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[PMID]:28406051
[Au] Autor:Siddiqui PJA; Khan A; Uddin N; Khaliq S; Rasheed M; Nawaz S; Hanif M; Dar A
[Ad] Endereço:a Centre of Excellence in Marine Biology, University of Karachi , Karachi , Pakistan.
[Ti] Título:Antidepressant-like deliverables from the sea: evidence on the efficacy of three different brown seaweeds via involvement of monoaminergic system.
[So] Source:Biosci Biotechnol Biochem;81(7):1369-1378, 2017 Jul.
[Is] ISSN:1347-6947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Brown seaweeds exhibit several health benefits in treating and managing wide array of ailments. In this study, the antidepressant-like effect of methaolic extracts from Sargassum swartzii (SS), Stoechospermum marginatum (SM), and Nizamuddinia zanardinii (NZ) was examined in forced swimming test (FST), in rats. Oral administration of SS, SM, and NZ extract (30-60 mg/kg) exhibited antidepressant-like activity in FST by reducing immobility time as compared to control group, without inducing significant change in ambulatory behavior in open field test. In order to evaluate the involvement of monoaminergic system, rats were pretreated with the inhibitor of brain serotonin stores p-chlorophenylalanin (PCPA), dopamine (SCH23390 and sulpiride), and adrenoceptor (prazosin and propranolol) antagonists. Rats receiving treatment for 28 days were decapitated and brains were analyzed for monoamine levels. It may be concluded that the extracts of SS, SM, and NZ produces antidepressant-like activity via modulation of brain monoaminergic system in a rat model.
[Mh] Termos MeSH primário: Antidepressivos/farmacologia
Depressão/prevenção & controle
Feófitas/química
Receptores Adrenérgicos/genética
Receptores Dopaminérgicos/genética
Receptores de Serotonina/genética
Alga Marinha/química
[Mh] Termos MeSH secundário: Antagonistas Adrenérgicos/farmacologia
Animais
Antidepressivos/isolamento & purificação
Benzazepinas/farmacologia
Depressão/genética
Depressão/metabolismo
Depressão/fisiopatologia
Antagonistas de Dopamina/farmacologia
Fenclonina/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Metanol
Prazosina/farmacologia
Propranolol/farmacologia
Ratos
Ratos Wistar
Receptores Adrenérgicos/metabolismo
Receptores Dopaminérgicos/metabolismo
Receptores de Serotonina/metabolismo
Antagonistas da Serotonina/farmacologia
Solventes
Sulpirida/farmacologia
Natação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Antagonists); 0 (Antidepressive Agents); 0 (Benzazepines); 0 (Dopamine Antagonists); 0 (Receptors, Adrenergic); 0 (Receptors, Dopamine); 0 (Receptors, Serotonin); 0 (SCH 23390); 0 (Serotonin Antagonists); 0 (Solvents); 7MNE9M8287 (Sulpiride); 9Y8NXQ24VQ (Propranolol); R5J7E3L9SP (Fenclonine); XM03YJ541D (Prazosin); Y4S76JWI15 (Methanol)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170707
[Lr] Data última revisão:
170707
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1080/09168451.2017.1313697


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[PMID]:28233634
[Au] Autor:Sasaki-Hamada S; Suzuki A; Ueda Y; Matsumoto K; Oka JI
[Ad] Endereço:Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Japan.
[Ti] Título:Serotonergic and dopaminergic systems are implicated in antidepressant-like effects of chotosan, a Kampo formula, in mice.
[So] Source:J Pharmacol Sci;133(2):110-113, 2017 Feb.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:We previously demonstrated that chotosan (CTS), a traditional herbal formula called Kampo medicine, improves diabetes-induced cognitive deficits. In the present study, we investigated the antidepressant-like effects of CTS in mice. The administration of CTS (1.0 g/kg, for 3 days) decreased the immobility time in the forced-swim test, and this decrease was prevented by the prior administration of sulpiride (an antagonist of D receptors) and WAY100635 (an antagonist of 5-HT receptors). None of the treatments tested altered the locomotor activity of mice. These results suggest that CTS exerts antidepressant-like effects through changes in the serotonergic and dopaminergic systems.
