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[PMID]:28987407
[Au] Autor:Shao HY; Wu MH; Deng F; Xu G; Liu N; Li X; Tang L
[Ad] Endereço:School of Environmental and Chemical Engineering, Shanghai University, Shanghai, 200444, PR China; Shanghai Environmental Monitoring Center, Shanghai, 200235, PR China.
[Ti] Título:Electron beam irradiation induced degradation of antidepressant drug fluoxetine in water matrices.
[So] Source:Chemosphere;190:184-190, 2018 Jan.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:With the development of psychiatric disorder in the current society, abuse of antidepressant drug fluoxetine (FLX) has made such compound an emerging contaminant in natural waters, and causes endocrine systems disturbance on some aquatic species. Herein, an efficient advanced oxidation process (AOP), electron beam irradiation was carried out to investigate the decomposition characteristics of such novel environmental pollutant, including the effects of initial concentration, pH, radical scavengers and anions. The results showed that FLX degradation followed pseudo-first-order kinetics. The degradation rate and dose constant decreased with increasing initial FLX concentration; and G-values elevated with the increase of initial concentration but reduced with increase of absorbed dose. Acidic condition was more conducive to FLX destruction than neutral and alkaline. The radical scavenger experiments indicated OH was the main reactive species for the decomposition of FLX, while the reductive species e and H played an adjuvant role. The presence of anions slightly decreased or even no impact on FLX degradation rate. Various water matrices influenced degradation processes of FLX. Experimental results suggested radiolytic degradation showed the best performance in pure water rather than natural water no matter with filtration or not. Moreover, with the occurrence of defluorination and dealkylation during degradation process, some organic and inorganic intermediates were detected, and the possible degradation mechanisms and pathways of FLX were proposed.
[Mh] Termos MeSH primário: Fluoxetina/efeitos da radiação
Purificação da Água/métodos
[Mh] Termos MeSH secundário: Ânions/farmacologia
Antidepressivos/efeitos da radiação
Elétrons
Fluoxetina/química
Cinética
Oxirredução
Poluentes Químicos da Água/química
Poluentes Químicos da Água/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anions); 0 (Antidepressive Agents); 0 (Water Pollutants, Chemical); 01K63SUP8D (Fluoxetine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171009
[St] Status:MEDLINE


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[PMID]:28452902
[Au] Autor:Fan KY; Liu HC
[Ad] Endereço:*Department of Psychiatry, Taipei City Psychiatric Center, Taipei City Hospital; and †Department of Psychiatry, School of Medicine, Taipei Medical University, Taipei, Taiwan.
[Ti] Título:Delirium Associated With Fluoxetine Discontinuation: A Case Report.
[So] Source:Clin Neuropharmacol;40(3):152-153, 2017 May/Jun.
[Is] ISSN:1537-162X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Withdrawal symptoms on selective serotonin reuptake inhibitor (SSRI) discontinuation have raised clinical attention increasingly. However, delirium is rarely reported in the SSRI discontinuation syndrome. CASE: We report a case of delirium developing after fluoxetine discontinuation in a 65-year-old female patient with major depressive disorder. She experienced psychotic depression with limited response to treatment of fluoxetine 40 mg/d and quetiapine 100 mg/d for 3 months. After admission, we tapered fluoxetine gradually in 5 days because of its limited effect. However, delirious pictures developed 2 days after we stopped fluoxetine. Three days later, we added back fluoxetine 10 mg/d. Her delirious features gradually improved, and the clinical presentation turned into previous psychotic depression state. We gradually increased the medication to fluoxetine 60 mg/d and olanzapine 20 mg/d in the following 3 weeks. Her psychotic symptoms decreased, and there has been no delirious picture noted thereafter. CONCLUSIONS: Delirium associated with fluoxetine discontinuation is a much rarer complication in SSRI discontinuation syndrome. The symptoms of SSRI discontinuation syndrome may be attributable to a rapid decrease in serotonin availability. In general, the shorter the half-life of any medication, the greater the likelihood patients will experience discontinuation symptoms. Genetic vulnerability might be a potential factor to explain that SSRI discontinuation syndrome also occurred rapidly in people taking long-half-life fluoxetine. The genetic polymorphisms of both pharmacokinetic and pharmacodynamic pathways might be potentially associated with SSRI discontinuation syndrome.
