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Pesquisa : D12.776.624.664.520.750.887 [Categoria DeCS]
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[PMID]:28903063
[Au] Autor:Ghouili F; Martin LJ
[Ad] Endereço:Biology Department, Université de Moncton, Moncton, New-Brunswick E1A 3E9, Canada.
[Ti] Título:Cooperative regulation of Gja1 expression by members of the AP-1 family cJun and cFos in TM3 Leydig and TM4 Sertoli cells.
[So] Source:Gene;635:24-32, 2017 Nov 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Within the testis, connexin43 encoded by Gja1 plays an important role in cell-to-cell communication between Leydig cells as well as between Sertoli cells and spermatogonia. In the adult male, Leydig cells are the principal producers of testosterone sustaining spermatogenesis, while Sertoli cells nourish, protect and support the differentiating germ cells. It has been shown previously that members of the AP-1 family regulate Gja1 expression in myometrial cells, suggesting that such regulatory mechanism may also be relevant within the testis. Thus, we performed cotransfections of AP-1 expression plasmids with different mouse Gja1 promoter/luciferase reporter constructs within TM3 Leydig and TM4 Sertoli cells. We showed that a functional cooperation between cJun and cFos activates Gja1 expression and requires an AP-1 DNA regulatory element located between -132 and -26 bp. In addition, such synergy relies on the recruitment of cFos to this region of the mouse Gja1 promoter. Hence, our data indicate that AP-1 members are important for optimal expression of Gja1 within Sertoli and Leydig cells from the testis.
[Mh] Termos MeSH primário: Comunicação Celular/genética
Conexina 43/genética
Proteínas Oncogênicas v-fos/genética
Fator de Transcrição AP-1/genética
[Mh] Termos MeSH secundário: Animais
Conexina 43/biossíntese
Regulação da Expressão Gênica no Desenvolvimento
Células Intersticiais do Testículo/metabolismo
Masculino
Camundongos
Proteínas Oncogênicas v-fos/biossíntese
Regiões Promotoras Genéticas
Células de Sertoli/metabolismo
Espermatogênese/genética
Testículo/crescimento & desenvolvimento
Testículo/metabolismo
Testosterona/genética
Fator de Transcrição AP-1/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (GJA1 protein, mouse); 0 (Oncogene Proteins v-fos); 0 (Transcription Factor AP-1); 3XMK78S47O (Testosterone)
[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:170914
[St] Status: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


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[PMID]:28267582
[Au] Autor:Füredi N; Nagy Á; Mikó A; Berta G; Kozicz T; Pétervári E; Balaskó M; Gaszner B
[Ad] Endereço:Department of Anatomy, Medical School, University of Pécs, Hungary.
[Ti] Título:Melanocortin 4 receptor ligands modulate energy homeostasis through urocortin 1 neurons of the centrally projecting Edinger-Westphal nucleus.
[So] Source:Neuropharmacology;118:26-37, 2017 May 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The role of the urocortin 1 (Ucn1) expressing centrally projecting Edinger-Westphal (EWcp) nucleus in energy homeostasis and stress adaptation response has previously been investigated. Morphological and functional studies have proven that orexigenic and anorexigenic peptidergic afferents and receptors for endocrine messengers involved in the energy homeostasis are found in the EWcp. The central role of the hypothalamic melanocortin system in energy homeostasis is well known, however, no data have been published so far on possible crosstalk between melanocortins and EWcp-Ucn1. First, we hypothesized that members of the melanocortin system [i.e. alpha-melanocyte stimulating hormone (alpha-MSH), agouti-related peptide (AgRP), melanocortin 4 receptor (MC4R)] would be expressed in the EWcp. Second, we put forward, that alpha-MSH and AgRP contents as well as neuronal activity and Ucn1 peptide content of the EWcp would be affected by fasting. Third, we assumed that the intra-EWcp injections of exogenous MC4R agonists and antagonist would cause food intake-related and metabolic changes. Ucn1 neurons were found to carry MC4Rs, and they were contacted both by alpha-MSH and AgRP immunoreactive nerve fibers in the rat. The alpha-MSH immunosignal was reduced, while that of AgRP was increased upon starvation. These were associated with the elevation of FosB and Ucn1 expression. The intra-EWcp administration of MC4R blocker (i.e. HS024) had a similar, but enhanced effect on FosB and Ucn1. Furthermore, alpha-MSH injected into the EWcp had anorexigenic effect, increased oxygen consumption and caused peripheral vasodilation. We conclude that the melanocortin system influences the EWcp that contributes to energy-homeostasis.
