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  1 / 61596 MEDLINE  
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[PMID]:28463109
[Au] Autor:Tang X; Roessingh S; Hayley SE; Chu ML; Tanaka NK; Wolfgang W; Song S; Stanewsky R; Hamada FN
[Ad] Endereço:Visual Systems Group, Abrahamson Pediatric Eye Institute, Division of Pediatric Ophthalmology, Cincinnati Children's Hospital Medical Center, Cincinnati, United States.
[Ti] Título:The role of PDF neurons in setting the preferred temperature before dawn in .
[So] Source:Elife;6, 2017 05 02.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Animals have sophisticated homeostatic controls. While mammalian body temperature fluctuates throughout the day, small ectotherms, such as achieve a body temperature rhythm (BTR) through their preference of environmental temperature. Here, we demonstrate that pigment dispersing factor (PDF) neurons play an important role in setting preferred temperature before dawn. We show that small lateral ventral neurons (sLNvs), a subset of PDF neurons, activate the dorsal neurons 2 (DN2s), the main circadian clock cells that regulate temperature preference rhythm (TPR). The number of temporal contacts between sLNvs and DN2s peak before dawn. Our data suggest that the thermosensory anterior cells (ACs) likely contact sLNvs via serotonin signaling. Together, the ACs-sLNs-DN2s neural circuit regulates the proper setting of temperature preference before dawn. Given that sLNvs are important for sleep and that BTR and sleep have a close temporal relationship, our data highlight a possible neuronal interaction between body temperature and sleep regulation.
[Mh] Termos MeSH primário: Temperatura Corporal
Drosophila/fisiologia
Rede Nervosa/fisiologia
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Animais
Relógios Circadianos
Drosophila/efeitos da radiação
Proteínas de Drosophila/metabolismo
Homeostase
Neurônios/química
Neuropeptídeos/metabolismo
Serotonina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Drosophila Proteins); 0 (Neuropeptides); 0 (pdf protein, Drosophila); 333DO1RDJY (Serotonin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  2 / 61596 MEDLINE  
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[PMID]:27778165
[Au] Autor:Bai M; Liu H; Xu K; Oso AO; Wu X; Liu G; Tossou MC; Al-Dhabi NA; Duraipandiyan V; Xi Q; Yin Y
[Ad] Endereço:Key Laboratory of Agro-ecological Processes in Subtropical Region, Institute of Subtropical Agriculture, Chinese Academy of Sciences, Hunan Provincial Engineering Research Center for Healthy Livestock and Poultry Production, Changsha, 410125, Hunan, China.
[Ti] Título:A review of the immunomodulatory role of dietary tryptophan in livestock and poultry.
[So] Source:Amino Acids;49(1):67-74, 2017 01.
[Is] ISSN:1438-2199
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:Tryptophan, a nutritionally essential amino acid, is active in the regulation of immune responses in animals. The products of tryptophan metabolism, such as indoleamine 2,3-dioxygenase, kynurenine, quinolinic acid, and melatonin, may improve immunity in an organism and induce anti-inflammatory responses. The immune tolerance processes mediated by tryptophan metabolites are not well understood. Recent studies have reported that the enzymes that break down tryptophan through the kynurenine metabolic pathway are found in numerous cell types, including immunocytes. Moreover, some tryptophan metabolites have been shown to play a role in the inhibition of T lymphocyte proliferation, elevation of immunoglobulin levels in the blood, and promotion of antigen-presenting organization in tissues. This review summarizes the effects and mechanisms of tryptophan and metabolites in immune functions in livestock and poultry. It also highlights the areas in which our understanding of the role(s) of tryptophan is incomplete and suggests possible future research that might prove of benefit to livestock and poultry producers.
