Enhancing VTA Cav1.3 L-type Ca2+ channel activity promotes cocaine and mood-related behaviors via overlapping AMPA receptor mechanisms in the nucleus accumbens
Open accessAbstract
Genetic factors significantly influence susceptibility for substance abuse and mood disorders. Rodent studies have begun to elucidate a role of Ca v 1.3 L-type Ca 2+ channels in neuropsychiatric-related behaviors, such as addictive and depressive-like behaviors. Human studies have also linked the CACNA1D gene, which codes for the Ca v 1.3 protein, with bipolar disorder. However, the neurocircuitry and the molecular mechanisms underlying the role of Ca v 1.3 in neuropsychiatric phenotypes are not well established. In the present study, we directly manipulated Ca v 1.3 channels in Ca v 1.2 dihydropyridine insensitive mutant mice and found that ventral tegmental area (VTA) Ca v 1.3 channels mediate cocaine-related and depressive-like behavior through a common nucleus accumbens (NAc) shell calcium-permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (CP-AMPAR) mechanism that requires GluA1 phosphorylation at S831. Selective activation of VTA Ca v 1.3 with (±)-BayK-8644 (BayK) enhanced cocaine conditioned place preference and cocaine psychomotor activity while inducing depressive-like behavior, an effect not observed in S831A phospho-mutant mice. Infusion of the CP-AMPAR-specific blocker Naspm into the NAc shell reversed the cocaine and depressive-like phenotypes. In addition, activation of VTA Ca v 1.3 channels resulted in social behavioral deficits. In contrast to the cocaine- and depression-related phenotypes, GluA1/A2 AMPARs in the NAc core mediated social deficits, independent of S831-GluA1 phosphorylation. Using a candidate gene analysis approach, we also identified single-nucleotide polymorphisms in the CACNA1D gene associated with cocaine dependence in human subjects. Together, our findings reveal novel, overlapping mechanisms through which VTA Ca v 1.3 mediates cocaine-related, depressive-like and social phenotypes, suggesting that Ca v 1.3 may serve as a target for the treatment of neuropsychiatric symptoms.
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Increased ventral tegmental area Cav1.3 channel activity enhances anhedonia and social-behavior deficits.
“Increased VTA Cav1.3 channel activity enhances anhedonia and social-behavior deficits [56]”
From The molecular and cellular mechanisms of depression: a focus on reward circuitry (2019) · cites this paper as [56]
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The molecular and cellular mechanisms of depression: a focus on reward circuitry
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- Authors
- Martínez-Rivera, A., Hao, J., Tropea, T. F., Giordano, T. P., Kosovsky, M., Rice, R. C., Lee, A., Huganir, R. L., Striessnig, J., Addy, N. A., Han, S., & Rajadhyaksha, A. M.
- Affiliations
- Weill Cornell Medicine (US)
- University of Iowa (US)
- Johns Hopkins University (US)
- Universität Innsbruck (AT)
- Yale University (US)
- Cornell University (US)
- Corresponding author
- Han, S
- Rajadhyaksha, A M
- ORCID
- Venue
- Molecular Psychiatry
- Published
- 2017-02-14
- Volume
- 22
- Issue
- 12
- Pages
- 1735-1745
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC5555837
- OpenAlex
- W2587893207
- Cited by
- 55
- References
- 81
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 7 · 2023: 5 · 2022: 12 · 2021: 6 · 2020: 7 · 2019: 4 · 2018: 5 · 2017: 5
- FWCI
- 2.81
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Johns Hopkins University
- Austrian Science Fund
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (R01AA022994, U10AA008401)
- National Heart, Lung, and Blood Institute (R01HL087120)
- National Institute on Drug Abuse (R01DA029122, R21DA038048, R21DA023686, R01DA013423)
- National Human Genome Research Institute (U01HG004422, U01HG004446, U01HG004438, HHSN268200782096C)
- National Cancer Institute (P01CA089392)
- National Institute on Deafness and Other Communication Disorders (R01DC009433)
- National Institute of Neurological Disorders and Stroke (R01NS084190)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- Cav1.3 L-type calcium channel, CACNA1D, ventral tegmental area, nucleus accumbens shell, cocaine conditioned place preference, depression-like behavior, social behavior deficits, Bay K 8644, single nucleotide polymorphisms, cocaine dependence, bipolar disorder, substance abuse, mood disorders
- MeSH terms
- Affect, Animals, Cocaine, Conditioning, Psychological, Depression, Disease Models, Animal, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Motor Activity, Nucleus Accumbens, Social Behavior, Ventral Tegmental Area, Receptors, AMPA, Dopamine Uptake Inhibitors, Cocaine-Related Disorders, Calcium Channels, L-Type, Genetic Association Studies, Post-Synaptic Density
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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