Antidepressant effect of optogenetic stimulation of the medial prefrontal cortex
Open accessAbstract
Brain stimulation and imaging studies in humans have highlighted a key role for the prefrontal cortex in clinical depression; however, it remains unknown whether excitation or inhibition of prefrontal cortical neuronal activity is associated with antidepressant responses. Here, we examined cellular indicators of functional activity, including the immediate early genes (IEGs) zif268 ( egr1 ), c-fos , and arc , in the prefrontal cortex of clinically depressed humans obtained postmortem. We also examined these genes in the ventral portion of the medial prefrontal cortex (mPFC) of mice after chronic social defeat stress, a mouse model of depression. In addition, we used viral vectors to overexpress channel rhodopsin 2 (a light-activated cation channel) in mouse mPFC to optogenetically drive “burst” patterns of cortical firing in vivo and examine the behavioral consequences. Prefrontal cortical tissue derived from clinically depressed humans displayed significant reductions in IEG expression, consistent with a deficit in neuronal activity within this brain region. Mice subjected to chronic social defeat stress exhibited similar reductions in levels of IEG expression in mPFC. Interestingly, some of these changes were not observed in defeated mice that escape the deleterious consequences of the stress, i.e., resilient animals. In those mice that expressed a strong depressive-like phenotype, i.e., susceptible animals, optogenetic stimulation of mPFC exerted potent antidepressant-like effects, without affecting general locomotor activity, anxiety-like behaviors, or social memory. These results indicate that the activity of the mPFC is a key determinant of depression-like behavior, as well as antidepressant responses.
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In mice subjected to social defeat stress, optogenetic stimulation of the ventral medial PFC increased social interaction and reduced anhedonia as measured via the sucrose preference test.
“In mice subjected to social defeat stress, optogenetic stimulation of the ventral medial PFC increased social interaction and reduced anhedonia as measured via the sucrose preference test (174).”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [174]
Non-selective activation of the mPFC can reverse behavioral deficits in depression models.
“Our findings build upon prior studies showing that non-selective activation of the mPFC can reverse behavioral deficits in depression models [36–39]”
From A nucleus accumbens-projecting prefrontal cortex circuit underlies chronic social stress-induced depression-like behaviors (2026) · cites this paper as [36]
After optogenetic stimulation of the medial prefrontal cortex in susceptible mice, susceptible mice show a reduction in social avoidance similar to what has been previously observed after antidepressant treatments.
“After this manipulation in the medial prefrontal cortex, susceptible mice show a reduction in social avoidance similar to what has been previously observed after antidepressant treatments.”
From A standardized protocol for repeated social defeat stress in mice (2011) · cites this paper as [44]
Each glutamatergic projection to the NAcc from the PFC, thalamus, amygdala, and hippocampus has a distinct contribution to modulating social anhedonia following social stress.
“each of these projections has been shown to have a distinct contribution to modulating social anhedonia following social stress”
From Social functioning in major depressive disorder (2016) · cites this paper as Covington et al., 2010
Increased activity of thalamo-NAcc projections leads to increased social avoidance after social stress.
“increased activity of thalamo-NAcc projections leads to increased social avoidance after social stress”
From Social functioning in major depressive disorder (2016) · cites this paper as Covington et al., 2010
High-frequency optogenetic stimulation of the PFC-NAcc pathway reverses social avoidance.
“high-frequency optogenetic stimulation of this pathway reverses social avoidance (Covington et al., 2010;Vialou et al., 2014).”
From Social functioning in major depressive disorder (2016) · cites this paper as Covington et al., 2010
PFC-NAcc afferents may promote resiliency.
“PFC-NAcc afferents may promote resiliency”
From Social functioning in major depressive disorder (2016) · cites this paper as Covington et al., 2010
Optogenetic bursting stimulation of the medial prefrontal cortex in chronically socially defeated mice drives immediate early gene expression changes like those in antidepressant-medicated human prefrontal cortex.
