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Cited by 68Nicotinic Acetylcholine Receptors StudySmoking Behavior and CessationNeuroscience and Neuropharmacology Research

Targeted Deletion of the Mouse α2 Nicotinic Acetylcholine Receptor Subunit Gene (Chrna 2) Potentiates Nicotine-Modulated Behaviors

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Lotfipour, Shahrdad, Byun, Janet S., Leach, Prescott, Fowler, Christie D., Murphy, Niall P., Kenny, Paul J., Gould, Thomas J., Boulter, Jim·2013·The Journal of Neuroscience
DOI 10.1523/jneurosci.4731-12.2013PMC PMC3831006
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Abstract

Baseline and nicotine-modulated behaviors were assessed in mice harboring a null mutant allele of the nicotinic acetylcholine receptor (nAChR) subunit gene α2 (Chrna 2). Homozygous Chrna 2−/−mice are viable, show expected sex and Mendelian genotype ratios, and exhibit no gross neuroanatomical abnormalities. A broad range of behavioral tests designed to assess genotype-dependent effects on anxiety (elevated plus maze and light/dark box), motor coordination (narrow bean traverse and gait), and locomotor activity revealed no significant differences between mutant mice and age-matched wild-type littermates. Furthermore, a panel of tests measuring traits, such as body position, spontaneous activity, respiration, tremors, body tone, and startle response, revealed normal responses for Chrna 2-null mutant mice. However,Chrna 2−/−mice do exhibit a mild motor or coordination phenotype (a decreased latency to fall during the accelerating rotarod test) and possess an increased sensitivity to nicotine-induced analgesia in the hotplate assay. Relative to wild-type,Chrna 2−/−mice show potentiated nicotine self-administration and withdrawal behaviors and exhibit a sex-dependent enhancement of nicotine-facilitated cued, but not trace or contextual, fear conditioning. Overall, our results suggest that loss of the mouse nAChR α2 subunit has very limited effects on baseline behavior but does lead to the potentiation of several nicotine-modulated behaviors.

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  • α2 knockout mice self-administer larger doses of nicotine than wild-type controls.

    “α2 KO mice also self-administer higher doses of nicotine than WT controls (Lotfipour et al. 2013).”

    From Nicotine Withdrawal (2015) · cites this paper as Lotfipour et al. 2013

    The Results (Food and nicotine reinforcement; page not provided) report enhanced self-administration by α2 knockout mice during the first two days of acquisition and at the highest dose tested (0.4 mg/kg/infusion). The unqualified comparison overstates the finding: the paper reports no significant overall genotype effect during acquisition or across the four-dose response test. (LLM, conf=0.86)

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  • α2 knockout mice show more somatic withdrawal symptoms in novel environments but no somatic withdrawal signs in habituated environments.

    “α2 KO mice exhibit more somatic symptoms of withdrawal in novel environments (Lotfipour et al. 2013), but display no somatic signs of withdrawal in habituated environments (i.e., the home cage) (Salas et al. 2009).”

    From Nicotine Withdrawal (2015) · cites this paper as Lotfipour et al. 2013

  • In male mice, deletion of Chrna2 causes withdrawal-induced deficits in cued fear conditioning.

    “In male mice, Chrna2 deletion also produces nicotine withdrawal-induced deficits of cued FC (Lotfipour et al. 2013).”

    From Nicotine Withdrawal (2015) · cites this paper as Lotfipour et al. 2013

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Authors
Lotfipour, S., Byun, J. S., Leach, P., Fowler, C. D., Murphy, N. P., Kenny, P. J., Gould, T. J., & Boulter, J.
Affiliations
  • University of California, Los Angeles (US)
  • Temple University (US)
  • Scripps Research Institute (US)
ORCID
Venue
The Journal of Neuroscience
Publisher
Society for Neuroscience
Published
2013-05-01
Volume
33
Issue
18
Pages
7728-7741
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
DOI
10.1523/jneurosci.4731-12.2013
PMC
PMC3831006
OpenAlex
W2023768026
Cited by
68
References
62
Citations by year
2026: 4 · 2025: 2 · 2024: 5 · 2023: 6 · 2022: 5 · 2021: 1 · 2020: 7 · 2019: 4 · 2018: 5 · 2017: 5 · 2016: 4 · 2015: 10 · 2014: 8 · 2013: 2
FWCI
3.58
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Tobacco-Related Disease Research Program
  • National Alliance for Research on Schizophrenia and Depression
  • National Institute of Mental Health (T32MH017140, MH 17140)
  • National Institute on Drug Abuse (DA024787, R01DA030929, DA007237-23, R01DA024787, T32DA007237)
  • Jane and Terry Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles
  • Jonsson Cancer Center Foundation
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
nicotinic acetylcholine receptors, CHRNA2, alpha2 subunit, null mice, nicotine self-administration, nicotine withdrawal, fear conditioning, motor coordination, anxiety, locomotor activity, sex differences
MeSH terms
Analysis of Variance, Animals, Anxiety, Conditioning, Classical, Drug Administration Schedule, Escape Reaction, Exploratory Behavior, Fear, Female, Male, Mice, Inbred C57BL, Morphine, Nicotine, Psychomotor Performance, Reaction Time, Receptors, Nicotinic, Reflex, Reflex, Startle, Substance Withdrawal Syndrome, Mice, Knockout, Neurotransmitter Agents, Nicotinic Agonists, Mice

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