[Mh] Termos MeSH primário: Suplementos Nutricionais
Imunomodulação/efeitos dos fármacos
Indolamina-Pirrol 2,3,-Dioxigenase/imunologia
Linfócitos/efeitos dos fármacos
Triptofano/imunologia
[Mh] Termos MeSH secundário: Ração Animal
Animais
Seres Humanos
Imunidade Inata
Indolamina-Pirrol 2,3,-Dioxigenase/metabolismo
Cinurenina/imunologia
Cinurenina/metabolismo
Gado
Linfócitos/citologia
Linfócitos/imunologia
Melatonina/imunologia
Melatonina/metabolismo
Aves Domésticas/imunologia
Ácido Quinolínico/imunologia
Ácido Quinolínico/metabolismo
Serotonina/imunologia
Serotonina/metabolismo
Suínos/imunologia
Triptofano/administração & dosagem
Triptofano/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Indoleamine-Pyrrole 2,3,-Dioxygenase); 333DO1RDJY (Serotonin); 343-65-7 (Kynurenine); 8DUH1N11BX (Tryptophan); F6F0HK1URN (Quinolinic Acid); JL5DK93RCL (Melatonin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1007/s00726-016-2351-8


  3 / 61596 MEDLINE  
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[PMID]:28460583
[Au] Autor:Nielsen BS; Larsen EH; Ladefoged O; Lam HR
[Ad] Endereço:1 Environment and Toxicology, DHI, Hørsholm, Denmark.
[Ti] Título:Subchronic, Low-Level Intraperitoneal Injections of Manganese (IV) Oxide and Manganese (II) Chloride Affect Rat Brain Neurochemistry.
[So] Source:Int J Toxicol;36(3):239-251, 2017 May/Jun.
[Is] ISSN:1092-874X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Manganese (Mn) is neurotoxic and can induce manganism, a Parkinson-like disease categorized as being a serious central nervous system irreversible neurodegenerative disease. An increased risk of developing symptoms of Parkinson disease has been linked to work-related exposure, for example, for workers in agriculture, horticulture, and people living near areas with frequent use of Mn-containing pesticides. In this study, the focus was placed on neurochemical effects of Mn. Rats were dosed intraperitoneally with 0.9% NaCl (control), 1.22 mg Mn (as MnO )/kg bodyweight (bw)/day, or 2.5 mg Mn (as MnCl )/kg bw/day for 7 d/wk for 8 or 12 weeks. This dosing regimen adds relevant new knowledge about Mn neurotoxicity as a consequence of low-dose subchronic Mn dosing. Manganese concentrations increased in the striatum, the rest of the brain, and in plasma, and regional brain neurotransmitter concentrations, including noradrenaline, dopamine (DA), 5-hydroxytrytamine, glutamate, taurine, and γ-amino butyric acid, and the activity of acetylcholinesterase changed. Importantly, a target parameter for Parkinson disease and manganism, the striatal DA concentration, was reduced after 12 weeks of dosing with MnCl . Plasma prolactin concentration was not significantly affected due to a potentially reduced dopaminergic inhibition of the prolactin release from the anterior hypophysis. No effects on the striatal α-synuclein and synaptophysin protein levels were detected.
[Mh] Termos MeSH primário: Química Encefálica/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Cloretos/toxicidade
Óxidos/toxicidade
[Mh] Termos MeSH secundário: Acetilcolinesterase/metabolismo
Animais
Encéfalo/metabolismo
Cloretos/sangue
Cloretos/farmacocinética
Dopamina/metabolismo
Ácido Glutâmico/metabolismo
Injeções Intraperitoneais
Masculino
Manganês/sangue
Manganês/metabolismo
Compostos de Manganês/sangue
Compostos de Manganês/farmacocinética
Norepinefrina/metabolismo
Óxidos/sangue
Óxidos/farmacocinética
Ratos Sprague-Dawley
Serotonina/metabolismo
Taurina/metabolismo
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chlorides); 0 (Manganese Compounds); 0 (Oxides); 1EQV5MLY3D (Taurine); 333DO1RDJY (Serotonin); 3KX376GY7L (Glutamic Acid); 42Z2K6ZL8P (Manganese); 56-12-2 (gamma-Aminobutyric Acid); 64J2OA7MH3 (manganese oxide); EC 3.1.1.7 (Acetylcholinesterase); QQE170PANO (manganese chloride); VTD58H1Z2X (Dopamine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1177/1091581817704378


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[PMID]:29253878
[Au] Autor:Asam K; Staniszewski A; Zhang H; Melideo SL; Mazzeo A; Voronkov M; Huber KL; Pérez E; Stock M; Stock JB; Arancio O; Nicholls RE
[Ad] Endereço:Department of Pathology and Cell Biology, Columbia University, New York, NY, United States of America.
