Structural and synaptic plasticity in stress-related disorders
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Abstract Stress can have a lasting impact on the structure and function of brain circuitry that results in long-lasting changes in the behavior of an organism. Synaptic plasticity is the mechanism by which information is stored and maintained within individual synapses, neurons, and neuronal circuits to guide the behavior of an organism. Although these mechanisms allow the organism to adapt to its constantly evolving environment, not all of these adaptations are beneficial. Under prolonged bouts of physical or psychological stress, these mechanisms become dysregulated, and the connectivity between brain regions becomes unbalanced, resulting in pathological behaviors. In this review, we highlight the effects of stress on the structure and function of neurons within the mesocorticolimbic brain systems known to regulate mood and motivation. We then discuss the implications of these spine adaptations on neuronal activity and pathological behaviors implicated in mood disorders. Finally, we end by discussing recent brain imaging studies in human depression within the context of these basic findings to provide insight into the underlying mechanisms leading to neural dysfunction in depression.
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Chronic stress reduces dendritic arborization and glutamatergic dendritic spine density of pyramidal neurons in PFC and hippocampus, reduces hippocampal neurogenesis, and increases dendritic spine number or branching in amygdala and NAc.
“chronic stress reduces dendritic arborization and glutamatergic dendritic spine density of pyramidal neurons in PFC and hippocampus, and reduces hippocampus neurogenesis, while increasing dendritic spine number or branching in amygdala and NAc (for review see63).”
From Neurobiology of resilience (2012) · cites this paper as [63]
Alterations in VTA DA activity affect activity in multiple downstream targets, including the NAc and mPFC, which appear to be particularly important for mediating social avoidance.
“Alterations in VTA DA activity will affect activity in multiple downstream targets, including the NAc and mPFC, which appear to be particularly important for mediating social avoidance [149, 150, 156-159].”
From Neural circuits regulating prosocial behaviors (2023) · cites this paper as [159]
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- Authors
- Christoffel, D. J., Golden, S. A., & Russo, S. J.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Russo, Scott J.
- Venue
- Reviews in the Neurosciences
- Publisher
- Walter de Gruyter GmbH
- Published
- 2011-01-01
- Volume
- 22
- Issue
- 5
- Pages
- 535-49
- ISSN
- 0334-1763 (ISSN-L)
- 2191-0200
- PMC
- PMC3212803
- OpenAlex
- W2034154165
- Cited by
- 334
- References
- 185
- Citations by year
- 2026: 14 · 2025: 22 · 2024: 18 · 2023: 19 · 2022: 31 · 2021: 30 · 2020: 21 · 2019: 31 · 2018: 31 · 2017: 27 · 2016: 21 · 2015: 17 · 2014: 14 · 2013: 17 · 2012: 17
- FWCI
- 1.46
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Reviews in the Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (R01MH090264)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- stress, synaptic plasticity, structural plasticity, mesocorticolimbic system, dendritic spine morphology, mood disorders, depression, psychological stress, neuronal activity
- MeSH terms
- Animals, Brain, Humans, Neuronal Plasticity, Stress, Psychological, Synapses
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