Multiple Nicotinic Acetylcholine Receptor Subtypes in the Mouse Amygdala Regulate Affective Behaviors and Response to Social Stress
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Electrophysiological and neurochemical studies implicate cholinergic signaling in the basolateral amygdala (BLA) in behaviors related to stress. Both animal studies and human clinical trials suggest that drugs that alter nicotinic acetylcholine receptor (nAChR) activity can affect behaviors related to mood and anxiety. Clinical studies also suggest that abnormalities in cholinergic signaling are associated with major depressive disorder, whereas pre-clinical studies have implicated both β2 subunit-containing (β2*) and α7 nAChRs in the effects of nicotine in models of anxiety- and depression-like behaviors. We therefore investigated whether nAChR signaling in the amygdala contributes to stress-mediated behaviors in mice. Local infusion of the non-competitive non-selective nAChR antagonist mecamylamine or viral-mediated downregulation of the β2 or α7 nAChR subunit in the amygdala all induced robust anxiolytic- and antidepressant-like effects in several mouse behavioral models. Further, whereas α7 nAChR subunit knockdown was somewhat more effective at decreasing anxiety-like behavior, only β2 subunit knockdown decreased resilience to social defeat stress and c-fos immunoreactivity in the BLA. In contrast, α7, but not β2, subunit knockdown effectively reversed the effect of increased ACh signaling in a mouse model of depression. These results suggest that signaling through β2* nAChRs is essential for baseline excitability of the BLA, and a decrease in signaling through β2 nAChRs alters anxiety- and depression-like behaviors even in unstressed animals. In contrast, stimulation of α7 nAChRs by acetylcholine may mediate the increased depression-like behaviors observed during the hypercholinergic state observed in depressed individuals.
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Knockdown of either α7 or β2 nAChR subunits in the BLA decreases cFos immunoreactivity and attenuates avoidance of anxiogenic stimuli, immobility in response to inescapable stress, and avoidance after social defeat.
“knockdown of either α7 or β2 nAChR subunits in BLA decreases cFos immunoreactivity in the structure and attenuates avoidance of anxiogenic stimuli, immobility in response to inescapable stress, and avoidance after social defeat (Mineur et al. 2016).”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Mineur et al. 2016
In the section on downregulation of α7 and β2* receptors, both knockdowns reduced dark-compartment time and tail-suspension immobility. But only β2 knockdown significantly reduced c-fos immunoreactivity and increased social interaction after social defeat; α7 knockdown did neither. The claim incorrectly extends those two effects to both subunits. (LLM, conf=0.90)
Experimental — accuracy not yet measuredInfusion of mecamylamine into the BLA decreases stress-induced immobility.
“Infusion of the broad nAChR antagonist mecamylamine into the BLA decreases stress-induced immobility”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Mineur et al. 2016
In animal studies, the α7 subtype nAChR modifies anxiolytic behavior.
“In animal studies, the α7 subtype nAChR modifies anxiolytic behavior”
Cholinergic signaling in the amygdala is necessary for social recognition, social memory formation, social stress responsivity, and fear learning.
“Cholinergic signaling in the amygdala is necessary for social recognition [56], social memory formation [57,58], social stress responsivity [59] and fear learning [60].”
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“…mecamylamine and the partial agonist cytisine are both effective in mouse models of antidepressant efficacy and converge to decrease neuronal activity in the basolateral amygdala (BLA) (Mineur et al, 2007), a brain region that is often hyperactivated in depressed patients (Drevets et al, 2008).”
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- Authors
- Mineur, Y. S., Fote, G. M., Blakeman, S., Cahuzac, E. L. M., Newbold, S. A., & Picciotto, M. R.
- Affiliations
- Yale University (US)
- Corresponding author
- Picciotto, Marina R
- Venue
- Neuropsychopharmacology
- Published
- 2015-10-16
- Volume
- 41
- Issue
- 6
- Pages
- 1579-1587
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC4832019
- OpenAlex
- W2334642065
- Cited by
- 90
- References
- 51
- Citations by year
- 2026: 5 · 2025: 11 · 2024: 5 · 2023: 11 · 2022: 9 · 2021: 11 · 2020: 9 · 2019: 6 · 2018: 10 · 2017: 8 · 2016: 5
- FWCI
- 3.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (DA033945)
- National Institute of Mental Health (MH077681, MH105824, R03MH105824, R01MH077681)
- National Institute on Drug Abuse (R01DA037566, P50DA033945, DA033945)
- Office of Research on Women's Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- nicotinic acetylcholine receptors, basolateral amygdala, beta2 nAChR, alpha7 nAChR, social defeat stress, anxiety-like behavior, depression-like behavior, mecamylamine, cholinergic neurotransmission, c-fos, major depressive disorder, stress resilience
- MeSH terms
- Amygdala, Animals, Male, Mecamylamine, Mice, Inbred C57BL, Physostigmine, Receptors, Nicotinic, Stress, Psychological, Signal Transduction, Mice, Knockout, Nicotinic Antagonists, Mice, alpha7 Nicotinic Acetylcholine Receptor
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