[Mh] Termos MeSH primário: Antidepressivos/farmacologia
Dopaminérgicos/farmacologia
Medicamentos de Ervas Chinesas/farmacologia
Medicina Kampo
Serotoninérgicos/farmacologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Fenclonina/química
Imipramina/química
Imipramina/farmacologia
Ketanserina/química
Ketanserina/farmacologia
Locomoção
Masculino
Metergolina/química
Camundongos
Piperazinas/química
Piperazinas/farmacologia
Piridinas/química
Piridinas/farmacologia
Sulpirida/química
Sulpirida/farmacologia
Natação
Ioimbina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents); 0 (Dopamine Agents); 0 (Drugs, Chinese Herbal); 0 (Piperazines); 0 (Pyridines); 0 (Serotonin Agents); 0 (choto-san); 1501393LY5 (Metergoline); 2Y49VWD90Q (Yohimbine); 71IH826FEG (N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamide); 7MNE9M8287 (Sulpiride); 97F9DE4CT4 (Ketanserin); OGG85SX4E4 (Imipramine); R5J7E3L9SP (Fenclonine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE


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[PMID]:28057699
[Au] Autor:Anderberg RH; Richard JE; Eerola K; López-Ferreras L; Banke E; Hansson C; Nissbrandt H; Berqquist F; Gribble FM; Reimann F; Wernstedt Asterholm I; Lamy CM; Skibicka KP
[Ad] Endereço:Department of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
[Ti] Título:Glucagon-Like Peptide 1 and Its Analogs Act in the Dorsal Raphe and Modulate Central Serotonin to Reduce Appetite and Body Weight.
[So] Source:Diabetes;66(4):1062-1073, 2017 Apr.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glucagon-like peptide 1 (GLP-1) and serotonin play critical roles in energy balance regulation. Both systems are exploited clinically as antiobesity strategies. Surprisingly, whether they interact in order to regulate energy balance is poorly understood. Here we investigated mechanisms by which GLP-1 and serotonin interact at the level of the central nervous system. Serotonin depletion impaired the ability of exendin-4, a clinically used GLP-1 analog, to reduce body weight in rats, suggesting that serotonin is a critical mediator of the energy balance impact of GLP-1 receptor (GLP-1R) activation. Serotonin turnover and expression of 5-hydroxytryptamine (5-HT) 2A (5-HT ) and 5-HT serotonin receptors in the hypothalamus were altered by GLP-1R activation. We demonstrate that the 5-HT , but surprisingly not the 5-HT , receptor is critical for weight loss, anorexia, and fat mass reduction induced by central GLP-1R activation. Importantly, central 5-HT receptors are also required for peripherally injected liraglutide to reduce feeding and weight. Dorsal raphe (DR) harbors cell bodies of serotonin-producing neurons that supply serotonin to the hypothalamic nuclei. We show that GLP-1R stimulation in DR is sufficient to induce hypophagia and increase the electrical activity of the DR serotonin neurons. Finally, our results disassociate brain metabolic and emotionality pathways impacted by GLP-1R activation. This study identifies serotonin as a new critical neural substrate for GLP-1 impact on energy homeostasis and expands the current map of brain areas impacted by GLP-1R activation.
