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1.
Schizophr Res ; 153(1-3): 150-9, 2014 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-24556469

RESUMO

Studies have suggested that the endocannabinoid system is implicated in the pathophysiology of schizophrenia. We have recently reported that Spontaneously Hypertensive Rats (SHRs) present a deficit in social interaction that is ameliorated by atypical antipsychotics. In addition, SHRs display hyperlocomotion - reverted by atypical and typical antipsychotics. These results suggest that this strain could be useful to study negative symptoms (modeled by a decrease in social interaction) and positive symptoms (modeled by hyperlocomotion) of schizophrenia and the effects of potential drugs with an antipsychotic profile. The aim of this study was to investigate the effects of WIN55-212,2 (CB1/CB2 agonist), ACEA (CB1 agonist), rimonabant (CB1 inverse agonist), AM404 (anandamide uptake/metabolism inhibitor), capsaicin (agonist TRPV1) and capsazepine (antagonist TRPV1) on the social interaction and locomotion of control animals (Wistar rats) and SHRs. The treatment with rimonabant was not able to alter either the social interaction or the locomotion presented by Wistar rats (WR) and SHR at any dose tested. The treatment with WIN55-212,2 decreased locomotion (1mg/kg) and social interaction (0.1 and 0.3mg/kg) of WR, while the dose of 1mg/kg increased social interaction of SHR. The treatment with ACEA increased (0.3mg/kg) and decreased (1mg/kg) locomotion of both strain. The administration of AM404 increased social interaction and decreased locomotion of SHR (5mg/kg), and decreased social interaction and increased locomotion in WR (1mg/kg). The treatment with capsaicin (2.5mg/kg) increased social interaction of both strain and decreased locomotion of SHR (2.5mg/kg) and WR (0.5mg/kg and 2.5mg/kg). In addition, capsazepine (5mg/kg) decreased locomotion of both strains and increased (5mg/kg) and decreased (10mg/kg) social interaction of WR. Our results indicate that the schizophrenia-like behaviors displayed by SHR are differently altered by cannabinoid and vanilloid drugs when compared to control animals and suggest the endocannabinoid and the vanilloid systems as a potential target for the treatment of schizophrenia.


Assuntos
Moduladores de Receptores de Canabinoides/uso terapêutico , Relações Interpessoais , Atividade Motora/efeitos dos fármacos , Esquizofrenia/tratamento farmacológico , Psicologia do Esquizofrênico , Canais de Cátion TRPV/metabolismo , Análise de Variância , Animais , Ácidos Araquidônicos/administração & dosagem , Benzoxazinas/administração & dosagem , Capsaicina/análogos & derivados , Capsaicina/uso terapêutico , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Masculino , Morfolinas/administração & dosagem , Naftalenos/administração & dosagem , Piperidinas/uso terapêutico , Pirazóis/uso terapêutico , Ratos , Ratos Endogâmicos SHR , Ratos Wistar , Rimonabanto , Esquizofrenia/fisiopatologia , Canais de Cátion TRPV/agonistas , Canais de Cátion TRPV/antagonistas & inibidores
2.
Med Hypotheses ; 80(5): 606-12, 2013 May.
Artigo em Inglês | MEDLINE | ID: mdl-23484676

RESUMO

Curcumin is a polyphenolic nonflavonoid compound extracted from the rhizome of turmeric (Curcuma longa), a plant commonly used in Indian and Chinese traditional medicine to treat rheumatism, cough, inflammation and wounds. Curcumin putative targets, known based on studies of diverse central nervous system disorders other than bipolar disorders (BD) include several proteins currently implicated in the pathophysiology of BD. These targets include, but are not limited to, transcription factors activated by environmental stressors and pro-inflammatory cytokines, protein kinases (PKA, PKC), enzymes, growth factors, inflammatory mediators, and anti-apoptotic proteins (Bcl-XL). Herein, we review previous studies on the anti-inflammatory and anti-oxidant properties of curcumin and discuss its therapeutic potential in BD.


Assuntos
Transtorno Bipolar/tratamento farmacológico , Transtorno Bipolar/metabolismo , Encéfalo/metabolismo , Curcumina/uso terapêutico , Citocinas/metabolismo , Fatores Imunológicos/metabolismo , Modelos Biológicos , Fatores de Transcrição/metabolismo , Anti-Inflamatórios não Esteroides/uso terapêutico , Encéfalo/efeitos dos fármacos , Humanos
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