Interactive effects of morphine and nicotine on memory function depend on the central amygdala cannabinoid CB1 receptor function in rats
| Autor: | Sakineh Alijanpour, Ameneh Rezayof, Fatemeh Tirgar, Nima Yazdanbakhsh |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
Male
0301 basic medicine Agonist AM251 Nicotine Cannabinoid receptor medicine.drug_class medicine.medical_treatment Amnesia Pharmacology 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Receptor Cannabinoid CB1 Memory Avoidance Learning medicine Animals Arachidonylcyclopropylamide Rats Wistar Biological Psychiatry Dose-Response Relationship Drug Morphine business.industry Central Amygdaloid Nucleus 030104 developmental biology chemistry Cannabinoid medicine.symptom business psychological phenomena and processes 030217 neurology & neurosurgery Central Nervous System Agents medicine.drug |
| Zdroj: | Progress in Neuro-Psychopharmacology and Biological Psychiatry. 82:62-68 |
| ISSN: | 0278-5846 |
| Popis: | The present study investigated the possible involvement of the central amygdala (CeA) cannabinoid receptors type-1 (CB1Rs) in the interactive effects of morphine and nicotine on memory formation in a passive avoidance learning task. Our results showed that systemic administration of morphine (3 and 6mg/kg, s.c.) immediately after training phase impaired memory consolidation and induced amnesia. Administration of nicotine (0.3 and 0.6mg/kg, s.c.) before testing phase significantly restored morphine-induced amnesia, suggesting a cross state-dependent learning between morphine and nicotine. The results showed that while the administration of the lower dose of nicotine (0.1mg/kg, s.c.) per se did not induce a significant effect on morphine-induced amnesia, intra-CeA injection of arachidonylcyclopropylamide (ACPA), a cannabinoid CB1 receptor agonist (3 and 4ng/rat), significantly potentiated the nicotine response. Furthermore, the blockade of the CeA cannabinoid CB1 receptors by the injection of AM251 (0.75 and 1ng/rat) reversed the potentiative effect of nicotine (0.6mg/kg, s.c.) on morphine-induced amnesia. It should be considered that bilateral injection of the same doses of ACPA or AM251 (0.5-1ng/rat) into the CeA by itself had no effect on morphine response in a passive avoidance learning task. Confirmed by the cubic interpolation planes, the dose-response data revealed a cross-state-dependent learning between morphine and nicotine which may be mediated by the CeA endocannabinoid system via CB1 receptors. |
| Databáze: | OpenAIRE |
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