[Mh] Termos MeSH primário: Apetite/efeitos dos fármacos
Peso Corporal/efeitos dos fármacos
Núcleo Dorsal da Rafe/metabolismo
Peptídeo 1 Semelhante ao Glucagon/farmacologia
Receptor do Peptídeo Semelhante ao Glucagon 1/efeitos dos fármacos
Hipoglicemiantes/farmacologia
Receptor 5-HT2A de Serotonina/efeitos dos fármacos
Receptor 5-HT2C de Serotonina/efeitos dos fármacos
Serotonina/metabolismo
[Mh] Termos MeSH secundário: Aminopiridinas/farmacologia
Animais
Anorexia
Comportamento Alimentar/efeitos dos fármacos
Fenclonina/farmacologia
Receptor do Peptídeo Semelhante ao Glucagon 1/metabolismo
Indóis/farmacologia
Liraglutida/farmacologia
Masculino
Peptídeos/farmacologia
Pirrolidinas/farmacologia
Ratos
Ratos Sprague-Dawley
Receptor 5-HT2A de Serotonina/metabolismo
Receptor 5-HT2C de Serotonina/metabolismo
Antagonistas da Serotonina/farmacologia
Peçonhas/farmacologia
Perda de Peso/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((2R,4R)-4-hydroxy-2-(2-(2-(2-(3-methoxy)phenyl)ethyl)phenoxy)ethyl-1-methylpyrrolidine hydrochloride); 0 (6-chloro-5-methyl-1-((2-(2-methylpyrid-3-yloxy)pyrid-5-yl)carbamoyl)indoline); 0 (Aminopyridines); 0 (Glucagon-Like Peptide-1 Receptor); 0 (Hypoglycemic Agents); 0 (Indoles); 0 (Peptides); 0 (Pyrrolidines); 0 (Receptor, Serotonin, 5-HT2A); 0 (Receptor, Serotonin, 5-HT2C); 0 (Serotonin Antagonists); 0 (Venoms); 333DO1RDJY (Serotonin); 839I73S42A (Liraglutide); 89750-14-1 (Glucagon-Like Peptide 1); 9P1872D4OL (exenatide); R5J7E3L9SP (Fenclonine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170107
[St] Status:MEDLINE
[do] DOI:10.2337/db16-0755


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[PMID]:27730334
[Au] Autor:Zhou C; Shi L; Ye B; Feng H; Zhang J; Zhang R; Yan X
[Ad] Endereço:Department of Microbiology, College of Life Sciences, Key Laboratory for Microbiological Engineering of Agricultural, Environment of Ministry of Agriculture, Nanjing Agricultural University, 6 Tongwei Road, Nanjing, Jiangsu, 210095, People's Republic of China.
[Ti] Título:pheS , an effective host-genotype-independent counter-selectable marker for marker-free chromosome deletion in Bacillus amyloliquefaciens.
[So] Source:Appl Microbiol Biotechnol;101(1):217-227, 2017 Jan.
[Is] ISSN:1432-0614
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Aside from applications in the production of commercial enzymes and metabolites, Bacillus amyloliquefaciens is also an important group of plant growth-promoting rhizobacteria that supports plant growth and suppresses phytopathogens. A host-genotype-independent counter-selectable marker would enable rapid genetic manipulation and metabolic engineering, accelerating the study of B. amyloliquefaciens and its development as both a microbial cell factory and plant growth-promoting rhizobacteria. Here, a host-genotype-independent counter-selectable marker pheS was constructed through a point mutation of the gene pheS, which encodes the α-subunit of phenylalanyl-tRNA synthetase in Bacillus subtilis strain 168. In the presence of 5 mM p-chloro-phenylalanine, 100 % of B. amyloliquefaciens strain SQR9 cells carrying pheS were killed, whereas the wild-type strain SQR9 showed resistance to p-chloro-phenylalanine. A simple pheS and overlap-PCR-based strategy was developed to create the marker-free deletion of the amyE gene as well as a 37-kb bmy cluster in B. amyloliquefaciens SQR9. The effectiveness of pheS as a counter-selectable marker in B. amyloliquefaciens was further confirmed through the deletion of amyE genes in strains B. amyloliquefaciens FZB42 and NJN-6. In addition, the potential use of pheS in other Bacillus species was preliminarily assessed. The expression of PheS in B. subtilis strain 168 and B. cereus strain ATCC 14579 caused pronounced sensitivity of both hosts to p-chloro-phenylalanine, indicating that pheS could be used as a counter-selectable marker (CSM) in these strains.
