Navegando por Palavras-chave "inhibitory avoidance learning"

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    Cholinergic modulation of inhibitory avoidance impairment induced by paradoxical sleep deprivation
    (Elsevier B.V., 2000-05-01) Bueno, OFA; Oliveira, MGM; Lobo, L. L.; Morais, P. R.; Melo, FHM; Tufik, Sergio [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    1. Male Wister rats were submitted to paradoxical sleep deprivation for 96 hr by a modified multiple platform technique.2. Training of step-through inhibitory avoidance was performed immediately after the last day of paradoxical sleep deprivation. Twenty-four hr after training the animals were submitted to the retention test.3. in Experiment 1, pilocarpine (4 mg/kg, i.p.) or atropine (4 mg/kg, i.p.) were administered daily during. the paradoxical sleep deprivation period. Pilocarpine, but not atropine, reversed the impairment induced by PS deprivation.4. in Experiment 2, pilocarpine (4, 8 and 12 mg/kg, i.p.) was injected 1 hr before training in order to verify if the reversal of memory impairment was an effect secondary to residual enhanced blood levels of pilocarpine during training. Acute treatment with pilocarpine, in any dose, did not reverse the impairment produced by paradoxical sleep deprivation5. Activation of the cholinergic system during the period ol:deprivation is able to prevent memory deficits induced by paradoxical sleep deprivation.
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    Learning deficits induced by sleep deprivation and recovery are not associated with altered [H-3]muscimol and [H-3]flunitrazepam binding
    (Elsevier B.V., 2005-03-10) Dubiela, Francisco Paulino [UNIFESP]; Oliveira, MGM; Moreira, K. M.; Nobrega, J. N.; Tufik, S.; Hipólide, Débora Cristina [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Ctr Addict & Mental Hlth
    Several studies have shown that sleep deprivation produces deficits in learning tasks, but mechanisms underlying these effects remain unclear. Other lines of evidence indicate an involvement of brain GABA systems in cognitive processes. Here, we investigated the possibility that alterations in GABA(A) or benzodiazepine (BDZ) receptor binding might underlie avoidance deficits induced by sleep deprivation. Rats were deprived of sleep for 96 h using the platform method and then trained in a step-through inhibitory avoidance task, or allowed to recover sleep for 24 h before training (sleep rebound group). Thirty minutes after training, animals were given a retention test. Both sleep-deprived and sleep-recovered animals showed a significant impairment in avoidance responding compared to cage controls, and the sleep-deprived group performed significant worse than the sleep-recovered group. A separate group of animals was sacrificed either immediately after 96 h of sleep deprivation or after 96 h of sleep deprivation followed by 24 h of sleep recovery. [H-3]muscimol and [H-3]flunitrazepam binding were examined by quantitative autoradiography in 42 brain regions, including areas involved in cognitive processes. No significant differences among groups were found in any brain region, except for a reduction in [H-3]flunitrazepam binding in the frontal cortex of sleep-recovered animals. These results confirm the deleterious effects of sleep loss on inhibitory avoidance learning, but suggest that such deficits cannot be attributed to altered GABA(A) or BDZ binding in brain. (c) 2005 Elsevier B.V. All rights reserved.