[Ti] Título:Eicosanoyl-5-hydroxytryptamide (EHT) prevents Alzheimer's disease-related cognitive and electrophysiological impairments in mice exposed to elevated concentrations of oligomeric beta-amyloid.
[So] Source:PLoS One;12(12):e0189413, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Soluble forms of oligomeric beta-amyloid (Aß) are thought to play a central role in Alzheimer's disease (AD). Transgenic manipulation of methylation of the serine/threonine protein phosphatase, PP2A, was recently shown to alter the sensitivity of mice to AD-related impairments resulting from acute exposure to elevated levels of Aß. In addition, eicosanoyl-5-hydroxytryptamide (EHT), a naturally occurring component from coffee beans that modulates PP2A methylation, was shown to confer therapeutic benefits in rodent models of AD and Parkinson's disease. Here, we tested the hypothesis that EHT protects animals from the pathological effects of exposure to elevated levels of soluble oligomeric Aß. We treated mice with EHT-containing food at two different doses and assessed the sensitivity of these animals to Aß-induced behavioral and electrophysiological impairments. We found that EHT administration protected animals from Aß-induced cognitive impairments in both a radial-arm water maze and contextual fear conditioning task. We also found that both chronic and acute EHT administration prevented Aß-induced impairments in long-term potentiation. These data add to the accumulating evidence suggesting that interventions with pharmacological agents, such as EHT, that target PP2A activity may be therapeutically beneficial for AD and other neurological conditions.
[Mh] Termos MeSH primário: Doença de Alzheimer/tratamento farmacológico
Peptídeos beta-Amiloides/química
Transtornos Cognitivos/prevenção & controle
Serotonina/análogos & derivados
[Mh] Termos MeSH secundário: Doença de Alzheimer/patologia
Animais
Café
Cognição/efeitos dos fármacos
Condicionamento (Psicologia)
Modelos Animais de Doenças
Eletrofisiologia
Medo
Feminino
Potenciação de Longa Duração
Masculino
Aprendizagem em Labirinto
Metilação
Camundongos
Camundongos Endogâmicos C57BL
Doenças do Sistema Nervoso/tratamento farmacológico
Doenças do Sistema Nervoso/patologia
Plasticidade Neuronal
Fosforilação
Serotonina/farmacologia
Solubilidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Coffee); 0 (eicosanoyl-5-hydroxytryptamide); 333DO1RDJY (Serotonin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189413


  5 / 61596 MEDLINE  
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[PMID]:29281635
[Au] Autor:Takahashi M; Takagi S
[Ad] Endereço:Division of Biological Science, Nagoya University Graduate School of Science Chikusa-ku, Nagoya, Japan.
[Ti] Título:Optical silencing of body wall muscles induces pumping inhibition in Caenorhabditis elegans.