“For example, optogenetic stimulation of the mPFC in a bursting pattern, not unlike that occurring during ketamine-induced gamma oscillations, in mice subjected to chronic social defeat drives changes in immediate early gene expression like those seen in the PFC of human patients medicated with antidepressants and has an antidepressant-like effect in sucrose and social interaction preference tests”
From Plasticity of synapses and reward circuit function in the genesis and treatment of depression (2023) · cites this paper as [194]
Optogenetic bursting stimulation of the medial prefrontal cortex has antidepressant-like effects in sucrose preference and social interaction tests in chronically stressed mice.
“For example, optogenetic stimulation of the mPFC in a bursting pattern, not unlike that occurring during ketamine-induced gamma oscillations, in mice subjected to chronic social defeat drives changes in immediate early gene expression like those seen in the PFC of human patients medicated with antidepressants and has an antidepressant-like effect in sucrose and social interaction preference tests”
From Plasticity of synapses and reward circuit function in the genesis and treatment of depression (2023) · cites this paper as [194]
Immediate early genes and synaptic-function genes are decreased in the prefrontal cortex of depressed humans and rodent models.
“Consistent with the decrease in excitation, expression of several immediate early genes and genes associated with synaptic function are decreased in the PFC of depressed humans and in rodent models [194,195].”
From Plasticity of synapses and reward circuit function in the genesis and treatment of depression (2023) · cites this paper as [194]
Burst-like 100 Hz stimulation of the prefrontal cortex promotes antidepressive outcomes in mice.
“For instance, burst-like 100Hz stimulation of the PFC is promotes antidepressive outcomes in mice (44, 45) and “high frequency” 20Hz TMS stimulation of the PFC in humans is antidepressant (46).”
From Emerging Role for Nucleus Accumbens Medium Spiny Neuron Subtypes in Depression (2017) · cites this paper as [44]
Direct optogenetic stimulation of mPFC neurons with channel rhodopsin promotes resilience to social defeat stress.
“Covington et al. showed that direct optogenetic stimulation of mPFC neurons with channel rhodopsin (ChR2) promotes resilience to social defeat stress65.”
From Neurobiology of resilience (2012) · cites this paper as [65]
Resilient mice show greater c-Fos, FosB, or ΔFosB expression in glutamatergic neurons of mPFC after chronic predator or social defeat stress.
“Recent studies have shown a greater degree of c–Fos, FosB, or ΔFosB expression in glutamatergic neurons of mPFC (infralimbic, paralimbic PFC) of resilient mice following chronic predator or social defeat stress25, 64, 65.”
From Neurobiology of resilience (2012) · cites this paper as [65]
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- Authors
- Covington, H. E., Lobo, M. K., Maze, I., Vialou, V., Hyman, J. M., Zaman, S., LaPlant, Q., Mouzon, E., Ghose, S., Tamminga, C. A., Neve, R. L., Deisseroth, K., & Nestler, E. J.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- University of British Columbia (CA)
- Duke University (US)
- The University of Texas Southwestern Medical Center (US)
- Massachusetts Institute of Technology (US)
- Stanford University (US)
- Corresponding author
- Nestler, Eric J.
- ORCID
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2010-12-01
- Volume
- 30
- Issue
- 48
- Pages
- 16082-16090
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3004756
- OpenAlex
- W2025204726
- Cited by
- 621
- References
- 71
- Citations by year
- 2026: 10 · 2025: 23 · 2024: 30 · 2023: 29 · 2022: 41 · 2021: 55 · 2020: 48 · 2019: 52 · 2018: 38 · 2017: 38 · 2016: 45 · 2015: 51 · 2014: 38 · 2013: 41 · 2012: 53
- FWCI
- 28.78
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc)
- Funders
- National Alliance for Research on Schizophrenia and Depression
- National Institute of Mental Health (R01MH051399, P50MH066172)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- depression, medial prefrontal cortex, optogenetic stimulation, antidepressant effects, immediate early genes, Zif268, c-fos, Arc, chronic social defeat stress, channelrhodopsin-2, neuronal activity, postmortem brain, depression resilience, depression vulnerability, depression-like behavior
- MeSH terms
- Channelrhodopsins, Animals, Depressive Disorder, Gene Expression Regulation, Humans, Interpersonal Relations, Male, Mice, Inbred C57BL, Prefrontal Cortex, Genes, Immediate-Early, Mice, Early Growth Response Protein 1
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