ArticleThe European journal of neuroscience2009
Nicotine withdrawal-induced deficits in trace fear conditioning in C57BL/6 mice--a role for high-affinity beta2 subunit-containing nicotinic acetylcholine receptors.
Article in The European journal of neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 53 citations in OpenAlex.
- Neurobiological Mechanisms of Nicotine Reward and Aversion.Pharmacological reviews · 2022Review
- Rodent models for nicotine withdrawal.Journal of psychopharmacology (Oxford, England) · 2021Review
- Translational Research in Nicotine Addiction.Cold Spring Harbor perspectives in medicine · 2021Review
- Cotinine Enhances Fear Extinction and Astrocyte Survival by Mechanisms Involving the Nicotinic Acetylcholine Receptors Signaling.Frontiers in pharmacology · 2020Article
- Chronic fluoxetine ameliorates adolescent chronic nicotine exposure-induced long-term adult deficits in trace conditioning.Neuropharmacology · 2017Article
- Nicotine disrupts safety learning by enhancing fear associated with a safety cue via the dorsal hippocampus.Journal of psychopharmacology (Oxford, England) · 2017Article
- Impairment of contextual fear extinction by chronic nicotine and withdrawal from chronic nicotine is associated with hippocampal nAChR upregulation.Neuropharmacology · 2016Article
- Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction.Learning & memory (Cold Spring Harbor, N.Y.) · 2016Review
- Nicotinic modulation of hippocampal cell signaling and associated effects on learning and memory.Physiology & behavior · 2016Review
- Cognitive control deficits during mecamylamine-precipitated withdrawal in mice: Possible links to frontostriatal BDNF imbalance.Neurobiology of learning and memory · 2016Article
- Cognitive Dysfunction, Affective States, and Vulnerability to Nicotine Addiction: A Multifactorial Perspective.Frontiers in psychiatry · 2016Review
- Negative affective states and cognitive impairments in nicotine dependence.Neuroscience and biobehavioral reviews · 2015Review
- Nicotine modulation of fear memories and anxiety: Implications for learning and anxiety disorders.Biochemical pharmacology · 2015Review
- Withdrawal From Chronic Nicotine Reduces Thyroid Hormone Levels and Levothyroxine Treatment Ameliorates Nicotine Withdrawal-Induced Deficits in Hippocampus-Dependent Learning in C57BL/6J Mice.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2015Article
- Nicotine Addiction and Psychiatric Disorders.International review of neurobiology · 2015Article
- The effects of acute nicotine on contextual safety discrimination.Journal of psychopharmacology (Oxford, England) · 2014Article
- Donepezil reverses nicotine withdrawal-induced deficits in contextual fear conditioning in C57BL/6J mice.Behavioral neuroscience · 2014Article
- Involvement of neuronal β2 subunit-containing nicotinic acetylcholine receptors in nicotine reward and withdrawal: implications for pharmacotherapies.Journal of clinical pharmacy and therapeutics · 2014Review
- Chronic nicotine pretreatment is sufficient to upregulate α4* nicotinic receptors and increase oral nicotine self-administration in mice.BMC neuroscience · 2014Article
- Substance abuse, memory, and post-traumatic stress disorder.Neurobiology of learning and memory · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Nicotine alters cognitive processes that include working memory and long-term memory. Trace fear conditioning may involve working memory during acquisition while also allowing the assessment of long-term memory. The present study used trace fear conditioning in C57BL/6 mice to investigate the effects of acute nicotine, chronic nicotine and withdrawal of chronic nicotine on processes active during acquisition and recall 24 h later and to examine the nicotinic acetylcholine receptor subtypes (nAChRs) involved in withdrawal deficits in trace fear conditioning. During training, acute nicotine (0.09 mg/kg) enhanced, but chronic nicotine (6.3 mg/kg/day, 13 days) and withdrawal of chronic nicotine (6.3 mg/kg/day, 12 days) had no significant effect on, acquisition of trace conditioning. At recall, acute treatment enhanced conditioning while chronic nicotine had no effect and withdrawal of chronic nicotine resulted in deficits. Antagonist-precipitated withdrawal was used to characterize the nAChRs involved in the withdrawal deficits. The low-affinity nAChR antagonist MLA (1.5, 3 or 9 mg/kg) had no effect on trace fear conditioning, but the high-affinity nAChR antagonist DHbetaE (3 mg/kg) precipitated deficits in trace fear conditioning if administered at training or training and testing, but not if administered at testing alone. The beta2 nAChR subunit is involved in the withdrawal effects as withdrawal of chronic nicotine produced deficits in trace fear conditioning in wildtype but not in beta2-knockout mice. Thus, nicotine alters processes involved in both acquisition and long-term memory of trace fear conditioning, and high-affinity beta2 subunit-containing nAChRs are critically involved in the effects of nicotine withdrawal on trace fear conditioning.
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Registered trials
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.