[So] Source:PLoS Genet;13(12):e1007134, 2017 12.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Feeding, a vital behavior in animals, is modulated depending on internal and external factors. In the nematode Caenorhabditis elegans, the feeding organ called the pharynx ingests food by pumping driven by the pharyngeal muscles. Here we report that optical silencing of the body wall muscles, which drive the locomotory movement of worms, affects pumping. In worms expressing the Arch proton pump or the ACR2 anion channel in the body wall muscle cells, the pumping rate decreases after activation of Arch or ACR2 with light illumination, and recovers gradually after terminating illumination. Pumping was similarly inhibited by illumination in locomotion-defective mutants carrying Arch, suggesting that perturbation of locomotory movement is not critical for pumping inhibition. Analysis of mutants and cell ablation experiments showed that the signals mediating the pumping inhibition response triggered by activation of Arch with weak light are transferred mainly through two pathways: one involving gap junction-dependent mechanisms through pharyngeal I1 neurons, which mediate fast signals, and the other involving dense-core vesicle-dependent mechanisms, which mediate slow signals. Activation of Arch with strong light inhibited pumping strongly in a manner that does not rely on either gap junction-dependent or dense-core vesicle-dependent mechanisms. Our study revealed a new aspect of the neural and neuroendocrine controls of pumping initiated from the body wall muscles.
[Mh] Termos MeSH primário: Optogenética/métodos
Músculos Faríngeos/metabolismo
Bombas de Próton/metabolismo
[Mh] Termos MeSH secundário: Animais
Caenorhabditis elegans
Proteínas de Caenorhabditis elegans/metabolismo
Ingestão de Alimentos/fisiologia
Locomoção/fisiologia
Neurônios Motores/metabolismo
Músculo Esquelético/metabolismo
Faringe/metabolismo
Serotonina
Transdução de Sinais/fisiologia
Canais de Ânion Dependentes de Voltagem/genética
Canais de Ânion Dependentes de Voltagem/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (Proton Pumps); 0 (Voltage-Dependent Anion Channels); 333DO1RDJY (Serotonin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171228
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007134


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[PMID]:28460173
[Au] Autor:Cabrera R; Filevich O; García-Acosta B; Athilingam J; Bender KJ; Poskanzer KE; Etchenique R
[Ad] Endereço:Departamento de Química Inorgánica, Analítica y Química Física, INQUIMAE, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, CONICET, Ciudad Universitaria Pabellón 2, AR1428EHA Buenos Aires, Argentina.
[Ti] Título:A Visible-Light-Sensitive Caged Serotonin.
[So] Source:ACS Chem Neurosci;8(5):1036-1042, 2017 05 17.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Serotonin, or 5-hydroxytryptamine (5HT), is an important neurotransmitter in the nervous system of both vertebrates and invertebrates. Deficits in 5HT signaling are responsible for many disabling psychiatric conditions, and its molecular machinery is the target of many pharmaceuticals. We present a new 5HT phototrigger, the compound [Ru(bpy) (PMe )(5HT)] , where PMe is trimethylphosphine. As with other ruthenium-bipyridyl based caged compounds, [Ru(bpy) (PMe )(5HT)] presents activity in the visible region of the spectrum. We characterize and discuss the photochemical properties of the caged compound, and demonstrate its use by modulating the excitability of mouse prefrontal principal neurons.
[Mh] Termos MeSH primário: Luz
Neurônios/efeitos dos fármacos
Córtex Pré-Frontal/efeitos dos fármacos
Rutênio/química
Serotonina/química
[Mh] Termos MeSH secundário: Animais
Camundongos
Neurônios/metabolismo
Córtex Pré-Frontal/metabolismo
Serotonina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
333DO1RDJY (Serotonin); 7UI0TKC3U5 (Ruthenium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1021/acschemneuro.7b00083


  7 / 61596 MEDLINE  
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[PMID]:28460160
[Au] Autor:Huot P; Sgambato-Faure V; Fox SH; McCreary AC
[Ad] Endereço:Centre de Recherche du Centre Hospitalier de l'Université de Montréal , Montreal, QC H2X 0A9, Canada.
[Ti] Título:Serotonergic Approaches in Parkinson's Disease: Translational Perspectives, an Update.
