N-methyl-D-aspartate receptors and protein synthesis are necessary for reinstatement of conditioned fear
Autor: | Norio Matsuki, Hikaru Igarashi, Huilian Shen, Natsuko Imamura, Hiroshi Nomura |
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Rok vydání: | 2013 |
Předmět: |
Male
medicine.drug_class Pharmacology Receptors N-Methyl-D-Aspartate Extinction Psychological chemistry.chemical_compound Mice Neurochemical Cannabinoid receptor type 1 Conditioning Psychological medicine Animals Anisomycin Protein Synthesis Inhibitors Benzodiazepine Behavior Animal business.industry General Neuroscience Classical conditioning Extinction (psychology) Fear Mice Inbred C57BL chemistry Protein Biosynthesis NMDA receptor business Diazepam psychological phenomena and processes medicine.drug |
Zdroj: | Neuroreport. 24(14) |
ISSN: | 1473-558X |
Popis: | Conditioned fear is extinguished if a conditioned animal receives the conditioned stimulus without an unconditioned stimulus. The extinguished fear response can be reinstated after the animal experiences a mild unconditioned stimulus. Although extensive studies on the neuronal circuitry and neurochemical mechanisms leading to fear acquisition and extinction have been carried out, few studies have focused on reinstatement. In this study, we investigated the effects of N-methyl-D-aspartic acid receptor (NMDAR) antagonists, protein synthesis inhibitors, cannabinoid receptor type 1 (CB1R) antagonists, and benzodiazepine on reinstatement of conditioned fear in mice. An intraperitoneal injection of the NMDAR antagonist MK-801 or the protein synthesis inhibitor anisomycin before the reminder shock attenuated fear reinstatement tested the next day. However, anisomycin had no effect on fear reinstatement tested 2 h after the reminder shock. CB1R antagonists, SR141716, and a benzodiazepine, diazepam, had no effect on fear reinstatement. These results suggested that NMDAR and protein synthesis-dependent plasticity contributed toward the reinstatement of conditioned fear and that protein synthesis was involved in consolidation of reinstated fear. |
Databáze: | OpenAIRE |
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