[Mh] Termos MeSH primário: Bacillus amyloliquefaciens/genética
Técnicas de Inativação de Genes/métodos
Genética Microbiana/métodos
Fenilalanina-tRNA Ligase/genética
Seleção Genética
[Mh] Termos MeSH secundário: Antibacterianos/toxicidade
Bacillus amyloliquefaciens/fisiologia
Bacillus subtilis/genética
Bacillus subtilis/fisiologia
Fenclonina/toxicidade
Genótipo
Viabilidade Microbiana/efeitos dos fármacos
Proteínas Mutantes/genética
Proteínas Mutantes/metabolismo
Fenilalanina-tRNA Ligase/metabolismo
Mutação Puntual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Mutant Proteins); EC 6.1.1.20 (Phenylalanine-tRNA Ligase); R5J7E3L9SP (Fenclonine)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161013
[St] Status:MEDLINE
[do] DOI:10.1007/s00253-016-7906-9


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[PMID]:27639596
[Au] Autor:Kino Y; Nakayama-Imaohji H; Fujita M; Tada A; Yoneda S; Murakami K; Hashimoto M; Hayashi T; Okazaki K; Kuwahara T
[Ad] Endereço:Department of Microbiology, Faculty of Medicine, Kagawa University, 1750-1, Miki, Kagawa 761-0793, Japan.
[Ti] Título:Counterselection employing mutated pheS for markerless genetic deletion in Bacteroides species.
[So] Source:Anaerobe;42:81-88, 2016 Dec.
[Is] ISSN:1095-8274
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Markerless gene deletion is necessary for multiple gene disruptions due to the limited number of antibiotic resistant markers for some bacteria. However, even in transformable strains, obtaining the expected mutation without a marker requires laborious screening of a large number of colonies. Previous studies had success in various bacteria with a counter-selection system where a conditional lethal gene was incorporated into the vector. We examined the efficacy of the mutated pheS gene (pheS*) as a counter-selective marker for gene deletion in Bacteroides. This mutation produces an amino acid substitution (A303G) in the alpha subunit of Bacteroides phenylalanyl tRNA synthetase, which in E. coli alters the specificity of the tRNA synthetase resulting in a conditional lethal mutation due to the incorporation of p-chloro-phenylalanine (p-Cl-Phe) into protein. B. fragilis YCH46 and B. thetaiotaomicron VPI-5482 transformed with a pheS*-harboring shuttle vector were clearly growth-inhibited in the presence of >5 mM p-Cl-Phe in liquid defined minimal media (DMM) and on DMM agar plates. A targeting plasmid was constructed to delete the genetic region for capsular polysaccharide PS2 in B. fragilis or PS1 in B. thetaiotaomicron. After counterselection, p-Cl-Phe-resistant colonies were generated at a frequency of 8.1 × 10 for B. fragilis and 1.7 × 10 for B. thetaiotaomicron. Of the p-Cl-Phe-resistant colonies, 4.2% and 72% harbored the correct genetic deletion for B. fragilis and B. thetaiotaomicron, respectively. These results indicate that mutated pheS is a useful counter-selective gene to construct markerless genetic deletions in Bacteroides.
[Mh] Termos MeSH primário: Proteínas de Bactérias/genética
Bacteroides/genética
Deleção de Genes
Mutação
Fenilalanina-tRNA Ligase/genética
Subunidades Proteicas/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Substituição de Aminoácidos
Cápsulas Bacterianas/metabolismo
Proteínas de Bactérias/metabolismo
Bacteroides/metabolismo
Meios de Cultura/farmacologia
Escherichia coli/genética
Escherichia coli/metabolismo
Fenclonina/farmacologia
Expressão Gênica
Genes Letais
Engenharia Genética
Marcadores Genéticos
Vetores Genéticos/química
Vetores Genéticos/metabolismo
Fenilalanina-tRNA Ligase/metabolismo
Polissacarídeos Bacterianos/metabolismo
Subunidades Proteicas/metabolismo
Alinhamento de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Culture Media); 0 (Genetic Markers); 0 (Polysaccharides, Bacterial); 0 (Protein Subunits); EC 6.1.1.20 (Phenylalanine-tRNA Ligase); R5J7E3L9SP (Fenclonine)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


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[PMID]:27421789
[Au] Autor:Aydin TH; Can ÖD; Demir Özkay Ü; Turan N
[Ad] Endereço:Department of Pharmacology, Faculty of Pharmacy, Anadolu University, 26470, Eskisehir, Turkey.
[Ti] Título:Effect of subacute agomelatine treatment on painful diabetic neuropathy: involvement of catecholaminergic mechanisms.