[So] Source:ACS Chem Neurosci;8(5):973-986, 2017 05 17.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Parkinson's disease (PD) has long been seen as a disorder caused by degeneration of the dopaminergic system, leading to the classic motor manifestations of the disease. However, there is now overwhelming evidence that PD is more than a disease merely caused by dopamine depletion. It is well-known that a myriad of other neurotransmitters are affected by the disease process. One such neurotransmitter is serotonin (5-HT). 5-HT has been shown to play a role in several motor and nonmotor manifestations of PD, including tremor, cognition, depression and psychosis. 5-HT also seems to play a critical role in L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia. A breadth of preclinical studies and clinical trials have been conducted that aimed at modulating the 5-HT system in order to alleviate depression, cognitive deficits, psychosis, and dyskinesia. In this Review, we summarize recent advances in the 5-HT field in PD, but with a translational emphasis. We start by presenting a novel nonhuman primate model of PD that presents with dual dopamine and 5-HT lesions. We then present preclinical and clinical data that introduce new concepts, such as the use of biased and partial agonists, as well as molecules recently introduced to the field of PD, such as eltoprazine, pimavanserin, nelotanserin, and SYN-120, to enhance therapeutic benefit while minimizing adverse events, notably on parkinsonian disability.
[Mh] Termos MeSH primário: Antiparkinsonianos/uso terapêutico
Doença de Parkinson/metabolismo
Serotoninérgicos/uso terapêutico
Serotonina/metabolismo
[Mh] Termos MeSH secundário: Animais
Antiparkinsonianos/farmacologia
Modelos Animais de Doenças
Seres Humanos
Atividade Motora/efeitos dos fármacos
Doença de Parkinson/tratamento farmacológico
Serotoninérgicos/farmacologia
Pesquisa Médica Translacional
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antiparkinson Agents); 0 (Serotonin Agents); 333DO1RDJY (Serotonin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1021/acschemneuro.6b00440


  8 / 61596 MEDLINE  
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[PMID]:28459524
[Au] Autor:Bécamel C; Berthoux C; Barre A; Marin P
[Ad] Endereço:Centre National de la Recherche Scientifique, UMR-5203, Institut de Génomique Fonctionnelle, F-34094 Montpellier, France.
[Ti] Título:Growing Evidence for Heterogeneous Synaptic Localization of 5-HT2A Receptors.
[So] Source:ACS Chem Neurosci;8(5):897-899, 2017 05 17.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The serotonin 2A (5-HT2A) receptor subtype continues to attract attention as a target for numerous psychoactive drugs including psychedelic hallucinogens, antidepressants, anxiolytics, and atypical antipsychotics. 5-HT2A receptors are a principal G protein-coupled receptor subtype mediating the excitatory effects of serotonin. Nonetheless, pre- vs postsynaptic localization of 5HT2A receptors, relative to glutamatergic synapses, has remained controversial. Here, we discuss recent findings highlighting the existence and roles of presynaptic 5-HT2A receptors in regulating glutamatergic transmission and cognition.
[Mh] Termos MeSH primário: Neurônios/metabolismo
Receptor 5-HT2A de Serotonina/metabolismo
Serotonina/metabolismo
Sinapses/metabolismo
Transmissão Sináptica/fisiologia
[Mh] Termos MeSH secundário: Animais
Ácido Glutâmico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptor, Serotonin, 5-HT2A); 333DO1RDJY (Serotonin); 3KX376GY7L (Glutamic Acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1021/acschemneuro.6b00409


  9 / 61596 MEDLINE  
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[PMID]:28450636
[Au] Autor:Chen WV; Nwakeze CL; Denny CA; O'Keeffe S; Rieger MA; Mountoufaris G; Kirner A; Dougherty JD; Hen R; Wu Q; Maniatis T
[Ad] Endereço:Department of Biochemistry and Molecular Biophysics, Columbia University, New York, NY 10032, USA.
[Ti] Título:Pcdhαc2 is required for axonal tiling and assembly of serotonergic circuitries in mice.
