Navegando por Palavras-chave "Extinction"
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- ItemSomente MetadadadosAcute systemic blockade of D2 receptors does not accelerate the extinction of cocaine-associated place preference(Elsevier B.V., 2009-12-04) Yim Júnior, Alberto [UNIFESP]; Andersen, M. L. [UNIFESP]; Soeiro, A. C. [UNIFESP]; Tufik, Sergio [UNIFESP]; Oliveira, Maria Gabriela Menezes de [UNIFESP]; Univ Fed Tocantins; Universidade Federal de São Paulo (UNIFESP)Facilitation of extinction can be used as a therapeutic tool in treatment of both post-traumatic stress disorder and drug addiction. the present study examined whether the blockade of D2 receptors before each extinction trial would accelerate the extinction of cocaine-induced place preference. Male Wistar rats were initially conditioned and tested for a cocaine-associated place-preference (20 mg/kg). On the following day after the initial test, the animals were submitted to extinction training. This training consisted of daily sessions in which the subjects were alternatively confined during 30 min in the saline and cocaine-associated environment. However, 30 min before each extinction trial the animals received a systemic injection of D2 antagonist sulpiride. While one group was treated with a dose of 50 mg/kg (ip), the other group was treated with a dose of 100 mg/kg. An additional control group received injections of saline during extinction trials. Twenty-four hours after the last extinction trial, the animals were tested again for their preferences to cocaine and saline associated environments. Since one round of extinction trial was not sufficient to produce extinction of cocaine associated place preference, the animals were submitted to a second cycle of extinction trials and test. the systemic administration of the two doses of sulpiride (50 and 100 mg/kg) 30 min before each conditioning did not enhance the extinction of cocaine-associated place preference. This finding suggests that the D2 receptors are not involved in a acute protocol of extinction of cocaine-induced place preference. (C) 2009 Elsevier B.V. All rights reserved.
- ItemAcesso aberto (Open Access)Análise dos marcadores moleculares associados a formação de memória de supressão condicionada na formação hipocampal dorsal e ventral(Universidade Federal de São Paulo, 2018-11) Kubota, Silvia Megumi [UNIFESP]; Cerutti, Suzete Maria [UNIFESP]; Gaiardo, Renan Barretta; http://lattes.cnpq.br/6686023038561523; http://lattes.cnpq.br/9076343601956182; http://lattes.cnpq.br/5830225508865434A formação hipocampal tem sido descrita como uma estrutura chave na consolidação de memórias de longa duração, do tipo declarativa, isto é, memórias que requerem a consciência do indivíduo durante sua evocação ou lembrança de informações sobre ambientes, pessoas ou objetos. Poucos estudos avaliam o papel da FH (formação hipocampal) na supressão de um comportamento em curso em detrimento do aumento da atenção e vigilância. Este estudo avaliou o papel da formação hipocampal dorsal e ventral na formação da memória de supressão condicionada por meio da análise da expressão diferencial da proteína cálcio -calmodulina – quinase II α (CaMKIIα), conhecidamente envolvida no processo de formação e da extinção do medo condicionado. Para isso, foram utilizados ratos Wistar, machos, adultos, distribuídos aleatoriamente em nove grupos experimentais (n=10/grupo), sendo eles: controle, condicionamento, teste 1 com uma tentativa, teste 1 com 10 tentativas e teste 3 com 10 tentativas, todos com eutanásia após 1 hora e 24 horas. O protocolo comportamental envolveu: i) aquisição da resposta de lamber (1º ao 5º dia); ii) aquisição da memória de supressão condicionada da resposta de lamber, por meio da associação som (CS, estímulo condicionado) e choque (US, estímulo incondicionado) (6 O dia); iii) reaquisição da resposta de lamber (7º dia) e iv) teste para avaliar a retenção da memória de supressão condicionada (8º dia). No teste 1 (8º dia) os animais foram submetidos a 1 ou 10 exposições ao CS- sem associação com US. No teste 2 ou 3 (9º e 10º dia) foram apresentados 10 CS-sem US. 1 hora ou 24 horas após o teste os animais foram eutanasiados para a retirada da formação hipocampal dorsal e ventral e a expressão proteica diferencial, avaliada pela técnica de Western blotting. Os dados mostraram que houve uma redução nos níveis de pCaMKII/CaMKII, no hipocampo dorsal (P<0,05) e ventral (P<0,05) dos animais submetidos ao teste de retenção com 10 tentativas de exposição ao CS, em comparação com o grupo controle. Os níveis reduzidos de pCaMKII podem estar relacionados a extinção da memória de supressão condicionada. Dados adicionais podem esclarecer sobre os diferentes níveis proteicos de CaMKII e pCaMKIIα em cada um dos subcampos que compõem a formação hipocampal dorsal e ventral.