[Mh] Termos MeSH primário: Antidepressivos de Segunda Geração/efeitos adversos
Delírio/etiologia
Fluoxetina/efeitos adversos
Inibidores da Captação de Serotonina/efeitos adversos
Síndrome de Abstinência a Substâncias/etiologia
[Mh] Termos MeSH secundário: Idoso
Antipsicóticos/uso terapêutico
Benzodiazepinas/uso terapêutico
Delírio/prevenção & controle
Transtorno Depressivo Maior/tratamento farmacológico
Monitoramento de Medicamentos
Resistência a Múltiplos Medicamentos
Quimioterapia Combinada
Feminino
Fluoxetina/uso terapêutico
Seres Humanos
Inibidores da Captação de Serotonina/uso terapêutico
Síndrome de Abstinência a Substâncias/fisiopatologia
Síndrome de Abstinência a Substâncias/prevenção & controle
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents, Second-Generation); 0 (Antipsychotic Agents); 0 (Serotonin Uptake Inhibitors); 01K63SUP8D (Fluoxetine); 12794-10-4 (Benzodiazepines); N7U69T4SZR (olanzapine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1097/WNF.0000000000000214


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[PMID]:28456685
[Au] Autor:Gassó P; Rodríguez N; Boloc D; Blázquez A; Torres T; Gortat A; Plana MT; Lafuente A; Mas S; Arnaiz JA; Lázaro L
[Ad] Endereço:Department of Basic Clinical Practice, Unit of Pharmacology, University of Barcelona, Spain; Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
[Ti] Título:Association of regulatory TPH2 polymorphisms with higher reduction in depressive symptoms in children and adolescents treated with fluoxetine.
[So] Source:Prog Neuropsychopharmacol Biol Psychiatry;77:236-240, 2017 Jul 03.
[Is] ISSN:1878-4216
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Genetic variability related to the brain serotonergic system has a significant impact on both the susceptibility to psychiatric disorders, such as major depressive disorder (MDD), and the response to antidepressant drugs, such as fluoxetine. TPH2 is one of the most important serotonergic candidate genes in selective serotonin reuptake inhibitors (SSRIs) pharmacogenetic studies. The aim of the present study was to evaluate the influence of regulatory polymorphisms that are specifically located in human TPH2 transcription factor binding sites (TFBSs), and therefore could be functional by altering gene expression, on clinical improvement in children and adolescents treated with fluoxetine. The selection of SNPs was also based on their linkage disequilibrium with TPH2 rs4570625, a genetic variant with questionable functionality, which was previously associated with clinical response in our pediatric population. A total of 83 children and adolescents were clinically evaluated 12weeks after initiating antidepressant treatment with fluoxetine for the first time. Clinical improvement was assessed by reductions in depressive symptoms measured using the Children's Depression Inventory (CDI) scale. The polymorphisms rs11179002, rs60032326 and rs34517220 were, for the first time in the literature, significantly associated with higher clinical improvement. The strongest association was found for rs34517220. In particular, minor allele homozygotes showed higher score reductions on the CDI scale compared with the major allele carriers. Interestingly, this polymorphism is located in a human TPH2 TFBS for two relevant transcription factors in the serotoninergic neurons, Foxa1 and Foxa2, which together with the high level of significance found for this SNP, could indicate that rs34517220 is in fact the crucial functional genetic variant related to the fluoxetine response. These results provide new evidence for the role of regulatory genetic variants that could modulate human TPH2 expression in the SSRI antidepressant response.
[Mh] Termos MeSH primário: Depressão/tratamento farmacológico
Depressão/genética
Fluoxetina/uso terapêutico
Polimorfismo de Nucleotídeo Único/genética
Triptofano Hidroxilase/genética
[Mh] Termos MeSH secundário: Adolescente
Antidepressivos/farmacocinética
Antidepressivos/uso terapêutico
Criança
Feminino
Fluoxetina/farmacocinética
Frequência do Gene
Genótipo
Haplótipos/genética
Seres Humanos
Masculino
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents); 01K63SUP8D (Fluoxetine); EC 1.14.16.4 (TPH2 protein, human); EC 1.14.16.4 (Tryptophan Hydroxylase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:29206826
[Au] Autor:Ontiveros-Sánchez de la Barquera JA
[Ad] Endereço:Departamento de Psiquiatría, Hospital Universitario, Universidad Autónoma de Nuevo León; Instituto de Información e Investigación en Salud Mental A.C., Monterrey, N.L., México.
