ArticleBMC neuroscience2013
Working memory- and anxiety-related behavioral effects of repeated nicotine as a stressor: the role of cannabinoid receptors.
Article in BMC neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 20 citations in OpenAlex.
- Interrelated involvement of the endocannabinoid/endovanilloid (TRPV1) systems and epigenetic processes in anxiety- and working memory impairment-related behavioural effects of nicotine as a stressor.Addiction biology · 2024Article
- Recent Studies on the Development of Nicotine Abuse and Behavioral Changes Induced by Chronic Stress Depending on Gender.Brain sciences · 2023Review
- Article
- SAHA Improves Depressive Symptoms, Cognitive Impairment and Oxidative Stress: Rise of a New Antidepressant Class.Neurochemical research · 2021Article
- Nicotine sensitization (Part 2): Time spent in the centre of an open field sensitizes to repeated nicotine into the drug-free state in female rats.Psychopharmacology · 2021Article
- Behavioral and Biochemical Interaction Between Nicotine and Chronic Unpredictable Mild Stress in Mice.Molecular neurobiology · 2017Article
- Article
- Combined effects of marijuana and nicotine on memory performance and hippocampal volume.Behavioural brain research · 2015Article
- New Insights into the Mechanisms of Action of Cotinine and its Distinctive Effects from Nicotine.Neurochemical research · 2015Review
- Cotinine halts the advance of Alzheimer's disease-like pathology and associated depressive-like behavior in Tg6799 mice.Frontiers in aging neuroscience · 2014Article
- Physical exercise prevents stress-induced activation of granule neurons and enhances local inhibitory mechanisms in the dentate gyrus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
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1 author at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundLike emotional symptoms such as anxiety, modulations in working memory are among the frequently-reported but controversial psychiatric symptoms associated with nicotine (NC) administration. In the present study, repeated NC-induced modulations in working memory, along with concurrently-observed anxiety-related behavioral alterations, were investigated in mice, and compared with the effects of a typical cognition-impairing stressor, immobilization stress (IM). Furthermore, considering the structural and functional contributions of brain cannabinoid (CB) receptors in NC-induced psychiatric symptoms including emotional symptoms, the interactive effects of brain CB receptor ligands (CB ligands) and NC and/or IM on the working memory- and anxiety-related behaviors were examined.
resultsStatistically significant working memory impairment-like behavioral alterations in the Y-maze test and anxiety-like behavioral alterations in the elevated plus-maze (EPM) test were observed in the groups of mice treated with 0.8 mg/kg NC (subcutaneous (s.c.) 0.8 mg/kg treatment, 4 days) and/or IM (10 min treatment, 4 days). In the group of mice treated with NC plus IM (NC-IM group), an enhancement of the behavioral alterations was observed. Among the CB type 1 (CB1) antagonist AM 251 (AM), the non-selective CB agonist CP 55,940 (CP), and the CB1 partial agonist/antagonist virodhamine (VD), significant recovering effects were provided by AM (0.2-2.5 mg/kg) and VD (5 mg/kg) against the working memory impairment-like behaviors, whereas significant anxiolytic-like effects (recoveries from both attenuated percentage of entries into open arms and attenuated percentage of time spent on open arms) were provided by VD (1-10 mg/kg) and CP (2 mg/kg) against the anxiety-like behaviors.
conclusionsAlthough working memory impairment- and anxiety-like behavioral alterations were commonly induced in the NC, IM, and NC-IM groups and the therapeutic involvement of CB receptors was shown, there were discrepancies in the types of effective CB ligands between the working memory- and anxiety-related behaviors. The differential involvements of CB receptor subtypes and indirectly activated neurotransmitter systems may contribute to these discrepancies.
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