ArticleBiochemical pharmacology2015
α2-Null mutant mice have altered levels of neuronal activity in restricted midbrain and limbic brain regions during nicotine withdrawal as demonstrated by cfos expression.
Article in Biochemical pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Deletion or enhancement of alpha-2 nAChRs (Chrna2) induces unique lifespan behavioral deficits.Neuropharmacology · 2026Article
- Functions and pharmacology of α2β2 nicotinic acetylcholine receptors; in and out of the shadow of α4β2 nicotinic acetylcholine receptors.Biochemical pharmacology · 2024Article
- A neuronal coping mechanism linking stress-induced anxiety to motivation for reward.Science advances · 2023Article
- Expression of Chrna9 is regulated by Tbx3 in undifferentiated pluripotent stem cells.Scientific reports · 2023Article
- Dynamic activity of interpeduncular nucleus GABAergic neurons controls expression of nicotine withdrawal in male mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Article
- Increased Response to 3,4-Methylenedioxymethamphetamine (MDMA) Reward and Altered Gene Expression in Zebrafish During Short- and Long-Term Nicotine Withdrawal.Molecular neurobiology · 2021Article
- Nicotinic Acetylcholine Receptor Accessory Subunits Determine the Activity Profile of Epibatidine Derivatives.Molecular pharmacology · 2020Article
- Abrogation of atypical neurogenesis and vascular-derived EphA4 prevents repeated mild TBI-induced learning and memory impairments.Scientific reports · 2020Article
- Maternal overnutrition programs hedonic and metabolic phenotypes across generations through sperm tsRNAs.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Cholinergic regulation of mood: from basic and clinical studies to emerging therapeutics.Molecular psychiatry · 2019Review
- α2* Nicotinic acetylcholine receptors influence hippocampus-dependent learning and memory in adolescent mice.Learning & memory (Cold Spring Harbor, N.Y.) · 2017Article
- Multiple Nicotinic Acetylcholine Receptor Subtypes in the Mouse Amygdala Regulate Affective Behaviors and Response to Social Stress.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Neuronal nicotinic acetylcholine receptors (nAChRs) are the primary binding sites for nicotine within the brain. Using alpha(α)2 nAChR subunit-null mutant mice, the current study evaluates whether the absence of this gene product during mecamylamine-precipitated nicotine withdrawal eliminates neuronal activity within selective midbrain and limbic brain regions, as determined by the expression of the immediate early gene, cfos. Our results demonstrate that nicotine withdrawal enhances neuronal activity within the interpeduncular nucleus and dorsal hippocampus, which is absent in mice null for α2-containing nAChRs. In contrast, we observe that α2-null mutant mice exhibit a suppression of neuronal activity in the dentate gyrus in mice undergoing nicotine withdrawal. Interestingly, α2-null mutant mice display potentiated neuronal activity specifically within the stratum lacunosum moleculare layer of the hippocampus, independent of nicotine withdrawal. Overall, our findings demonstrate that α2-null mutant mice have altered cfos expression in distinct populations of neurons within selective midbrain and limbic brain structures that mediate baseline and nicotine withdrawal-induced neuronal activity.
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