[Ti] Título:[Response to serotonergic and noradrenergic antidepressants: a crossover study of fluoxetine and desipramine in patients with first major depression episode].
[Ti] Título:Respuesta a antidepresivos serotoninérgicos y noradrenérgicos: estudio cruzado con fluoxetina y desipramina en pacientes con un primer episodio depresivo mayor..
[So] Source:Gac Med Mex;153(6):688-694, 2017 Nov-Dec.
[Is] ISSN:0016-3813
[Cp] País de publicação:Mexico
[La] Idioma:spa
[Ab] Resumo:BACKGROUND: Response rate data from studies with different kinds of antidepressant drugs help in the development of guidelines for the rational prescription of pharmacotherapy. However, there are still few comparative studies with selective reuptake inhibition on serotonin or norepinephrine in the same sample of major depression patients. METHODS: First episode major depression (DSM-III-R) outpatients who completed 6 weeks in two double-blind randomized trials with fluoxetine and desipramine were crossed over to treatment with the other drug under open conditions for 6 weeks. Response was considered if patient's final Hamilton depression scale score decreased 50% or more from baseline. RESULTS: No significant differences were found by drug treatment or sequence of treatment. Ten of the 18 patients (55.5%) were responders to both fluoxetine and desipramine, 3 (16.6%) were resistant to fluoxetine, 3 (16.6%) to desipramine and 2 (11.1%) to both drugs. DISCUSSION: These data suggest that among first major depressive episode outpatients fluoxetine and desipramine are equally effective. In patients who have been non-responders to one of the studied drugs, the other one is strikingly effective; this kind of treatment maneuver should be considered in such patients.
[Mh] Termos MeSH primário: Transtorno Depressivo Maior/tratamento farmacológico
Desipramina/uso terapêutico
Fluoxetina/uso terapêutico
[Mh] Termos MeSH secundário: Inibidores da Captação Adrenérgica/uso terapêutico
Adulto
Estudos Cross-Over
Transtorno Depressivo Maior/fisiopatologia
Desipramina/farmacologia
Método Duplo-Cego
Feminino
Fluoxetina/farmacologia
Seres Humanos
Masculino
Meia-Idade
Escalas de Graduação Psiquiátrica
Inibidores da Captação de Serotonina/uso terapêutico
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Adrenergic Uptake Inhibitors); 0 (Serotonin Uptake Inhibitors); 01K63SUP8D (Fluoxetine); TG537D343B (Desipramine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.24875/GMM.17002671


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[PMID]:29175455
[Au] Autor:Kosari-Nasab M; Shokouhi G; Ghorbanihaghjo A; Abbasi MM; Salari AA
[Ad] Endereço:Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
[Ti] Título:Anxiolytic- and antidepressant-like effects of Silymarin compared to diazepam and fluoxetine in a mouse model of mild traumatic brain injury.
[So] Source:Toxicol Appl Pharmacol;338:159-173, 2018 01 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Clinical and experimental studies have shown that mild traumatic brain injury (mTBI) is associated with increased anxiety- and depression-related behaviors and inflammation in the brain. Unfortunately, there are no specific therapies for long-term behavioral consequences of mTBI. This study set out to determine whether silymarin treatment compared to diazepam (DZP) and fluoxetine (FLX) can reduce neuroinflammation, anxiety- and depression-like behaviors after mTBI induction in mice. We used open field, elevated plus maze, light-dark box, zero maze, sucrose preference, forced swim, and tail suspension tests to assess anxiety and depression-like behaviors in mTBI-induced mice. The levels of tumor necrosis factor (TNF)-α protein, a marker of inflammation, in the prefrontal cortex and hippocampus was also measured. This study identified that the long-term treatment with DZP, FLX or SIL results in decreased anxiety and depression-like behaviors in mTBI-induced mice. The results also showed that these drugs reduced TNF-α levels in the prefrontal cortex and hippocampus. In addition, there were no significant differences between the effects of SIL and DZP or SIL and FLX on behavioral and cytokine levels in mTBI-induced mice. Our findings support the idea that mTBI could be a risk factor for anxiety- and depression-related disorders and neuroinflammation in the brain. Taken together, this study demonstrates that DZP, FLX or SIL can significantly reduce anxiety- and depression-like symptoms, and neuroinflammation after mTBI induction in mice.