[Mh] Termos MeSH primário: Núcleo de Edinger-Westphal/citologia
Homeostase/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Consumo de Oxigênio/efeitos dos fármacos
Receptor Tipo 4 de Melanocortina
Urocortinas/metabolismo
[Mh] Termos MeSH secundário: Proteína Relacionada com Agouti/metabolismo
Animais
Temperatura Corporal/efeitos dos fármacos
Vias de Administração de Medicamentos
Ingestão de Alimentos/efeitos dos fármacos
Jejum
Ligantes
Masculino
Fibras Nervosas/efeitos dos fármacos
Fibras Nervosas/fisiologia
Proteínas Oncogênicas v-fos/metabolismo
Peptídeos Cíclicos/farmacologia
Ratos
Ratos Wistar
Receptor Tipo 4 de Melanocortina/agonistas
Receptor Tipo 4 de Melanocortina/antagonistas & inibidores
Receptor Tipo 4 de Melanocortina/metabolismo
alfa-MSH/metabolismo
alfa-MSH/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AGRP protein, rat); 0 (Agouti-Related Protein); 0 (HS 024); 0 (Ligands); 0 (Oncogene Proteins v-fos); 0 (Peptides, Cyclic); 0 (Receptor, Melanocortin, Type 4); 0 (Urocortins); 581-05-5 (alpha-MSH)
[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:170308
[St] Status:MEDLINE


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[PMID]:28131863
[Au] Autor:Core SL; Curtis KS
[Ad] Endereço:Oklahoma State University - Center for Health Sciences, Tulsa, OK 74107, United States.
[Ti] Título:Early oxytocin inhibition of salt intake after furosemide treatment in rats?
[So] Source:Physiol Behav;173:34-41, 2017 May 01.
[Is] ISSN:1873-507X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Body fluid homeostasis requires a complex suite of physiological and behavioral processes. Understanding of the role of the central nervous system (CNS) in integrating these processes has been advanced by research employing immunohistochemical techniques to assess responses to a variety of body fluid challenges. Such techniques have revealed sex/estrogen differences in CNS activation in response to hypotension and hypernatremia. In contrast, it has been difficult to conclusively identify specific CNS areas and neurotransmitter systems that are activated by hyponatremia using these techniques. In part, this difficulty is due to the temporal disconnect between the physiological effects of treatments commonly used to deplete body sodium and the behavioral response to such depletion. In some methods, sodium ingestion is delayed in association with increased oxytocin (OT), suggesting an inhibitory role for OT in sodium intake. Urinary sodium loss increases within an hour after treatment with furosemide, a natriuretic-diuretic, but sodium intake is delayed for 18-24h. Accordingly, we hypothesized that acute furosemide-induced sodium loss activates centrally-projecting OT neurons which provide an initial inhibition of sodium intake, and tested this hypothesis in ovariectomized Sprague-Dawley rats with or without estrogen using immunohistochemical methods. Neuronal activation in the hypothalamic paraventricular nuclei (PVN) after administration of furosemide corresponded to the timing of the physiological effects. The activation was not different in estrogen-treated rats, nor did estrogen alter the initial suppression of sodium intake. However, virtually no fos immunoreactive (fos-IR) neurons in the parvocellular PVN were also immunolabeled for OT. Thus, acute sodium loss after furosemide produces neural activation and an early inhibition of sodium intake that does not appear to involve activation of centrally-projecting OT neurons and is not influenced by estrogen.
