Navegando por Palavras-chave "emotional memory"

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    Effects of nociceptin/orphanin FQ in the acquisition of contextual and tone fear conditioning in rats
    (Amer Psychological Assoc, 2008-02-01) Fornari, Raquel V. [UNIFESP]; Soares, Juliana C. K. [UNIFESP]; Ferreira, Tatiana L. [UNIFESP]; Moreira, Karin M. [UNIFESP]; Oliveira, Maria G. M. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Nociceptin, or orphanin FQ (N/OFQ), the endogenous ligand of NOP receptors, is known to regulate learning and memory processes. To verify the role of N/OFQ in the acquisition of contextual (CFC) and tone fear conditioning (TFC), Wistar male rats received intracerebroventricular injections of N/OFQ (0.1-5.0 nmol) before training, and were tested 24 and 48 hr later to access the freezing response to context and tone, respectively. the intermediate doses (1.0 and 2.5 nmol) impaired the CFC test, sparing TFC. the highest dose (5.0 nmol) reduced freezing during both tests, a result that may be due to nonspecific effects. the posttraining injection of N/OFQ (1 or 5 nmol) did not interfere with CFC and TFC, suggesting a specific effect of the peptide in acquisition processes. Moreover, the impairment observed with N/OFQ (1 nmol) in CFC cannot be attributed to a state-dependent learning because it was not reversed by its pretest administration. the data support the negative role of N/OFQ in the acquisition of aversively motivated tasks, which encompass a spatial component and depend on the hippocampus.
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    Hippocampal NMDA receptor blockade impairs CREB phosphorylation in amygdala after contextual fear conditioning
    (Wiley-Blackwell, 2013-07-01) Oliveira Coelho, Cesar Augusto de [UNIFESP]; Ferreira, Tatiana Lima; Kramer Soares, Juliana Carlota [UNIFESP]; Menezes Oliveira, Maria Gabriela [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    In contextual fear conditioning (CFC), hippocampus is thought to process environmental stimuli into a configural representation of the context and send it to amygdala nuclei, which current evidences point to be the site of CS-US association and fear memory storage. If it is true, hippocampus should influence learning-induced plasticity in the amygdala nuclei after CFC acquisition. To test this, we infused wistar rats with saline or AP5, a NMDA receptor antagonist, in the dorsal hippocampus just before a CFC session, in which they were conditioned to a single shock, exposed to the context with no shocks or received an immediate shock. the rats were perfused, their brains harvested and immunohistochemically stained for cAMP element binding protein (CREB) phosphorylation ratio (pCREB/CREB) in lateral (LA), basal (B) and central (CeA) amygdala nuclei. CFC showed a learning-specific increase in pCREB ratio in B and CeA, in conditioned-saline rats compared to context and immediate shocked ones. Further, conditioned rats that received AP5 showed a decrease in pCREB ratio in LA, B and CeA. Our results support the current ideas that the role of hippocampus in contextual fear conditioning occurs by sending contextual information to amygdala to serve as conditioned stimulus. (c) 2013 Wiley Periodicals, Inc.
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    Modafinil Prevents Inhibitory Avoidance Memory Deficit Induced by Sleep Deprivation in Rats
    (Amer Acad Sleep Medicine, 2010-07-01) Moreira, Karin Monteiro [UNIFESP]; Ferreira, Tatiana Lima [UNIFESP]; Hipólide, Débora Cristina [UNIFESP]; Fomari, Raquel Vecchio [UNIFESP]; Tufik, Sergio [UNIFESP]; Menezes Oliveira, Maria Gabriela [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade Federal do ABC (UFABC); Univ Groningen, Univ Med Ctr Groningen
    Study Objectives: Evaluation of modafinil effects on the inhibitory avoidance task (IA).Design: Rats were trained on a multiple trial IA task after receiving modafinil or vehicle injections. In experiment 1 they were trained with a weak protocol under baseline condition and in experiment 2, with a stronger protocol under sleep-deprivation condition.Results: In experiment 1 modafinil improved rats' acquisition whereas the retention test remained unaffected. In Experiment 2 modafinil did not interfere with training performance, but the lower dose prevented the retention impairment in sleep-deprived animals.Conclusions: Modafinil is able to improve acquisition in normal rats and reverse the long-term memory impairment induced by sleep-deprivation.
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    Neuroleptic Drugs Revert the Contextual Fear Conditioning Deficit Presented by Spontaneously Hypertensive Rats: A Potential Animal Model of Emotional Context Processing in Schizophrenia?
    (Oxford Univ Press, 2009-07-01) Calzavara, Mariana Bendlin [UNIFESP]; Medrano, Wladimir Agostini [UNIFESP]; Levin, Raquel [UNIFESP]; Kameda, Sonia Regina [UNIFESP]; Andersen, Monica Levy [UNIFESP]; Tufik, Sergio [UNIFESP]; Silva, Regina Helena; Frussa-Filho, Roberto [UNIFESP]; Abilio, Vanessa Costhek [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Fed Rio Grande do Norte
    Schizophrenia, bipolar disorder, and attention deficit/hyperactivity disorder (ADHD) present abnormalities in emotion processing. A previous study showed that the spontaneously hypertensive rats (SHR), a putative animal model of ADHD, present reduced contextual fear conditioning (CFC). the aim of the present study was to characterize the deficit in CFC presented by SHR. Adult male normotensive Wistar rats and SHR were submitted to the CFC task. Sensitivity of the animals to the shock and the CFC performance after repeated exposure to the task were investigated. Pharmacological characterization consisted in the evaluation of the effects of the following drugs administered previously to the acquisition of the CFC: pentylenetetrazole (anxiogenic) and chlordiazepoxide (anxiolytic); methylphenidate and amphetamine (used for ADHD); lamotrigine, carbamazepine, and valproic acid (mood stabilizers); haloperidol, ziprasidone, risperidone, amisulpride, and clozapine (neuroleptic drugs); metoclopramide and SCH 23390 (dopamine antagonists without antipsychotic properties); and ketamine (a psychotomimmetic). the effects of paradoxical sleep deprivation (that worsens psychotic symptoms) and the performance in a latent inhibition protocol (an animal model of schizophrenia) were also verified. No differences in the sensitivity to the shock were observed. the repeated exposure to the CFC task did not modify the deficit in CFC presented by SHR. Considering pharmacological treatments, only the neuroleptic drugs reversed this deficit. This deficit was potentiated by proschizophrenia manipulations. Finally, a deficit in latent inhibition was also presented by SHR. These findings suggest that the deficit in CFC presented by SHR could be a useful animal model to study abnormalities in emotional context processing related to schizophrenia.