[So] Source:Fundam Clin Pharmacol;30(6):549-567, 2016 Dec.
[Is] ISSN:1472-8206
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In this study, we investigated the effects of subacute agomelatine (40 and 80 mg/kg) administration on chronic hyperglycemia, metabolic parameters, and pain perception in streptozotocin-induced diabetic rats. Fasting blood glucose measurements and oral glucose tolerance tests were performed to evaluate the effect of agomelatine on glycemia, while metabolic parameters were monitored using metabolic cages. Potential effect of agomelatine on diabetes-induced mechanical and thermal allodynia was evaluated using dynamic plantar aesthesiometer and warm plate (38 °C) tests, respectively. Additionally, influence of agomelatine on hyperalgesia occurring in connection with diabetic neuropathy was examined using the Randall-Selitto (mechanical nociceptive stimulus), Hargreaves (thermal nociceptive stimulus), and cold plate (4 °C, thermal nociceptive stimulus) tests. Obtained data indicated that, in diabetic rats, agomelatine significantly improved hyperalgesia and allodynia responses, without no effect on hyperglycemia or the associated polydipsia, polyuria, and hyperphagia. Therapeutic potential of agomelatine on neuropathic pain was suppressed with α-methyl-para-tyrosine methyl ester (an inhibitor of catecholamine synthesis), phentolamine (a nonselective α-adrenoceptor antagonist), and propranolol (a nonselective ß-adrenoceptor antagonist) administrations. However, p-chlorophenylalanine methyl ester (an inhibitor of serotonin synthesis) pretreatment could not be achieved to reverse these antihyperalgesic and antiallodynic effects. These results suggest that the curative effect of agomelatine on neuropathic pain is mediated through rising synaptic catecholamine levels as well as through interactions with both α- and ß-adrenoceptors. To our knowledge, this is the first study to show findings that indicate catecholaminergic system mediated antihyperalgesic and antiallodynic effects of agomelatine.
[Mh] Termos MeSH primário: Acetamidas/farmacologia
Catecolaminas/metabolismo
Neuropatias Diabéticas/tratamento farmacológico
Neuralgia/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Glicemia/efeitos dos fármacos
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/complicações
Diabetes Mellitus Experimental/metabolismo
Neuropatias Diabéticas/etiologia
Neuropatias Diabéticas/metabolismo
Fenclonina/análogos & derivados
Fenclonina/farmacologia
Hiperalgesia/tratamento farmacológico
Hiperalgesia/metabolismo
Hiperglicemia/tratamento farmacológico
Hiperglicemia/metabolismo
Metiltirosinas/farmacologia
Neuralgia/metabolismo
Fentolamina/farmacologia
Propranolol/farmacologia
Ratos
Ratos Sprague-Dawley
Receptores Adrenérgicos alfa/metabolismo
Receptores Adrenérgicos beta/metabolismo
Estreptozocina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetamides); 0 (Blood Glucose); 0 (Catecholamines); 0 (Methyltyrosines); 0 (Receptors, Adrenergic, alpha); 0 (Receptors, Adrenergic, beta); 138112-76-2 (S 20098); 23434-96-0 (4-chlorophenylalanine methyl ester); 4502-13-0 (alpha-methyltyrosine methyl ester); 5W494URQ81 (Streptozocin); 9Y8NXQ24VQ (Propranolol); R5J7E3L9SP (Fenclonine); Z468598HBV (Phentolamine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170328
[Lr] Data última revisão:
170328
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160717
[St] Status:MEDLINE
[do] DOI:10.1111/fcp.12224


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[PMID]:27251625
[Au] Autor:Goeden N; Velasquez J; Arnold KA; Chan Y; Lund BT; Anderson GM; Bonnin A
[Ad] Endereço:Neuroscience Graduate Program, Zilkha Neurogenetic Institute.
[Ti] Título:Maternal Inflammation Disrupts Fetal Neurodevelopment via Increased Placental Output of Serotonin to the Fetal Brain.