[Mh] Termos MeSH primário: Furosemida/farmacologia
Ocitocina/metabolismo
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Inibidores de Simportadores de Cloreto de Sódio e Potássio/farmacologia
Sódio na Dieta
Núcleo Supraóptico/efeitos dos fármacos
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Peso Corporal/efeitos dos fármacos
Anticoncepcionais/farmacologia
Ingestão de Líquidos/efeitos dos fármacos
Estradiol/análogos & derivados
Estradiol/farmacologia
Feminino
Proteínas Oncogênicas v-fos/metabolismo
Ovariectomia
Núcleo Hipotalâmico Paraventricular/metabolismo
Ratos
Ratos Sprague-Dawley
Sódio na Dieta/metabolismo
Sódio na Dieta/urina
Núcleo Supraóptico/metabolismo
Micção/efeitos dos fármacos
Útero/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Contraceptive Agents); 0 (Oncogene Proteins v-fos); 0 (Sodium Potassium Chloride Symporter Inhibitors); 0 (Sodium, Dietary); 1S4CJB5ZGN (estradiol 3-benzoate); 4TI98Z838E (Estradiol); 50-56-6 (Oxytocin); 7LXU5N7ZO5 (Furosemide)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170130
[St] Status:MEDLINE


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[PMID]:27933357
[Au] Autor:Kurose M; Imbe H; Nakatani Y; Hasegawa M; Fujii N; Takagi R; Yamamura K; Senba E; Okamoto K
[Ad] Endereço:Division of Oral Physiology, Niigata University Graduate School of Medical and Dental Sciences, 2-5274 Gakkocho-Dori Chuo-ku, Niigata City, 951-8514, Niigata, Japan.
[Ti] Título:Bilateral increases in ERK activation at the spinomedullary junction region by acute masseter muscle injury during temporomandibular joint inflammation in the rats.
[So] Source:Exp Brain Res;235(3):913-921, 2017 Mar.
[Is] ISSN:1432-1106
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:We determined the role of persistent monoarthritis of temporomandibular joint region (TMJ) on bilateral masseter muscle (MM) nociception in male rats using orofacial nocifensive behaviors, phosphorylated extracellular signal-regulated kinase and Fos induction at the trigeminal subnucleus caudalis/upper cervical spinal cord (Vc/C ) region in response to formalin injection to the MM region. TMJ inflammation was induced by local injection of CFA into the left TMJ region. Orofacial nocifensive behaviors evoked by formalin injection ipsilateral or contralateral to the TMJ inflammation appeared to be increased at 1-14 days or at 1, 10 and 14 days after induction of TMJ inflammation, respectively, while increases in behavioral duration were seen mainly in the late phase rather than the early phase. The number of pERK positive cells was investigated in superficial laminae at the Vc/C region at 3, 10, 20, 60 and 80 min after MM stimulation with formalin at 14 days after TMJ inflammation. TMJ-inflamed rats displayed greater responses of pERK expression by the ipsilateral MM stimulation at 3-60 min, while contralateral MM stimulation increased pERK expression at 3, 10 and 20 min compared to non-CFA rats. Fos expression by MM stimulation was increased at 14 days after induction of TMJ inflammation regardless of the affected side. These findings showed that persistent TMJ inflammation for 10 and 14 days is sufficient to enhance MM nociception indicated by behaviors and neural responses in superficial laminae at the Vc/C region.
[Mh] Termos MeSH primário: Lateralidade Funcional/fisiologia
Inflamação/complicações
Doenças Musculares/etiologia
Vias Neurais/metabolismo
Síndrome da Disfunção da Articulação Temporomandibular/complicações
eIF-2 Quinase/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Formaldeído/efeitos adversos
Adjuvante de Freund/toxicidade
Regulação da Expressão Gênica/efeitos dos fármacos
Masculino
Músculo Masseter/patologia
Doenças Musculares/patologia
Proteínas Oncogênicas v-fos/metabolismo
Medição da Dor
Ratos
Ratos Sprague-Dawley
Síndrome da Disfunção da Articulação Temporomandibular/induzido quimicamente
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oncogene Proteins v-fos); 1HG84L3525 (Formaldehyde); 9007-81-2 (Freund's Adjuvant); EC 2.7.11.1 (PERK kinase); EC 2.7.11.1 (eIF-2 Kinase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161210
[St] Status:MEDLINE
[do] DOI:10.1007/s00221-016-4852-9


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[PMID]:27539452
[Au] Autor:Billwiller F; Renouard L; Clement O; Fort P; Luppi PH
[Ad] Endereço:UMR 5292 CNRS/U1028 INSERM, Faculté de Médecine RTH Laennec, Centre de Recherche en Neurosciences de Lyon (CRNL), SLEEP Team, Université Claude Bernard Lyon I, 7 Rue Guillaume Paradin, 69372, Lyon Cedex 08, France.