[Mh] Termos MeSH primário: Ansiolíticos/farmacologia
Antidepressivos/farmacologia
Lesões Encefálicas Traumáticas/psicologia
Diazepam/farmacologia
Fluoxetina/farmacologia
Silimarina/farmacologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Aprendizagem em Labirinto/efeitos dos fármacos
Camundongos
Fator de Necrose Tumoral alfa/análise
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Anxiety Agents); 0 (Antidepressive Agents); 0 (Silymarin); 0 (Tumor Necrosis Factor-alpha); 01K63SUP8D (Fluoxetine); Q3JTX2Q7TU (Diazepam)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:29241236
[Au] Autor:Querido AL
[Ad] Endereço:Larenseweg 14, Hilversum, The Netherlands, bram@praktijkquerido.nl.
[Ti] Título:Diving and antidepressants.
[So] Source:Diving Hyperb Med;47(4):253-256, 2017 Dec.
[Is] ISSN:1833-3516
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Psychoactive drugs pose a risk to both the diver and his or her buddy. Little is known about the safety of diving with antidepressants. Amongst the potential interactions with the diving environment are: somnolence; convulsions; a bleeding tendency (potentially worsening decompression illness, DCI), alterations to glucose metabolism and psychiatric side effects. Fluoxetine may potentially reduce the inflammatory process associated with DCI. This article presents guidelines for recreational diving in combination with antidepressants. These guidelines were endorsed at a meeting of the Dutch Association for Diving Medicine in 2015 and are solely based on 'expert' opinion.
[Mh] Termos MeSH primário: Antidepressivos/efeitos adversos
Mergulho/psicologia
Fluoxetina/efeitos adversos
[Mh] Termos MeSH secundário: Glicemia/efeitos dos fármacos
Glicemia/metabolismo
Doença da Descompressão/etiologia
Mergulho/efeitos adversos
Hemorragia/induzido quimicamente
Seres Humanos
Convulsões/induzido quimicamente
Transtornos do Sono-Vigília/induzido quimicamente
[Pt] Tipo de publicação:GUIDELINE; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antidepressive Agents); 0 (Blood Glucose); 01K63SUP8D (Fluoxetine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.28920/dhm47.4.253-256


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[PMID]:29245320
[Au] Autor:Wei A; Peng J; Gu Z; Li J
[Ad] Endereço:aDepartment of Pharmacy, Tongji HospitalbDepartment of Endocrinology, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, WuhancDepartment of Pharmacy, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
[Ti] Título:QTc prolongation and torsades de pointes due to a coadministration of fluoxetine and amiodarone in a patient with implantable cardioverter-defibrillator: Case report and review of the literature.
[So] Source:Medicine (Baltimore);96(49):e9071, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Drug-induced prolongation of the corrected QT interval (QTc) may lead to serious and potentially life-threatening ventricular tachyarrhythmia, such as torsades de pointes (Tdp), which is worthy of clinical attention. Here, we report 1 case of Tdp after a coadministration of fluoxetine and amiodarone. PATIENT CONCERNS: A 62-year-old Chinese male who placed with the implanted cardioverter-defibrillator (ICD) appeared the QTc prolongation and Tdp after the concurrent administration of fluoxetine and amiodarone. DIAGNOSES: Torsades de pointes (Tdp). INTERVENTIONS: The patient was treated with magnesium and potassium immediately. Her ICD-brady pacing mode was reprogrammed to 90 bpm. Meanwhile, both of fluoxetine and amiodarone were discontinued. OUTCOMES: The further episodes of Tdp were prevented. After a few days, the QTc gradually decreased without clinically significant arrhythmias. LESSONS: The present case demonstrates that a potential drug-drug interaction (DDI) may lead to a life-threatening drug adverse reaction (ADR) especially in special subjects. Therefore, clinicians should closely monitor the electrocardiogram (ECG) when QTc-prolonging agents are given to patients with cardiac abnormalities, and avoid combining 2 QTc-prolonging drugs.