[So] Source:J Neurosci;36(22):6041-9, 2016 Jun 01.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Maternal inflammation during pregnancy affects placental function and is associated with increased risk of neurodevelopmental disorders in the offspring. The molecular mechanisms linking placental dysfunction to abnormal fetal neurodevelopment remain unclear. During typical development, serotonin (5-HT) synthesized in the placenta from maternal l-tryptophan (TRP) reaches the fetal brain. There, 5-HT modulates critical neurodevelopmental processes. We investigated the effects of maternal inflammation triggered in midpregnancy in mice by the immunostimulant polyriboinosinic-polyribocytidylic acid [poly(I:C)] on TRP metabolism in the placenta and its impact on fetal neurodevelopment. We show that a moderate maternal immune challenge upregulates placental TRP conversion rapidly to 5-HT through successively transient increases in substrate availability and TRP hydroxylase (TPH) enzymatic activity, leading to accumulation of exogenous 5-HT and blunting of endogenous 5-HT axonal outgrowth specifically within the fetal forebrain. The pharmacological inhibition of TPH activity blocked these effects. These results establish altered placental TRP conversion to 5-HT as a new mechanism by which maternal inflammation disrupts 5-HT-dependent neurogenic processes during fetal neurodevelopment. SIGNIFICANCE STATEMENT: The mechanisms linking maternal inflammation during pregnancy with increased risk of neurodevelopmental disorders in the offspring are poorly understood. In this study, we show that maternal inflammation in midpregnancy results in an upregulation of tryptophan conversion to serotonin (5-HT) within the placenta. Remarkably, this leads to exposure of the fetal forebrain to increased concentrations of this biogenic amine and to specific alterations of crucially important 5-HT-dependent neurogenic processes. More specifically, we found altered serotonergic axon growth resulting from increased 5-HT in the fetal forebrain. The data provide a new understanding of placental function playing a key role in fetal brain development and how this process is altered by adverse prenatal events such as maternal inflammation. The results uncover important future directions for understanding the early developmental origins of mental disorders.
[Mh] Termos MeSH primário: Desenvolvimento Fetal/fisiologia
Doenças Fetais/etiologia
Inflamação/complicações
Placenta/metabolismo
Efeitos Tardios da Exposição Pré-Natal/fisiopatologia
Serotonina/metabolismo
[Mh] Termos MeSH secundário: 5-Hidroxitriptofano/biossíntese
5-Hidroxitriptofano/metabolismo
Animais
Encéfalo/embriologia
Encéfalo/metabolismo
Citocinas/genética
Citocinas/metabolismo
Modelos Animais de Doenças
Feminino
Fenclonina/toxicidade
Desenvolvimento Fetal/efeitos dos fármacos
Doenças Fetais/induzido quimicamente
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Regulação da Expressão Gênica no Desenvolvimento/fisiologia
Inflamação/induzido quimicamente
Camundongos
Placenta/efeitos dos fármacos
Placenta/fisiologia
Polidesoxirribonucleotídeos/toxicidade
Gravidez
Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente
Antagonistas da Serotonina/toxicidade
Estatísticas não Paramétricas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Polydeoxyribonucleotides); 0 (Serotonin Antagonists); 25853-45-6 (poly d(I-C)); 333DO1RDJY (Serotonin); C1LJO185Q9 (5-Hydroxytryptophan); R5J7E3L9SP (Fenclonine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170706
[Lr] Data última revisão:
170706
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160603
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2534-15.2016


  8 / 2564 MEDLINE  
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[PMID]:26989517
[Au] Autor:Majeed ZR; Abdeljaber E; Soveland R; Cornwell K; Bankemper A; Koch F; Cooper RL
[Ad] Endereço:Department of Biology, University of Kentucky, Lexington, KY 40506, USA; Department of Biology, College of Science, Salahaddin University-Erbil, Erbil, Iraq.
[Ti] Título:Modulatory Action by the Serotonergic System: Behavior and Neurophysiology in Drosophila melanogaster.
[So] Source:Neural Plast;2016:7291438, 2016.