[Ti] Título:Differential origin of the activation of dorsal and ventral dentate gyrus granule cells during paradoxical (REM) sleep in the rat.
[So] Source:Brain Struct Funct;222(3):1495-1507, 2017 Apr.
[Is] ISSN:1863-2661
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:We recently demonstrated that granule cells located in the dorsal dentate gyrus (dDG) are activated by neurons located in the lateral supramammillary nucleus (SumL) during paradoxical sleep (PS) hypersomnia. To determine whether these neurons are glutamatergic and/or GABAergic, we combined FOS immunostaining with in situ hybridization of vesicular glutamate transporter 2 (vGLUT2, a marker of glutamatergic neurons) or that of the vesicular GABA transporter (vGAT, a marker of GABAergic neurons) mRNA in rats displaying PS hypersomnia (PSR). We found that 84 and 76 % of the FOS+ SumL neurons in PSR rats expressed vGLUT2 and vGAT mRNA, respectively. Then, we examined vGLUT2 and FOS immunostaining in the dorsal and ventral DG of PSR rats with a neurochemical lesion of the Sum. In PSR-lesioned animals but not in sham animals, nearly all vGLUT2+ fibers and FOS+ neurons disappeared in the dDG, but not in the ventral DG (vDG). To identify the pathway (s) responsible (s) for the activation of the vDG during PS hypersomnia, we combined Fluorogold (FG) injection in the vDG of PSR rats with FOS staining. We found a large number of neurons FOS-FG+, specifically in the medial entorhinal cortex (ENTm). Altogether, our results suggest that SumL neurons with a unique dual glutamatergic and GABAergic phenotype are responsible for the activation of the dDG during PS hypersomnia, while vDG granule neurons are activated by ENTm cortical neurons. These results suggest differential mechanisms and functions for the activation of the dDG and the vDG granule cells during PS.
[Mh] Termos MeSH primário: Giro Denteado/citologia
Neurônios/fisiologia
Sono REM/fisiologia
[Mh] Termos MeSH secundário: Animais
Contagem de Células
Giro Denteado/lesões
Eletroencefalografia
Eletromiografia
Hipotálamo Posterior/citologia
Masculino
Proteínas Oncogênicas v-fos/genética
Proteínas Oncogênicas v-fos/metabolismo
Fosfopiruvato Hidratase/metabolismo
Ratos
Ratos Sprague-Dawley
Privação do Sono
Estatísticas não Paramétricas
Estilbamidinas/metabolismo
Proteína Vesicular 2 de Transporte de Glutamato/genética
Proteína Vesicular 2 de Transporte de Glutamato/metabolismo
Vigília
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt); 0 (Oncogene Proteins v-fos); 0 (Slc17a6 protein, rat); 0 (Stilbamidines); 0 (Vesicular Glutamate Transport Protein 2); EC 4.2.1.11 (Phosphopyruvate Hydratase)
[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:160820
[St] Status:MEDLINE
[do] DOI:10.1007/s00429-016-1289-7


  7 / 629 MEDLINE  
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[PMID]:27901001
[Au] Autor:Xu QF; Zheng Y; Chen J; Xu XY; Gong ZJ; Huang YF; Lu C; Maibach HI; Lai W
[Ad] Endereço:Department of Dermato-Venereology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510630, China.
[Ti] Título:Ultraviolet A Enhances Cathepsin L Expression and Activity via JNK Pathway in Human Dermal Fibroblasts.
[So] Source:Chin Med J (Engl);129(23):2853-2860, 2016 12 05.
