AKT Signaling within the Ventral Tegmental Area Regulates Cellular and Behavioral Responses to Stressful Stimuli
Open accessAbstract
Background The neurobiological mechanisms by which only a minority of stress-exposed individuals develop psychiatric diseases remain largely unknown. Recent evidence suggests that dopaminergic neurons of the ventral tegmental area (VTA) play a key role in the manifestation of stress vulnerability.Methods Using a social defeat paradigm, we segregated susceptible mice (socially avoidant) from unsusceptible mice (socially interactive) and examined VTA punches for changes in neurotrophic signaling. Employing a series of viral vectors, we sought to causally implicate these neurotrophic changes in the development of avoidance behavior.Results Susceptibility to social defeat was associated with a significant reduction in levels of active/phosphorylated AKT (thymoma viral proto-oncogene) within the VTA, whereas chronic antidepressant treatment (in mice and humans) increased active AKT levels. This defeat-induced reduction in AKT activation in susceptible mice was both necessary and sufficient to recapitulate depressive behaviors associated with susceptibility. Pharmacologic reductions in AKT activity also significantly raised the firing frequency of VTA dopamine neurons, an important electrophysiologic hallmark of the susceptible phenotype.Conclusions These studies highlight a crucial role for decreases in VTA AKT signaling as a key mediator of the maladaptive cellular and behavioral response to chronic stress.
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Self-citation
- Authors
- Krishnan, V., Han, M.-H., Mazei-Robison, M., Iñiguez, S. D., Ables, J. L., Vialou, V., Berton, O., Ghose, S., Covington, H. E., Wiley, M. D., Henderson, R. P., Neve, R. L., Eisch, A. J., Tamminga, C. A., Russo, S. J., Bolaños, C. A., & Nestler, E. J.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Florida State University (US)
- Harvard University (US)
- ORCID
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2008-10
- Volume
- 64
- Issue
- 8
- Pages
- 691-700
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC2742561
- OpenAlex
- W1972601515
- Cited by
- 176
- References
- 53
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 5 · 2023: 10 · 2022: 14 · 2021: 6 · 2020: 8 · 2019: 11 · 2018: 2 · 2017: 15 · 2016: 7 · 2015: 8 · 2014: 14 · 2013: 12 · 2012: 13
- FWCI
- 6.34
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- AstraZeneca
- National Alliance for Research on Schizophrenia and Depression
- National Institute of Mental Health
- National Institute on Drug Abuse
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- Akt signaling, ventral tegmental area, social defeat, stress vulnerability, depression, dopaminergic neurons, neurotrophic signaling, antidepressant treatment, avoidance behavior, chronic stress, social avoidance
- MeSH terms
- Proto-Oncogene Mas, Adaptation, Psychological, Analysis of Variance, Animals, Antidepressive Agents, Avoidance Learning, Depressive Disorder, Disease Models, Animal, Dominance-Subordination, Escape Reaction, Humans, Male, Mice, Inbred C57BL, Social Behavior, Stress, Psychological, Down-Regulation, Rats, Sprague-Dawley, Ventral Tegmental Area, Statistics, Nonparametric, Immobility Response, Tonic, Proto-Oncogene Proteins c-akt, Mice, Rats, In Vitro Techniques
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