[Is] ISSN:1687-5443
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Serotonin modulates various physiological processes and behaviors. This study investigates the role of 5-HT in locomotion and feeding behaviors as well as in modulation of sensory-motor circuits. The 5-HT biosynthesis was dysregulated by feeding Drosophila larvae 5-HT, a 5-HT precursor, or an inhibitor of tryptophan hydroxylase during early stages of development. The effects of feeding fluoxetine, a selective serotonin reuptake inhibitor, during early second instars were also examined. 5-HT receptor subtypes were manipulated using RNA interference mediated knockdown and 5-HT receptor insertional mutations. Moreover, synaptic transmission at 5-HT neurons was blocked or enhanced in both larvae and adult flies. The results demonstrate that disruption of components within the 5-HT system significantly impairs locomotion and feeding behaviors in larvae. Acute activation of 5-HT neurons disrupts normal locomotion activity in adult flies. To determine which 5-HT receptor subtype modulates the evoked sensory-motor activity, pharmacological agents were used. In addition, the activity of 5-HT neurons was enhanced by expressing and activating TrpA1 channels or channelrhodopsin-2 while recording the evoked excitatory postsynaptic potentials (EPSPs) in muscle fibers. 5-HT2 receptor activation mediates a modulatory role in a sensory-motor circuit, and the activation of 5-HT neurons can suppress the neural circuit activity, while fluoxetine can significantly decrease the sensory-motor activity.
[Mh] Termos MeSH primário: Encéfalo/fisiologia
Comportamento Alimentar/fisiologia
Locomoção
Neurônios Serotoninérgicos/fisiologia
Serotonina/fisiologia
[Mh] Termos MeSH secundário: 5-Hidroxitriptofano/administração & dosagem
Animais
Proteínas de Drosophila/metabolismo
Drosophila melanogaster
Inibidores Enzimáticos/administração & dosagem
Potenciais Pós-Sinápticos Excitadores
Comportamento Alimentar/efeitos dos fármacos
Fenclonina/administração & dosagem
Locomoção/efeitos dos fármacos
Subunidades Proteicas/metabolismo
Receptores de Serotonina/fisiologia
Células Receptoras Sensoriais/fisiologia
Serotonina/administração & dosagem
Triptofano Hidroxilase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Drosophila Proteins); 0 (Enzyme Inhibitors); 0 (Protein Subunits); 0 (Receptors, Serotonin); 333DO1RDJY (Serotonin); C1LJO185Q9 (5-Hydroxytryptophan); EC 1.14.16.4 (Tryptophan Hydroxylase); R5J7E3L9SP (Fenclonine)
[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:160319
[St] Status:MEDLINE
[do] DOI:10.1155/2016/7291438


  9 / 2564 MEDLINE  
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[PMID]:26905688
[Au] Autor:Pettersson R; Hagsäter SM; Eriksson E
[Ad] Endereço:Department of Pharmacology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Box 431, SE-405 30, Gothenburg, Sweden.
[Ti] Título:Serotonin depletion eliminates sex differences with respect to context-conditioned immobility in rat.
[So] Source:Psychopharmacology (Berl);233(8):1513-21, 2016 Apr.
[Is] ISSN:1432-2072
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Previous studies have shown that male rats display more anxiety-like behavior than females as assessed using the elevated plus maze and that serotonin depletion abolishes this difference by exerting an anxiolytic-like effect in males only. OBJECTIVES: To compare male and female rats with respect to immobility and startle responses to sudden noise bursts after contextual fear conditioning and to explore to what extent any possible sex difference in this regard is influenced by serotonin depletion during testing (but not acquisition). RESULTS: In line with previous studies, males displayed more immobility following contextual conditioning induced by previous exposure to foot shocks than females. In males but not females, the immobility response was reduced by administration of the serotonin synthesis inhibitor para-chlorophenylalanine (PCPA) between shock exposure and testing, the consequence being that males and females no longer differed in this regard. Untreated males but not females displayed a negative correlation between fear-conditioned startle and immobility, suggesting that the latter behavior, when excessive, interferes with the former. In line with this assumption, the reduction in immobility following administration of PCPA in males coincided with an increase in startle that was not observed in females, hence revealing a sex difference in startle not seen in untreated controls. CONCLUSION: The greater display of context-conditioned immobility in males compared with females appears to be serotonin-dependent.