[Is] ISSN:0366-6999
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cathepsin L (CatL) is a cysteine protease with strong matrix degradation activity that contributes to photoaging. Mannose phosphate-independent sorting pathways mediate ultraviolet A (UVA)-induced alternate trafficking of CatL. Little is known about signaling pathways involved in the regulation of UVA-induced CatL expression and activity. This study aims to investigate whether a single UVA irradiation affects CatL expression and activity and whether mitogen-activated protein kinase (MAPK)/activator protein-1 (AP-1) pathway is involved in the regulation of UVA-induced CatL expression and activity in human dermal fibroblasts (HDFs). METHODS: Primary HDFs were exposed to UVA. Cell proliferation was determined by a cell counting kit. UVA-induced CatL production and activity were studied with quantitative real-time reverse transcription polymerase chain reaction (RT-PCR), Western blotting, and fluorimetric assay in cell lysates collected on three consecutive days after irradiation. Time courses of UVA-activated JNK and p38MAPK signaling were examined by Western blotting. Effects of MAPK inhibitors and knockdown of Jun and Fos on UVA-induced CatL expression and activity were investigated by RT-PCR, Western blotting, and fluorimetric assay. Data were analyzed by one-way analysis of variance. RESULTS: UVA significantly increased CatL gene expression, protein abundance, and enzymatic activity for three consecutive days after irradiation (F = 83.11, 56.14, and 71.19, respectively; all P < 0.05). Further investigation demonstrated phosphorylation of JNK and p38MAPK activated by UVA. Importantly, inactivation of JNK pathway significantly decreased UVA-induced CatL expression and activity, which were not affected by p38MAPK inhibition. Moreover, knockdown of Jun and Fos significantly attenuated basal and UVA-induced CatL expression and activity. CONCLUSIONS: UVA enhances CatL production and activity in HDFs, probably by activating JNK and downstreaming AP-1. These findings provide a new possible molecular approach for antiphotoaging therapy.
[Mh] Termos MeSH primário: Catepsina L/metabolismo
Fibroblastos/metabolismo
Fibroblastos/efeitos da radiação
Pele/citologia
Raios Ultravioleta
[Mh] Termos MeSH secundário: Antracenos/farmacologia
Células Cultivadas
Criança
Pré-Escolar
Inibidores Enzimáticos/farmacologia
MAP Quinases Reguladas por Sinal Extracelular/antagonistas & inibidores
Fibroblastos/citologia
Fibroblastos/efeitos dos fármacos
Seres Humanos
Imidazóis/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Sistema de Sinalização das MAP Quinases/efeitos da radiação
Proteínas Oncogênicas v-fos/genética
Proteínas Oncogênicas v-fos/metabolismo
Proteínas Proto-Oncogênicas c-jun/genética
Proteínas Proto-Oncogênicas c-jun/metabolismo
Piridinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracenes); 0 (Enzyme Inhibitors); 0 (Imidazoles); 0 (Oncogene Proteins v-fos); 0 (Proto-Oncogene Proteins c-jun); 0 (Pyridines); 1TW30Y2766 (pyrazolanthrone); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.4.22.15 (Cathepsin L); OU13V1EYWQ (SB 203580)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161201
[St] Status:MEDLINE
[do] DOI:10.4103/0366-6999.194654


  8 / 629 MEDLINE  
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[PMID]:27605618
[Au] Autor:de Guglielmo G; Crawford E; Kim S; Vendruscolo LF; Hope BT; Brennan M; Cole M; Koob GF; George O
[Ad] Endereço:Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, California 92037, and.
[Ti] Título:Recruitment of a Neuronal Ensemble in the Central Nucleus of the Amygdala Is Required for Alcohol Dependence.
