ABSTRACT
We investigated the relationship between deficits in fear memory induced by sleep deprivation and pCREB expression in the basal and central nuclei of the amygdala. Sleep deprivation reduced pCREB expression in the central nucleus compared to control or sleep recovered groups, and in the basal nucleus only compared to sleep recovered group. Moreover, 24h of sleep recovery prior to training prevented changes in both pCREB expression and performance.
Subject(s)
Amygdala/metabolism , Conditioning, Psychological/physiology , Cyclic AMP Response Element-Binding Protein/metabolism , Fear/physiology , Sleep Deprivation , Animals , Immunohistochemistry , Male , Memory/physiology , Phosphorylation , Psychomotor Performance/physiology , Rats , Rats, WistarABSTRACT
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.
Subject(s)
Avoidance Learning/drug effects , Benzhydryl Compounds/pharmacology , Memory Disorders/prevention & control , Neuroprotective Agents/pharmacology , Sleep Deprivation/complications , Analysis of Variance , Animals , Behavior, Animal/drug effects , Disease Models, Animal , Male , Memory Disorders/etiology , Modafinil , Rats , Rats, WistarABSTRACT
A number of studies have suggested that the glutamatergic and cholinergic systems are both involved in learning and memory processes and that they interact in order to facilitate these processes. However, the role of M1-muscarinic receptors in mediating this interaction has not been elucidated. The aim of this study was to determine whether the concomitant administration of MK-801 (non-competitive NMDA antagonist) and dicyclomine (M1-muscarinic antagonist--DIC) in sub-effective doses impairs contextual fear conditioning (hippocampal-dependent task) and tone fear conditioning tasks (hippocampal-independent task). The results showed that concomitant pre-training administration of DIC (8.0 mg/kg) and MK-801 (0.07 mg/kg)--two sub-effectives doses for the contextual fear conditioning task--does impair the performance of animals on this task (as measured by freezing behavior time). Tone fear conditioning tasks were not affected by the drugs either administered separately or concurrently. The pre-training administration of sub-effective doses of MK-801 and DIC in combination impairs performance on contextual fear conditioning task (hippocampal-dependent), but not on tone fear conditioning task (hippocampal-independent). These data support the hypothesis that the interaction between glutamatergic and cholinergic systems in hippocampus-dependent learning and memory processes probably occurs through M1 receptor.
