JA; Moratalla R
[Ad] Endereço:HM-CINAC, Hospital Universitario HM Puerta del Sur, Mostoles and Medical School, CEU-San Pablo University, Madrid, Spain.
[Ti] Título:Striatal activation by optogenetics induces dyskinesias in the 6-hydroxydopamine rat model of Parkinson disease.
[So] Source:Mov Disord;32(4):530-537, 2017 04.
[Is] ISSN:1531-8257
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Long-term levodopa (l-dopa) treatment is associated with the development of l-dopa-induced dyskinesias in the majority of patients with Parkinson disease (PD). The etiopathogonesis and mechanisms underlying l-dopa-induced dyskinesias are not well understood. METHODS: We used striatal optogenetic stimulation to induce dyskinesias in a hemiparkinsonian model of PD in rats. Striatal dopamine depletion was induced unilaterally by 6-hydroxydopamine injection into the medial forebrain bundle. For the optogenetic manipulation, we injected adeno-associated virus particles expressing channelrhodopsin to stimulate striatal medium spiny neurons with a laser source. RESULTS: Simultaneous optical activation of medium spiny neurons of the direct and indirect striatal pathways in the 6-hydroxydopamine lesion but l-dopa naïve rats induced involuntary movements similar to l-dopa-induced dyskinesias, labeled here as optodyskinesias. Noticeably, optodyskinesias were facilitated by l-dopa in animals that did not respond initially to the laser stimulation. In general, optodyskinesias lasted while the laser stimulus was applied, but in some instances remained ongoing for a few seconds after the laser was off. Postmortem tissue analysis revealed increased FosB expression, a molecular marker of l-dopa-induced dyskinesias, primarily in medium spiny neurons of the direct pathway in the dopamine-depleted hemisphere. CONCLUSION: Selective optogenetic activation of the dorsolateral striatum elicits dyskinesias in the 6-hydroxydopamine rat model of PD. This effect was associated with a preferential activation of the direct striato-nigral pathway. These results potentially open new avenues in the understanding of mechanisms involved in l-dopa-induced dyskinesias. © 2017 International Parkinson and Movement Disorder Society.
[Mh] Termos MeSH primário: Adrenérgicos/toxicidade
Corpo Estriado/metabolismo
Discinesias/etiologia
Optogenética/efeitos adversos
Oxidopamina/toxicidade
Doença de Parkinson/etiologia
[Mh] Termos MeSH secundário: Animais
Antiparkinsonianos/efeitos adversos
Encéfalo/metabolismo
Channelrhodopsins
Modelos Animais de Doenças
Dinorfinas/metabolismo
Lateralidade Funcional
Levodopa/efeitos adversos
Masculino
Doença de Parkinson/patologia
Doença de Parkinson/fisiopatologia
Proteínas Proto-Oncogênicas c-fos/metabolismo
Ratos
Ratos Sprague-Dawley
Transdução Genética
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agents); 0 (Antiparkinson Agents); 0 (Channelrhodopsins); 0 (Fosb protein, rat); 0 (Proto-Oncogene Proteins c-fos); 46627O600J (Levodopa); 74913-18-1 (Dynorphins); 8HW4YBZ748 (Oxidopamine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170304
[St] Status:MEDLINE
[do] DOI:10.1002/mds.26947


  7 / 1834 MEDLINE  
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[PMID]:28202248
[Au] Autor:Okada S; Yamaguchi N
[Ad] Endereço:Department of Pharmacology, Graduate School of Medicine, Aichi Medical University, 1-1 Yazakokarimata, Nagakute, Aichi 480-1195, Japan. Electronic address: okadas@aichi-med-u.ac.jp.
[Ti] Título:Possible role of adrenoceptors in the hypothalamic paraventricular nucleus in corticotropin-releasing factor-induced sympatho-adrenomedullary outflow in rats.
[So] Source:Auton Neurosci;203:74-80, 2017 Mar.