[So] Source:J Neurosci;36(36):9446-53, 2016 Sep 07.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Abstinence from alcohol is associated with the recruitment of neurons in the central nucleus of the amygdala (CeA) in nondependent rats that binge drink alcohol and in alcohol-dependent rats. However, whether the recruitment of this neuronal ensemble in the CeA is causally related to excessive alcohol drinking or if it represents a consequence of excessive drinking remains unknown. We tested the hypothesis that the recruitment of a neuronal ensemble in the CeA during abstinence is required for excessive alcohol drinking in nondependent rats that binge drink alcohol and in alcohol-dependent rats. We found that inactivation of the CeA neuronal ensemble during abstinence significantly decreased alcohol drinking in both groups. In nondependent rats, the decrease in alcohol intake was transient and returned to normal the day after the injection. In dependent rats, inactivation of the neuronal ensemble with Daun02 produced a long-term decrease in alcohol drinking. Moreover, we observed a significant reduction of somatic withdrawal signs in dependent animals that were injected with Daun02 in the CeA. These results indicate that the recruitment of a neuronal ensemble in the CeA during abstinence from alcohol is causally related to excessive alcohol drinking in alcohol-dependent rats, whereas a similar neuronal ensemble only partially contributed to alcohol-binge-like drinking in nondependent rats. These results identify a critical neurobiological mechanism that may be required for the transition to alcohol dependence, suggesting that focusing on the neuronal ensemble in the CeA may lead to a better understanding of the etiology of alcohol use disorders and improve medication development. SIGNIFICANCE STATEMENT: Alcohol dependence recruits neurons in the central nucleus of the amygdala (CeA). Here, we found that inactivation of a specific dependence-induced neuronal ensemble in the CeA reversed excessive alcohol drinking and somatic signs of alcohol dependence in rats. These results identify a critical neurobiological mechanism that is required for alcohol dependence, suggesting that targeting dependence neuronal ensembles may lead to a better understanding of the etiology of alcohol use disorders, with implications for diagnosis, prevention, and treatment.
[Mh] Termos MeSH primário: Alcoolismo/patologia
Núcleo Central da Amígdala/citologia
Rede Nervosa/fisiologia
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Animais
Núcleo Central da Amígdala/efeitos dos fármacos
Depressores do Sistema Nervoso Central/farmacologia
Condicionamento Operante/efeitos dos fármacos
Daunorrubicina/análogos & derivados
Daunorrubicina/farmacologia
Modelos Animais de Doenças
Etanol/administração & dosagem
Masculino
Rede Nervosa/efeitos dos fármacos
Neurônios/efeitos da radiação
Proteínas Oncogênicas v-fos/genética
Proteínas Oncogênicas v-fos/metabolismo
Ratos
Ratos Transgênicos
Esquema de Reforço
Autoadministração
Estatísticas não Paramétricas
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Central Nervous System Depressants); 0 (N-(4''-(galactopyranosyl)-3''-nitrobenzyloxycarbonyl)daunomycin); 0 (Oncogene Proteins v-fos); 3K9958V90M (Ethanol); ZS7284E0ZP (Daunorubicin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160909
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1395-16.2016


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[PMID]:27569537
[Au] Autor:Silva TM; Takakura AC; Moreira TS
[Ad] Endereço:Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, 05508-900 São Paulo, SP, Brazil.
[Ti] Título:Acute hypoxia activates hypothalamic paraventricular nucleus-projecting catecholaminergic neurons in the C1 region.
[So] Source:Exp Neurol;285(Pt A):1-11, 2016 Nov.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Catecholaminergic C1 cells reside in the rostral and intermediate portions of the ventrolateral medulla (RVLM) and can be activated by hypoxia. These neurons regulate the hypothalamic pituitary axis via direct projections to the hypothalamic paraventricular nucleus (PVH) and regulate the autonomic nervous system via projections to sympathetic and parasympathetic preganglionic neurons. Based on the various effects attributed to the C1 cells and what is currently known of their synaptic inputs, our hypothesis is that acute hypoxia (AH) activates RVLM projecting catecholaminergic neurons to PVH. Anterograde tracer, Phaseolus vulgaris leucoagglutinin (PHA-L) was unilaterally injected into the RVLM and a retrograde tracer Cholera toxin b (CTb) was unilaterally injected into the PVH region. After ten days, male Wistar rats that received CTb injection into the PVH were subjected to AH (8% O , balanced with N ) or normoxia (21% O ) for 3h. Acute hypoxia significantly increased Fos immunoreactivity in the C1 region (68±2 neurons), and half of the RVLM cells activated are catecholaminergic (35±2 neurons). We observed that 23±4% of the RVLM projecting PVH cells that were activated by AH were also C1 cells. The presence of varicosities containing PHA-L in PVH region was also observed. The present results suggest that catecholaminergic C1-PVH projection is hypoxia-sensitive and the pathway between these two important brain areas can be one more piece in the complex puzzle of neural control of autonomic regulation during hypoxia.