- ItemSomente MetadadadosDiazepam effects on aversive memory retrieval and extinction: Role of anxiety levels(Pergamon-Elsevier Science Ltd, 2016) Leão, Anderson Henrique França Figueiredo; Cabral, Alicia; Izídio, Geison Souza; Ribeiro, Alessandra Mussi [UNIFESP]; Silva, Regina Helena [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Benzodiazepines (BDZs) are anxiolytic drugs that impair memory acquisition. Previous studies using the plus maze discriminative avoidance task (PMDAT, which assesses memory and anxiety concomitantly) indicated that the effects of BDZs on anxiety and acquisition are related to each other. The possible influence of the anxiolytic action of BDZs on their effects on memory retrieval and extinction are poorly understood. This is relevant considering the relationship between aversive memories and anxiety disorders. We designed a modified protocol of PMDAT that evaluates anxiety during retrieval and extinction of the task. Male Wistar rats were trained in the PMDAT (plus-maze with two open and two enclosed arms) using a standard or a modified protocol. In the standard protocol, the aversive stimuli were presented in one of the enclosed arms during training, and the animal had free access to the whole apparatus. In the modified protocol, the open arms were blocked with glass walls. Twenty-four hours after training, the animals subjected to each of the protocols were treated with saline or 2.0 mg/kg of diazepam (DZP) 30 min before the test. There was a third session in the maze (retest) 24 h after the test. During the test, DZP impaired and improved retrieval in rats that had been trained in the standard and the modified protocol when compared to the respective saline-treated groups. In addition, treatment with DZP prior to the test induced anxiolysis, but only in the animals that were not pre-exposed to the open arms of the apparatus (modified protocol). In these animals, DZP impaired extinction, which was evaluated during retest session. The impairing effect of DZP on extinction seems to be related to its anxiolytic action during the test (extinction learning). Further, we suggest that aversive memory retrieval depends on both the treatment and the arousal elicited by exposure to the apparatus.
- ItemAcesso aberto (Open Access)Flavones from Erythrina falcata are modulators of fear memory(Biomed Central Ltd, 2014-08-05) Oliveira, Daniela Rodrigues de [UNIFESP]; Zamberlam, Claudia Raquel [UNIFESP]; Gaiardo, Renan Barreta [UNIFESP]; Rego, Gizelda Maia; Cerutti, Janete Maria [UNIFESP]; Cavalheiro, Alberto J.; Cerutti, Suzete Maria [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Empresa Brasileira de Pesquisa Agropecuária (EMBRAPA); Universidade de São Paulo (USP)Background: Flavonoids, which have been identified in a variety of plants, have been demonstrated to elicit beneficial effects on memory. Some studies have reported that flavonoids derived from Erythrina plants can provide such beneficial effects on memory. the aim of this study was to identify the flavonoids present in the stem bark crude extract of Erythrina falcata (CE) and to perform a bioactivity-guided study on conditioned fear memory.Methods: the secondary metabolites of CE were identified by high performance liquid chromatography combined with a diode array detector, electrospray ionization tandem mass spectrometry (HPLC-DAD-ESI/MSn) and nuclear magnetic resonance (NMR). the buthanolic fraction (BuF) was obtained by partitioning. Subfractions from BuF (BuF1 - BuF6) and fraction flavonoidic (FfA and FfB) were obtained by flash chromatography. the BuF3 and BuF4 fractions were used for the isolation of flavonoids, which was performed using HPLC-PAD. the isolated substances were quantified by HPLC-DAD and their structures were confirmed by nuclear magnetic resonance (NMR). the activities of CE and the subfractions were monitored using a one-trial, step-down inhibitory avoidance (IA) task to identify the effects of these substances on the acquisition and extinction of conditioned fear in rats.Results: Six subclasses of flavonoids were identified for the first time in CE. According to our behavioral data, CE, BuF, BuF3 and BuF4, the flavonoidic fractions, vitexin, isovitexin and 6-C-glycoside-diosmetin improved the acquisition of fear memory. Rats treated with BuF, BuF3 and BuF4 were particularly resistant to extinction. Nevertheless, rats treated with FfA and FfB, vitexin, isovitexin and 6-C-glycoside-diosmetin exhibited gradual reduction in conditioned fear response during the extinction retest session, which was measured at 48 to 480 h after conditioning.Conclusions: Our results demonstrate that vitexin, isovitexin and diosmetin-6-C-glucoside and flavonoidic fractions resulted in a significant retention of fear memory but did not prevent the extinction of fear memory. These results further substantiate that the treatment with pure flavonoids or flavanoid-rich fractions might represent potential therapeutic approaches for the treatment of neurocognitive disorders, improvement of memory acquisition and spontaneous recovery of fear.