[Is] ISSN:1872-7484
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: A functional interaction between the corticotropin-releasing factor (CRF) system and noradrenergic neurons in the brain has been suggested. In the present study, we investigated the interrelationship between the central CRF-induced elevation of plasma catecholamines and adrenoceptor activation in the paraventricular nucleus of the hypothalamus (PVN) using urethane-anesthetized rats. MAIN METHODS: In rats under urethane anesthesia, a femoral venous line was inserted for infusion of saline, and a femoral arterial line was inserted for collecting blood samples. Next, animals were placed in a stereotaxic apparatus for the application of test agents. Catecholamines in the plasma were extracted by alumina absorption and were assayed with high-performance liquid chromatography with electrochemical detection. Quantification of noradrenaline in rat PVN microdialysates was performed with high-performance liquid chromatography with electrochemical detection. KEY FINDINGS: We showed that centrally administered CRF elevated noradrenaline release in the PVN. Furthermore, we demonstrated that microinjection of phenylephrine into the PVN induced elevation of plasma levels of adrenaline, but not of noradrenaline, whereas microinjection of isoproterenol into the PVN induced elevation of plasma levels of noradrenaline, but not of adrenaline. Bilateral blockade of adrenoceptors in the PVN revealed that phentolamine significantly suppressed the CRF-induced elevation of plasma adrenaline level, while propranolol significantly CRF-induced elevation of plasma noradrenaline level. SIGNIFICANCE: Our results suggest that centrally administered CRF-induced elevation of plasma levels of adrenaline and noradrenaline can be mediated via activation of α-adrenoceptors and ß-adrenoceptors, respectively, in the rat PVN.
[Mh] Termos MeSH primário: Medula Suprarrenal/efeitos dos fármacos
Hormônio Liberador da Corticotropina/administração & dosagem
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Receptores Adrenérgicos alfa/metabolismo
Receptores Adrenérgicos beta/metabolismo
Sistema Nervoso Simpático/efeitos dos fármacos
[Mh] Termos MeSH secundário: Medula Suprarrenal/metabolismo
Adrenérgicos/farmacologia
Anestésicos Intravenosos/farmacologia
Animais
Hormônio Liberador da Corticotropina/metabolismo
Epinefrina/sangue
Isoproterenol/farmacologia
Masculino
Norepinefrina/sangue
Núcleo Hipotalâmico Paraventricular/metabolismo
Fentolamina/farmacologia
Fenilefrina/farmacologia
Propranolol/farmacologia
Ratos Wistar
Sistema Nervoso Simpático/metabolismo
Simpatomiméticos/farmacologia
Uretana/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agents); 0 (Anesthetics, Intravenous); 0 (Receptors, Adrenergic, alpha); 0 (Receptors, Adrenergic, beta); 0 (Sympathomimetics); 1WS297W6MV (Phenylephrine); 3IN71E75Z5 (Urethane); 9015-71-8 (Corticotropin-Releasing Hormone); 9Y8NXQ24VQ (Propranolol); L628TT009W (Isoproterenol); X4W3ENH1CV (Norepinephrine); YKH834O4BH (Epinephrine); Z468598HBV (Phentolamine)
[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:170217
[St] Status:MEDLINE


  8 / 1834 MEDLINE  
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[PMID]:28131727
[Au] Autor:Hao F; Yang C; Chen SS; Wang YY; Zhou W; Hao Q; Lu T; Hoffer B; Zhao LR; Duan WM; Xu QY
[Ad] Endereço:Department of Anatomy, Capital Medical University, Beijing 100069, China.
[Ti] Título:Long-term protective effects of AAV9-mesencephalic astrocyte-derived neurotrophic factor gene transfer in parkinsonian rats.
[So] Source:Exp Neurol;291:120-133, 2017 May.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intrastriatal injection of mesencephalic astrocyte-derived neurotrophic factor (MANF) protein has been shown to provide neuroprotective and neurorestorative effects in a 6-hydroxydopamine (6-OHDA) - lesioned rat model of Parkinson's disease. Here, we used an adeno-associated virus serotype 9 (AAV9) vector to deliver the human MANF (hMANF) gene into the rat striatum 10days after a 6-OHDA lesion to examine long-term effects of hMANF on nigral dopaminergic neurons and mechanisms underlying MANF neuroprotection. Intrastriatal injection of AAV9-hMANF vectors led to a robust and widespread expression of the hMANF gene in the injected striatum up to 24weeks. Increased levels of hMANF protein were also detected in the ipsilateral substantia nigra. The hMANF gene transfer promoted the survival of nigral dopaminergic neurons, regeneration of striatal dopaminergic fibers and an upregulation of striatal dopamine levels, resulting in a long-term improvement of rotational behavior up to 16weeks after viral injections. By using SH-SY5Y cells, we found that intra- and extracellular application of MANF protected cells against 6-OHDA-induced toxicity via inhibiting the endoplasmic reticulum stress and activating the PI3K/Akt/mTOR pathway. Our results suggest that AAV9-mediated hMANF gene delivery into the striatum exerts long-term neuroprotective and neuroregenerative effects on the nigrostriatal dopaminergic system in parkinsonian rats, and provide insights into mechanisms responsible for MANF neuroprotection.