[Mh] Termos MeSH primário: Condicionamento (Psicologia)/fisiologia
Imobilização/fisiologia
Inibidores da Captação de Serotonina/farmacologia
Serotonina/metabolismo
Caracteres Sexuais
[Mh] Termos MeSH secundário: Animais
Ansiolíticos/farmacologia
Ansiedade/metabolismo
Ansiedade/psicologia
Condicionamento (Psicologia)/efeitos dos fármacos
Medo/efeitos dos fármacos
Medo/fisiologia
Medo/psicologia
Feminino
Fenclonina/farmacologia
Masculino
Ratos
Ratos Wistar
Reflexo de Sobressalto/efeitos dos fármacos
Reflexo de Sobressalto/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Anxiety Agents); 0 (Serotonin Uptake Inhibitors); 333DO1RDJY (Serotonin); R5J7E3L9SP (Fenclonine)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160225
[St] Status:MEDLINE
[do] DOI:10.1007/s00213-016-4246-5


  10 / 2564 MEDLINE  
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[PMID]:26738969
[Au] Autor:Kawaura K; Ogata Y; Honda S; Soeda F; Shirasaki T; Takahama K
[Ad] Endereço:Department of Environmental and Molecular Health Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1 Oe-honmachi, Kumamoto 862-0973, Japan.
[Ti] Título:Tipepidine, a non-narcotic antitussive, exerts an antidepressant-like effect in the forced swimming test in adrenocorticotropic hormone-treated rats.
[So] Source:Behav Brain Res;302:269-78, 2016 Apr 01.
[Is] ISSN:1872-7549
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We investigated whether tipepidine exerts an antidepressant-like effect in the forced swimming test in adrenocorticotropic hormone (ACTH)-treated rats, which is known as a treatment-resistant depression model, and we studied the pharmacological mechanisms of the effects of tipepidine. Male Wistar rats (5-7 weeks old) were used in this study. Tipepidine (20 and 40 mg/kg, i.p.) decreased the immobility time in the forced swimming test in ACTH-treated rats. The anti-immobility effect of tipepidine was blocked by a catecholamine-depleting agent, alpha-methyl-p-tyrosine (300 mg/kg, s.c.), but not by a serotonin-depleting agent, p-chlorophenylalanine. The anti-immobility effect of tipepidine was also blocked by a dopamine D1 receptor antagonist, SCH23390 (0.02 mg/kg, s.c.) and an adrenaline α2 receptor antagonist, yohimbine (2 mg/kg, i.p.). In microdialysis technique, tipepidine (40 mg/kg, i.p.) increased the extracellular dopamine level of the nucleus accumbens (NAc) in ACTH-treated rats. These results suggest that tipepidine exerts an antidepressant-like effect in the forced swimming test in ACTH-treated rats, and that the effect of tipepidine is mediated by the stimulation of dopamine D1 receptors and adrenaline α2 receptors. The results also suggest that an increase in the extracellular dopamine level in the NAc may be involved in the antidepressant-like effect of tipepidine in ACTH-treated rats.
[Mh] Termos MeSH primário: Hormônio Adrenocorticotrópico/farmacologia
Antidepressivos/uso terapêutico
Depressão/tratamento farmacológico
Hormônios/farmacologia
Piperidinas/uso terapêutico
Natação/psicologia
[Mh] Termos MeSH secundário: Animais
Benzazepinas/farmacologia
Depressão/fisiopatologia
Modelos Animais de Doenças
Antagonistas de Dopamina/farmacologia
Relação Dose-Resposta a Droga
Interações Medicamentosas
Fenclonina/farmacologia
Imipramina/uso terapêutico
Resposta de Imobilidade Tônica/efeitos dos fármacos
Locomoção/efeitos dos fármacos
Masculino
Ratos
Ratos Wistar
Antagonistas da Serotonina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antidepressive Agents); 0 (Benzazepines); 0 (Dopamine Antagonists); 0 (Hormones); 0 (Piperidines); 0 (SCH 23390); 0 (Serotonin Antagonists); 2260ZP67IT (tipepidine); 9002-60-2 (Adrenocorticotropic Hormone); OGG85SX4E4 (Imipramine); R5J7E3L9SP (Fenclonine)
[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:160108
[St] Status:MEDLINE



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