The ever‐changing brain: Cellular and molecular mechanisms for the effects of stressful experiences
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The adult brain is capable of considerable structural and functional plasticity and the study of hormone actions in brain has contributed to our understanding of this important phenomenon. In particular, stress and stress‐related hormones such as glucocorticoids and mineralocorticoids play a key role in the ability of acute and chronic stress to cause reversible remodeling of neuronal connections in the hippocampus, prefrontal cortex, and amygdala. To produce this plasticity, these hormones act by both genomic and non‐genomic mechanisms together with ongoing, experience‐driven neural activity mediated by excitatory amino acid neurotransmitters, neurotrophic factors such as brain derived neurotrophic factor, extracellular molecules such as neural cell adhesion molecule, neuropeptides such as corticotrophin releasing factor, and endocannabinoids. The result is a dynamic brain architecture that can be modified by experience. Under this view, the role of pharmaceutical agents, such as antidepressants, is to facilitate such plasticity that must also be guided by experiences. © 2011 Wiley Periodicals, Inc. Develop Neurobiol 72: 878–890, 2012
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Oxidative stress may contribute to the slow emergence of psychoses by mistiming key windows of brain development.
“Given the pivotal role of PV cells and PNNs in regulating the onset and closure of brain plasticity (52,57), oxidative stress may contribute to the slow emergence of psychoses by mistiming key windows of brain development.”
From Perineuronal nets protect fast-spiking interneurons against oxidative stress (2013) · cites this paper as [57]
The “Initial evidence for adult brain plasticity” section discusses developmental critical periods, but not their mistiming by oxidative stress or a resulting emergence of psychoses. Searches of our copy for oxidative stress, psychosis, and related terms found no passage addressing that proposed link; pages were not supplied. (LLM, conf=0.75)
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- Authors
- McEwen, B. S.
- Affiliations
- Rockefeller University (US)
- Corresponding author
- McEwen, Bruce S.
- ORCID
- McEwen, Bruce S.
- Venue
- Developmental Neurobiology
- Publisher
- Wiley
- Published
- 2012-05-14
- Volume
- 72
- Issue
- 6
- Pages
- 878-890
- ISSN
- 1932-8451 (ISSN-L)
- 1932-846X
- PMC
- PMC3248634
- OpenAlex
- W2003627321
- Cited by
- 165
- References
- 22
- Citations by year
- 2026: 8 · 2025: 8 · 2024: 5 · 2023: 12 · 2022: 4 · 2021: 8 · 2020: 7 · 2019: 4 · 2018: 6 · 2017: 14 · 2016: 16 · 2015: 21 · 2014: 23 · 2013: 16 · 2012: 12
- FWCI
- 1.44
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Developmental Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (MH-41256, R37MH041256, MH-58911, P50MH058911, R01MH041256)
- National Institute of Neurological Disorders and Stroke (R01NS007080, NS 07080)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- stress, neuroplasticity, glucocorticoids, mineralocorticoids, hippocampus, prefrontal cortex, amygdala, excitatory amino acids, brain-derived neurotrophic factor, CD56, corticotropin-releasing factor, endocannabinoids, antidepressants, experience-dependent plasticity
- MeSH terms
- Animals, Brain, Glucocorticoids, Neuronal Plasticity, Stress, Physiological, Stress, Psychological, Brain-Derived Neurotrophic Factor
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