- ItemSomente MetadadadosSleep deprivation impairs the extinction of cocaine-induced environmental conditioning in mice(Elsevier B.V., 2014-09-01) Berro, Laís Fernanda [UNIFESP]; Hollais, André Willian [UNIFESP]; Patti, Camilla de Lima [UNIFESP]; Fukushiro, Daniela Fukue [UNIFESP]; Mari-Kawamoto, Elisa [UNIFESP]; Talhati, Fernanda [UNIFESP]; Costa, José M. [UNIFESP]; Zanin, Karina Agustini [UNIFESP]; Lopes-Silva, Leonardo Brito [UNIFESP]; Ceccon, Liliane Minglini Barbosa [UNIFESP]; Santos, Renan dos [UNIFESP]; Procopio-Souza, Roberta [UNIFESP]; Trombin, Thaís Fernanda [UNIFESP] ; Yokoyama, Thais Suemi [UNIFESP]; Wuo-Silva, Raphael [UNIFESP]; Tufik, Sergio [UNIFESP]; Andersen, Monica Levy [UNIFESP]; Frussa-Filho, Roberto [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Persistence of a drug-environment conditioning induced by repeated psychostimulant treatment is thought to play a key role in the addictive cycle. in addition, sleep disorders are a common feature in patients with addictive disorders. Sleep deprivation shares similar neurobiological effects with psychostimulants. Therefore, we investigated whether sleep deprivation would impair the extinction of previously established conditioning between the drug effect and the environmental cues. Four cohorts of male adult mice underwent a behavioral sensitization procedure pairing drug (cocaine at 15 mg/kg, i.p.) or saline with environment (open-field apparatus). the extinction of conditioned locomotion was evaluated after control (home-cage maintained) or sleep deprivation (gentle handling method for 6 h) conditions. Sleep deprivation both postponed the initiation and impaired the completeness of extinction of the conditioned locomotion promoted by previous drug-environment conditioning in cocaine-sensitized animals. While the cocaine control group required 5 free-drug sessions of exposure to the open-field apparatus to complete extinction of conditioned locomotion, the cocaine pre-treated group that experienced sleep deprivation before each extinction session still significantly differed from its respective control group on Day 5 of extinction. the possibility that the sleep condition can influence the extinction of a long-lasting association between drug effects and environmental cues can represent new outcomes for clinically relevant phenomena. (C) 2014 Elsevier Inc. All rights reserved.
- ItemSomente MetadadadosUnderstanding posttraumatic stress disorder through fear conditioning, extinction and reconsolidation(Pergamon-Elsevier Science Ltd, 2016) Careaga, Mariella Bodemeier Loayza [UNIFESP]; Girardi, Carlos Eduardo Neves [UNIFESP]; Suchecki, Deborah [UNIFESP]Careaga MBL, Girardi CEN, Suchecki D. Understanding posttraumatic stress disorder through fear conditioning, extinction and reconsolidation. NEUROSCI BIOBEHAV REV - Posttraumatic stress disorder (PTSD) is a psychopathology characterized by exacerbation of fear response. A dysregulated fear response may be explained by dysfunctional learning and memory, a hypothesis that was proposed decades ago. A key component of PTSD is fear conditioning and the study of this phenomenon in laboratory has expanded the understanding of the underlying neurobiological changes in PTSD. Furthermore, traumatic memories are strongly present even years after the trauma and maintenance of this memory is usually related to behavioral and physiological maladaptive responses. Persistence of traumatic memory may be explained by a dysregulation of two memory processes: extinction and reconsolidation. The former may explain the over-expression of fear responses as an imbalance between traumatic and extinction memory. The latter, in turn, explains the maintenance of fear responses as a result of enhancing trauma-related memories. Thus, this review will discuss the importance of fear conditioning for the establishment of PTSD and how failure in extinction or abnormal reconsolidation may contribute to the maintenance of fear response overtime. (C) 2016 Elsevier Ltd. All rights reserved.