[Mh] Termos MeSH primário: Amiodarona/efeitos adversos
Antiarrítmicos/efeitos adversos
Cardiomiopatia Dilatada/terapia
Desfibriladores Implantáveis
Interações Medicamentosas
Fluoxetina/efeitos adversos
Síndrome do QT Longo/induzido quimicamente
Inibidores da Captação de Serotonina/efeitos adversos
Torsades de Pointes/induzido quimicamente
[Mh] Termos MeSH secundário: Amiodarona/administração & dosagem
Antiarrítmicos/administração & dosagem
Eletrocardiografia
Fluoxetina/administração & dosagem
Seres Humanos
Masculino
Meia-Idade
Inibidores da Captação de Serotonina/administração & dosagem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Serotonin Uptake Inhibitors); 01K63SUP8D (Fluoxetine); N3RQ532IUT (Amiodarone)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009071


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[PMID]:29277782
[Au] Autor:Radin DP; Purcell R; Lippa AS
[Ad] Endereço:RespireRx Pharmaceuticals, Inc., Glen Rock, NJ, U.S.A. dradin@respirerx.com.
[Ti] Título:Oncolytic Properties of Ampakines .
[So] Source:Anticancer Res;38(1):265-269, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The 5-year survival rate of glioblastoma (GBM) is ~10%, demonstrating that a new therapeutic modality for this cancer is desperately needed. Complicating the search for such a modality is that most large molecules cannot pass through the blood brain barrier, so molecules demonstrating efficacy in vitro may not be useful in vivo because they never reach the brain. Recently, the selective serotonin reuptake inhibitor (SSRI) fluoxetine (FLX) was identified as an effective agent in targeting GBM in vitro and in vivo by agonizing AMPA-glutamate receptors (AMPARs), eliciting massive calcium influx and mitochondrial calcium overload and apoptosis. MATERIALS AND METHODS: In the current study, we used a colorimetric cell viability assay to determine if we could enhance the oncolytic effect of FLX in vitro by pre-treating cells with an AMPAR-positive allosteric modulator (Ampakine). RESULTS: Our results demonstrated for the first time that concentrations of the Class I ampakine CX614, which increase AMPAR agonist binding affinity, possess oncolytic activity as a sole agent and synergistically reduce GBM viability when paired with FLX. FLX also demonstrates a dose-dependent induction of apoptosis in cancer cells originating outside the CNS that overexpress calcium-permeable AMPARs. Likewise, CX614 inhibits cancer cell viability in a dose-dependent fashion and its combination with FLX synergistically reduces cell viability. These effects of CX614 were not seen with the Class II ampakines, CX717 and CX1739. CONCLUSION: CX614 inhibits the growth of multiple cancers in vitro and bolsters the oncolytic activity of FLX in several cancers.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Fluoxetina/farmacologia
Oxazinas/farmacologia
[Mh] Termos MeSH secundário: Neoplasias Encefálicas/tratamento farmacológico
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Glioblastoma/tratamento farmacológico
Seres Humanos
Receptores de AMPA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Oxazines); 0 (Receptors, AMPA); 01K63SUP8D (Fluoxetine); 87V631480W (2H,3H,6aH-pyrrolidino(2'',1''-3',2')1,3-oxazino(6',5'-5,4)benzo(e)1, 4-dioxan-10-one)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:29073219
[Au] Autor:Kalogeraki E; Pielecka-Fortuna J; Löwel S
[Ad] Endereço:Department of Systems Neuroscience, J.F.B. Institut für Zoologie und Anthropologie, Universität Göttingen, Göttingen, Germany.
[Ti] Título:Environmental enrichment accelerates ocular dominance plasticity in mouse visual cortex whereas transfer to standard cages resulted in a rapid loss of increased plasticity.