[Mh] Termos MeSH primário: Catecolaminas/metabolismo
Hipóxia/patologia
Bulbo/patologia
Vias Neurais/fisiologia
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Pressão Sanguínea/fisiologia
Contagem de Células
Toxina da Cólera/farmacocinética
Modelos Animais de Doenças
Esquema de Medicação
Glutamato Descarboxilase/metabolismo
Frequência Cardíaca/fisiologia
Hipóxia/fisiopatologia
Masculino
Proteínas Oncogênicas v-fos/metabolismo
Núcleo Hipotalâmico Paraventricular
Fito-Hemaglutininas/administração & dosagem
Fito-Hemaglutininas/farmacocinética
Ratos
Ratos Wistar
Tirosina 3-Mono-Oxigenase/metabolismo
Proteína Vesicular 2 de Transporte de Glutamato/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Catecholamines); 0 (Oncogene Proteins v-fos); 0 (Phytohemagglutinins); 0 (Vesicular Glutamate Transport Protein 2); 0 (leukoagglutinins, plants); 9012-63-9 (Cholera Toxin); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 4.1.1.15 (Glutamate Decarboxylase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170916
[Lr] Data última revisão:
170916
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160830
[St] Status:MEDLINE


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[PMID]:27553574
[Au] Autor:Nam H; Kerman IA
[Ad] Endereço:Department of Anatomy and Neurobiology, University of Maryland School of Medicine, United States.
[Ti] Título:A2 noradrenergic neurons regulate forced swim test immobility.
[So] Source:Physiol Behav;165:339-49, 2016 Oct 15.
[Is] ISSN:1873-507X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Wistar-Kyoto (WKY) rat is a widely used animal model of depression, which is characterized by dysregulation of noradrenergic signaling. We previously demonstrated that WKY rats show a unique behavioral profile on the forced swim test (FST), characterized by high levels of immobility upon initial exposure and a greater learning-like response by further increasing immobility upon re-exposure than the genetically related Wistar rats. In the current study we aimed to determine whether altered activation of brainstem noradrenergic cell groups contributes to this behavioral profile. We exposed WKY and Wistar rats, to either 5min of forced swim or to the standard two-day FST (i.e. 15min forced swim on Day 1, followed by 5min on Day 2). We then stained their brains for FOS/tyrosine hydroxylase double-immunocytochemistry to determine potential differences in the activation of the brainstem noradrenergic cell groups. We detected a relative hyperactivation in the locus coeruleus of WKY rats when compared to Wistars in response to both one- and two-day forced swim. In contrast, within the A2 noradrenergic cell group, WKY rats exhibited diminished levels of FOS across both days of the FST, suggesting their lesser activation. We followed up these observations by selectively lesioning the A2 neurons, using anti-dopamine-ß-hydroxylase-conjugated saporin, in Wistar rats, which resulted in increased FST immobility on both days of the test. Together these data indicate that the A2 noradrenergic cell group regulates FST behavior, and that its hypoactivation may contribute to the unique behavioral phenotype of WKY rats.
[Mh] Termos MeSH primário: Neurônios Adrenérgicos/fisiologia
Transtorno Depressivo/patologia
Resposta de Imobilidade Tônica/fisiologia
Natação/psicologia
[Mh] Termos MeSH secundário: Neurônios Adrenérgicos/efeitos dos fármacos
Animais
Modelos Animais de Doenças
Dopamina beta-Hidroxilase/farmacologia
Imunotoxinas/uso terapêutico
Masculino
Microinjeções
Proteínas Oncogênicas v-fos/metabolismo
Ratos
Ratos Endogâmicos WKY
Ratos Sprague-Dawley
Ratos Wistar
Proteínas Inativadoras de Ribossomos Tipo 1/farmacologia
Núcleo Solitário/efeitos dos fármacos
Núcleo Solitário/patologia
Especificidade da Espécie
Fatores de Tempo
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunotoxins); 0 (Oncogene Proteins v-fos); 0 (Ribosome Inactivating Proteins, Type 1); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 1.14.17.1 (Dopamine beta-Hydroxylase); EC 3.2.2.22 (saporin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160825
[St] Status:MEDLINE



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