Evidence map›Paper›PMID 37758936›Full record

ArticlePsychopharmacology2024

Cross state-dependent memory retrieval between tramadol and ethanol: involvement of dorsal hippocampal GABAA receptors.

Majid Jafari-Sabet, Shiva Amiri, Mohammad Sheibani, Navid Fatahi, Helia Aghamiri

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Article in Psychopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Majid Jafari-SabetRazi Drug Research Center, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. jafarisabet.m@iums.ac.ir.ORCID http://orcid.org/0000-0003-2962-5752
Shiva AmiriPharmaceutics Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.
Mohammad SheibaniRazi Drug Research Center, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Navid FatahiDepartment of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Helia AghamiriDepartment of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Iran University of Medical Sciences · IRKerman University of Medical Sciences · IR

Funding

Iran University of Medical Sciences 98-3-21-16177
6 · The paper itself

Abstract

rationaleTramadol and ethanol, as psychoactive agents, are often abused. Discovering the molecular pathways of drug-induced memory creation may contribute to preventing drug addiction and relapse.

objectiveThe tramadol- and ethanol-induced state-dependent memory (SDM) and cross-SDM retrieval between tramadol and ethanol were examined in this study. Moreover, because of the confirmed involvement of GABAA receptors and GABAergic neurotransmission in memory retrieval impairment, we assessed cross-SDM retrieval between tramadol and ethanol with a specific emphasis on the role of the GABAA receptors. The first hypothesis of this study was the presence of cross-SDM between tramadol and ethanol, and the second hypothesis was related to possible role of GABAA receptors in memory retrieval impairment within the dorsal hippocampus. The cannulae were inserted into the hippocampal CA1 area of NMRI mice, and a step-down inhibitory avoidance test was used to evaluate state dependence and memory recovery.

resultsThe post-training and/or pre-test administration of tramadol (2.5 and 5 mg/kg, i.p.) and/or ethanol (0.5 and 1 g/kg, i.p.) induced amnesia, which was restored after the administration of the drugs 24 h later during the pre-test period, proposing ethanol and tramadol SDM. The pre-test injection of ethanol (0.25 and 0.5 g/kg, i.p.) with tramadol at an ineffective dose (1.25 mg/kg) enhanced tramadol SDM. Moreover, tramadol injection (1.25 and 2.5 mg/kg) with ethanol at the ineffective dose (0.25 g/kg) promoted ethanol SDM. Furthermore, the pre-test intra-CA1 injection of bicuculline (0.0625, 0.125, and 0.25 μg/mouse), a GABAA receptor antagonist, 5 min before the injection of tramadol (5 mg/kg) or ethanol (1 g/kg) inhibited tramadol- and ethanol-induced SDM dose-dependently.

conclusionThe findings strongly confirmed cross-SDM between tramadol and ethanol and the critical role of dorsal hippocampal GABAA receptors in the cross-SDM between tramadol and ethanol.

Indexed as

TramadolAmnesiaAnimalsAvoidance LearningCA1 Region, HippocampalEthanolHippocampusMemoryMiceMice, Inbred StrainsReceptors, GABA-AEthanolReceptors, GABA-ATramadolBicucullineDorsal hippocampusEthanolMouseState-dependent memoryTramadol

Identifiers

PMID37758936
OpenAlexW4387085543

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.