AMPA receptors mediate passive avoidance deficits induced by sleep deprivation
Autor: | José N. Nobrega, Francisco Paulino Dubiela, Karin M. Moreira, Sergio Tufik, Luciane V. Sita, Débora Cristina Hipólide, Claudio Marcos Teixeira de Queiroz |
---|---|
Rok vydání: | 2013 |
Předmět: |
Male
medicine.medical_specialty Time Factors Passive avoidance task Hippocampus In situ hybridization AMPA receptor Hippocampal formation Tritium Benzodiazepines Behavioral Neuroscience GYKI-52466 Internal medicine Avoidance Learning medicine Animals Receptors AMPA Rats Wistar Nootropic Agents Analysis of Variance Learning Disabilities musculoskeletal neural and ocular physiology Antagonist ANATOMIA Sleep in non-human animals Pyrrolidinones Aniracetam Rats Sleep deprivation Endocrinology Gene Expression Regulation nervous system Sleep Deprivation medicine.symptom Psychology Excitatory Amino Acid Antagonists Neuroscience Protein Binding medicine.drug |
Zdroj: | Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual) Universidade de São Paulo (USP) instacron:USP Repositório Institucional da UFRN Universidade Federal do Rio Grande do Norte (UFRN) instacron:UFRN |
ISSN: | 0166-4328 |
Popis: | The present study addressed the effects of sleep deprivation (SD) on AMPA receptor (AMPAR) binding in brain regions associated with learning and memory, and investigated whether treatment with drugs acting on AMPAR could prevent passive avoidance deficits in sleep deprived animals. [(3)H]AMPA binding and GluR1 in situ hybridization signals were quantified in different brain regions of male Wistar rats either immediately after 96 h of sleep deprivation or after 24h of sleep recovery following 96 h of sleep deprivation. Another group of animals were sleep deprived and then treated with either the AMPAR potentiator, aniracetam (25, 50 and 100mg/kg, acute administration) or the AMPAR antagonist GYKI-52466 (5 and 10mg/kg, acute and chronic administration) before passive avoidance training. Task performance was evaluated 2h and 24h after training. A significant reduction in [(3)H]AMPA binding was found in the hippocampal formation of SD animals, while no alterations were observed in GluR1 mRNA levels. The highest dose of aniracetam (100mg/kg) reverted SD-induced impairment of passive avoidance performance in both retention tests, whereas GYKI-52466 treatment had no effect. Pharmacological enhancement of AMPAR function may revert hippocampal-dependent learning impairments produced after SD. We argue that such effects might be associated with reduced AMPAR binding in the hippocampus of sleep deprived animals. |
Databáze: | OpenAIRE |
Externí odkaz: |