[Mh] Termos MeSH primário: Técnicas de Transferência de Genes
Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo
Fatores de Crescimento Neural/metabolismo
Transtornos Parkinsonianos/terapia
[Mh] Termos MeSH secundário: Adenoviridae/genética
Adrenérgicos/toxicidade
Anfetamina/farmacologia
Animais
Células Cultivadas
Modelos Animais de Doenças
Dopamina/metabolismo
Feminino
Regulação da Expressão Gênica/genética
Fator Neurotrófico Derivado de Linhagem de Célula Glial/genética
Seres Humanos
Degeneração Neural/etiologia
Degeneração Neural/terapia
Fatores de Crescimento Neural/genética
Proteínas do Tecido Nervoso/metabolismo
Neuroblastoma/patologia
Oxidopamina/toxicidade
Transtornos Parkinsonianos/induzido quimicamente
Transtornos Parkinsonianos/complicações
Transtornos Parkinsonianos/patologia
Ratos
Ratos Sprague-Dawley
Comportamento Estereotipado/efeitos dos fármacos
Comportamento Estereotipado/fisiologia
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agents); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (MANF protein, human); 0 (Nerve Growth Factors); 0 (Nerve Tissue Proteins); 8HW4YBZ748 (Oxidopamine); CK833KGX7E (Amphetamine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170516
[Lr] Data última revisão:
170516
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170130
[St] Status:MEDLINE


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[PMID]:28131726
[Au] Autor:Fjodorova M; Torres EM; Dunnett SB
[Ad] Endereço:Brain Repair Group, School of Biosciences, Cardiff University, Museum Avenue, Cardiff, Wales CF10 3AX, UK. Electronic address: fjodorovam@cf.ac.uk.
[Ti] Título:Transplantation site influences the phenotypic differentiation of dopamine neurons in ventral mesencephalic grafts in Parkinsonian rats.
[So] Source:Exp Neurol;291:8-19, 2017 May.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Foetal midbrain progenitors have been shown to survive, give rise to different classes of dopamine neurons and integrate into the host brain alleviating Parkinsonian symptoms following transplantation in patients and animal models of the disease. Dopamine neuron subpopulations in the midbrain, namely A9 and A10, can be identified anatomically based on cell morphology and ascending axonal projections. G protein-gated inwardly rectifying potassium channel Girk2 and the calcium binding protein Calbindin are the two best available histochemical markers currently used to label (with some overlap) A9- and A10-like dopamine neuron subtypes, respectively, in tyrosine hydroxylase expressing neurons both in the midbrain and grafts. Both classes of dopamine neurons survive in grafts in the striatum and extend axonal projections to their normal dorsal and ventral striatal targets depending on phenotype. Nevertheless, grafts transplanted into the dorsal striatum, which is an A9 input nucleus, are enriched for dopamine neurons that express Girk2. It remains to be elucidated whether different transplantation sites favour the differential survival and/or development of concordant dopamine neuron subtypes within the grafts. Here we used rat foetal midbrain progenitors at two developmental stages corresponding to a peak in either A9 or A10 neurogenesis and examined their commitment to respective dopaminergic phenotypes by grafting cells into different forebrain regions that contain targets of either nigral A9 dopamine innervation (dorsal striatum), ventral tegmental area A10 dopamine innervation (nucleus accumbens and prefrontal cortex), or only sparse dopamine but rich noradrenaline innervation (hippocampus). We demonstrate that young (embryonic day, E12), but not older (E14), mesencephalic tissue and the transplant environment influence survival and functional integration of specific subtypes of dopamine neurons into the host brain. We also show that irrespective of donor age A9-like, Girk2-expressing neurons are more responsive to environmental cues in adopting a dopaminergic phenotype during differentiation post-grafting. These novel findings suggest that dopamine progenitors use targets of A9/A10 innervation in the transplantation site to complete maturation and the efficacy of foetal cell replacement therapy in patients may be improved by deriving midbrain tissue at earlier developmental stages than in current practice.