[So] Source:Science;356(6336):406-411, 2017 04 28.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Serotonergic neurons project their axons pervasively throughout the brain and innervate various target fields in a space-filling manner, leading to tiled arrangements of their axon terminals to allow optimal allocation of serotonin among target neurons. Here we show that conditional deletion of the mouse protocadherin α ( α) gene cluster in serotonergic neurons disrupts local axonal tiling and global assembly of serotonergic circuitries and results in depression-like behaviors. Genetic dissection and expression profiling revealed that this role is specifically mediated by Pcdhαc2, which is the only Pcdhα isoform expressed in serotonergic neurons. We conclude that, in contrast to neurite self-avoidance, which requires single-cell identity mediated by Pcdh diversity, a single cell-type identity mediated by the common C-type Pcdh isoform is required for axonal tiling and assembly of serotonergic circuitries.
[Mh] Termos MeSH primário: Axônios/patologia
Caderinas/fisiologia
Depressão/genética
Neurônios Serotoninérgicos/patologia
Serotonina/metabolismo
[Mh] Termos MeSH secundário: Animais
Caderinas/genética
Deleção de Genes
Sistema Límbico/metabolismo
Camundongos
Camundongos Mutantes
Família Multigênica
Neurônios Serotoninérgicos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cadherins); 0 (Pcdhalphac2 protein, mouse); 333DO1RDJY (Serotonin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1126/science.aal3231


  10 / 61596 MEDLINE  
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[PMID]:29294327
[Au] Autor:Ren C; Liu J; Zhou J; Liang H; Wang Y; Sun Y; Ma B; Yin Y
[Ad] Endereço:Departments of Human Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing 100191, China.
[Ti] Título:Low levels of serum serotonin and amino acids identified in migraine patients.
[So] Source:Biochem Biophys Res Commun;496(2):267-273, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Migraine is a highly disabling primary headache associated with a high socioeconomic burden and a generally high prevalence. The clinical management of migraine remains a challenge. This study was undertaken to identify potential serum biomarkers of migraine. Using Liquid Chromatography coupled to Mass Spectrometry (LC-MS), the metabolomic profile of migraine was compared with healthy individuals. Principal component analysis (PCA) and Orthogonal partial least squares-discriminant analysis (orthoPLS-DA) showed the metabolomic profile of migraine is distinguishable from controls. Volcano plot analysis identified 10 serum metabolites significantly decreased during migraine. One of these was serotonin, and the other 9 were amino acids. Pathway analysis and enrichment analysis showed tryptophan metabolism (serotonin metabolism), arginine and proline metabolism, and aminoacyl-tRNA biosynthesis are the three most prominently altered pathways in migraine. ROC curve analysis indicated Glycyl-l-proline, N-Methyl-dl-Alanine and l-Methionine are potential sensitive and specific biomarkers for migraine. Our results show Glycyl-l-proline, N-Methyl-dl-Alanine and l-Methionine may be as specific or more specific for migraine than serotonin which is the traditional biomarker of migraine. We propose that therapeutic manipulation of these metabolites or metabolic pathways may be helpful in the prevention and treatment of migraine.
[Mh] Termos MeSH primário: Alanina/análogos & derivados
Dipeptídeos/sangue
Metionina/sangue
Transtornos de Enxaqueca/diagnóstico
Serotonina/sangue
[Mh] Termos MeSH secundário: Adulto
Alanina/sangue
Arginina/sangue
Biomarcadores/sangue
Estudos de Casos e Controles
Cromatografia Líquida de Alta Pressão/métodos
Análise Discriminante
Feminino
Seres Humanos
Masculino
Metaboloma
Transtornos de Enxaqueca/sangue
Transtornos de Enxaqueca/fisiopatologia
Análise de Componente Principal
Prolina/sangue
Aminoacil-RNA de Transferência/sangue
Curva ROC
Triptofano/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Dipeptides); 0 (RNA, Transfer, Amino Acyl); 333DO1RDJY (Serotonin); 600-21-5 (N-methylalanine); 704-15-4 (glycylproline); 8DUH1N11BX (Tryptophan); 94ZLA3W45F (Arginine); 9DLQ4CIU6V (Proline); AE28F7PNPL (Methionine); OF5P57N2ZX (Alanine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE



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