[So] Source:PLoS One;12(10):e0186999, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In standard cage (SC) raised mice, experience-dependent ocular dominance (OD) plasticity in the primary visual cortex (V1) rapidly declines with age: in postnatal day 25-35 (critical period) mice, 4 days of monocular deprivation (MD) are sufficient to induce OD-shifts towards the open eye; thereafter, 7 days of MD are needed. Beyond postnatal day 110, even 14 days of MD failed to induce OD-plasticity in mouse V1. In contrast, mice raised in a so-called "enriched environment" (EE), exhibit lifelong OD-plasticity. EE-mice have more voluntary physical exercise (running wheels), and experience more social interactions (bigger housing groups) and more cognitive stimulation (regularly changed labyrinths or toys). Whether experience-dependent shifts of V1-activation happen faster in EE-mice and how long the plasticity promoting effect would persist after transferring EE-mice back to SCs has not yet been investigated. To this end, we used intrinsic signal optical imaging to visualize V1-activation i) before and after MD in EE-mice of different age groups (from 1-9 months), and ii) after transferring mice back to SCs after postnatal day 130. Already after 2 days of MD, and thus much faster than in SC-mice, EE-mice of all tested age groups displayed a significant OD-shift towards the open eye. Transfer of EE-mice to SCs immediately abolished OD-plasticity: already after 1 week of SC-housing and MD, OD-shifts could no longer be visualized. In an attempt to rescue abolished OD-plasticity of these mice, we either administered the anti-depressant fluoxetine (in drinking water) or supplied a running wheel in the SCs. OD-plasticity was only rescued for the running wheel- mice. Altogether our results show that raising mice in less deprived environments like large EE-cages strongly accelerates experience-dependent changes in V1-activation compared to the impoverished SC-raising. Furthermore, preventing voluntary physical exercise of EE-mice in adulthood immediately precludes OD-shifts in V1.
[Mh] Termos MeSH primário: Criação de Animais Domésticos
Dominância Ocular/fisiologia
Meio Ambiente
Plasticidade Neuronal
Córtex Visual/fisiologia
[Mh] Termos MeSH secundário: Envelhecimento/fisiologia
Animais
Dominância Ocular/efeitos dos fármacos
Feminino
Fluoxetina/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Plasticidade Neuronal/efeitos dos fármacos
Inibidores da Captação de Serotonina/farmacologia
Fatores de Tempo
Córtex Visual/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Serotonin Uptake Inhibitors); 01K63SUP8D (Fluoxetine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171027
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186999


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[PMID]:29049348
[Au] Autor:Lu Y; Ho CS; Liu X; Chua AN; Wang W; McIntyre RS; Ho RC
[Ad] Endereço:Department of Clinical Psychology and Psychiatry/School of Public Health, Zhejiang University College of Medicine, Hangzhou, China.
[Ti] Título:Chronic administration of fluoxetine and pro-inflammatory cytokine change in a rat model of depression.
[So] Source:PLoS One;12(10):e0186700, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study evaluated the chronic effects of fluoxetine, a commonly prescribed SSRI antidepressant, on the peripheral and central levels of inflammatory cytokines including IL-1ß, IL-6, TNF-α and IL-17 over a 4-interval in a rat model of chronic mild stress (CMS) which resembles the human experience of depression. Twenty-four Sprague-Dawley rats were randomly assigned to CMS+vehicle (n = 9), CMS+fluoxetine (n = 9) and the control (n = 6) groups. Sucrose preference and forced swim tests were performed to assess behavioral change. Blood samples were collected on day 0, 60, 90 and 120 for measurement of cytokine levels in plasma. On day 120, the brain was harvested and central level of cytokines was tested using Luminex. Four months of fluoxetine treatment resulted in changes in the sucrose preference and immobility time measurements, commensurate with antidepressant effects. The CMS+vehicle group exhibited elevated plasma levels of IL-1ß, IL-17, and TNF-α on day 60 or 120. Rats treated with fluoxetine demonstrated lower IL-1ß in plasma and brain after 90 and 120-day treatment respectively (p<0.05). There was a trend of reduction of IL-6 and TNF-α concentration. This study revealed the potential therapeutic effects of fluoxetine by reducing central and peripheral levels of IL-1ß in the alleviation of depressive symptoms.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Depressão/tratamento farmacológico
Modelos Animais de Doenças
Fluoxetina/administração & dosagem
Mediadores da Inflamação/metabolismo
Inibidores da Captação de Serotonina/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Citocinas/sangue
Feminino
Fluoxetina/uso terapêutico
Mediadores da Inflamação/sangue
Ratos
Ratos Sprague-Dawley
Inibidores da Captação de Serotonina/uso terapêutico
Natação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammation Mediators); 0 (Serotonin Uptake Inhibitors); 01K63SUP8D (Fluoxetine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171020
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186700



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