[Mh] Termos MeSH primário: Transplante de Tecido Encefálico
Neurônios Dopaminérgicos/fisiologia
Neurogênese/fisiologia
Transtornos Parkinsonianos/cirurgia
Área Tegmentar Ventral/transplante
[Mh] Termos MeSH secundário: Adrenérgicos/toxicidade
Anfetamina/farmacologia
Animais
Modelos Animais de Doenças
Agonistas de Dopamina/farmacologia
Embrião de Mamíferos
Feminino
Masculino
Feixe Prosencefálico Mediano/lesões
Oxidopamina/toxicidade
Transtornos Parkinsonianos/induzido quimicamente
Gravidez
Ratos
Ratos Sprague-Dawley
Comportamento Estereotipado/efeitos dos fármacos
Tirosina 3-Mono-Oxigenase/metabolismo
Área Tegmentar Ventral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agents); 0 (Dopamine Agonists); 8HW4YBZ748 (Oxidopamine); CK833KGX7E (Amphetamine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170516
[Lr] Data última revisão:
170516
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170130
[St] Status:MEDLINE


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[PMID]:28131725
[Au] Autor:Frau R; Savoia P; Fanni S; Fiorentini C; Fidalgo C; Tronci E; Stancampiano R; Meloni M; Cannas A; Marrosu F; Bortolato M; Devoto P; Missale C; Carta M
[Ad] Endereço:Dept. of Biomedical Sciences, University of Cagliari, Cittadella Universitaria SP 8, Monserrato 09042, Italy.
[Ti] Título:The 5-alpha reductase inhibitor finasteride reduces dyskinesia in a rat model of Parkinson's disease.
[So] Source:Exp Neurol;291:1-7, 2017 May.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Levodopa-induced dyskinesia (LID) is a disabling motor complication occurring in Parkinson's disease patients (PD) after long-term l-DOPA treatment. Although its etiology remains unclear, there is accumulating evidence that LID relies on an excessive dopamine receptor transmission, particularly at the downstream signaling of D receptors. We previously reported that the pharmacological blockade of 5-alpha reductase (5AR), the rate limiting enzyme in neurosteroids synthesis, rescued a number of behavioral aberrations induced by D receptor-selective and non-selective agonists, without inducing extrapyramidal symptoms. Thus, the present study was designed to verify whether the 5AR inhibitor finasteride (FIN) may counteract the dyskinesias induced by dopaminergic agonists in 6-hydroxydopamine (6-OHDA)-lesioned rats. First, we assessed the acute and chronic effect of different doses of FIN (30-60mg/kg) on LID, in male 6-OHDA-lesioned dyskinetic rats. Thereafter, to fully characterize the therapeutic potential of FIN on LID and its impact on l-DOPA efficacy, we assessed abnormal involuntary movements and forelimb use in hemiparkinsonian male rats chronically injected with FIN (30-60mg/kg/24days) either prior to- or concomitant with l-DOPA administration. In addition, to investigate whether the impact of FIN on LID may be ascribed to a modulation of the D - or D /D -receptor function, dyskinesias were assessed in l-DOPA-primed 6-OHDA-lesioned rats that received FIN in combination with selective direct dopaminergic agonists. Finally, we set to investigate whether FIN may produce similar effect in female hemiparkinsonian rats, as seen in males. The results indicated that FIN administrations significantly dampened LID in all tested treatment regimens, without interfering with the ability of l-DOPA to ameliorate forelimb use in the stepping test. The antidyskinetic effect appears to be due to modulation of both D - and D /D -receptor function, as FIN also reduced abnormal involuntary movements induced by the selective D receptor agonist SKF-82958 and the D /D receptor agonist ropinirole. Significant dampening of LID was also observed in female rats, although only at the higher tested dose. Clinical investigations are warranted to assess whether similar protection from dyskinesia is seen in PD patients.
[Mh] Termos MeSH primário: Inibidores de 5-alfa Redutase/uso terapêutico
Discinesia Induzida por Medicamentos/tratamento farmacológico
Finasterida/uso terapêutico
Doença de Parkinson/tratamento farmacológico
[Mh] Termos MeSH secundário: Adrenérgicos/toxicidade
Animais
Antiparkinsonianos/efeitos adversos
Benserazida/efeitos adversos
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Discinesia Induzida por Medicamentos/etiologia
Feminino
Lateralidade Funcional/efeitos dos fármacos
Levodopa/efeitos adversos
Masculino
Oxidopamina/toxicidade
Doença de Parkinson/etiologia
Transtornos Psicomotores/induzido quimicamente
Ratos
Ratos Sprague-Dawley
Fatores de Tempo
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-alpha Reductase Inhibitors); 0 (Adrenergic Agents); 0 (Antiparkinson Agents); 46627O600J (Levodopa); 57GNO57U7G (Finasteride); 762OS3ZEJU (Benserazide); 8HW4YBZ748 (Oxidopamine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170516
[Lr] Data última revisão:
170516
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170130
[St] Status:MEDLINE



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