The neuroendocrine impact of acute stress on synaptic plasticity
Open accessAbstract
Stress induces changes in nervous system function on different signaling levels, from molecular signaling to synaptic transmission to neural circuits to behavior—and on different time scales, from rapid onset and transient to delayed and long-lasting. The principal effectors of stress plasticity are glucocorticoids, steroid hormones that act with a broad range of signaling competency due to the expression of multiple nuclear and membrane receptor subtypes in virtually every tissue of the organism. Glucocorticoid and mineralocorticoid receptors are localized to each of the cellular compartments of the receptor-expressing cells—the membrane, cytosol, and nucleus. In this review, we cover the neuroendocrine effects of stress, focusing mainly on the rapid actions of acute stress–induced glucocorticoids that effect changes in synaptic transmission and neuronal excitability by modulating synaptic and intrinsic neuronal properties via activation of presumed membrane glucocorticoid and mineralocorticoid receptors. We describe the synaptic plasticity that occurs in 4 stress-associated brain structures, the hypothalamus, hippocampus, amygdala, and prefrontal cortex, in response to single or short-term stress exposure. The rapid transformative impact of glucocorticoids makes this stress signal a particularly potent effector of acute neuronal plasticity.
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Sex steroids, thyroid hormones, and glucocorticoids modulate synaptic transmission, dendritic spine dynamics, neuronal excitability, and circuit maturation, particularly in the hippocampus and hypothalamus.
“Sex steroids, thyroid hormones, and glucocorticoids modulate synaptic transmission, dendritic spine dynamics, neuronal excitability, and circuit maturation, particularly in plasticity-relevant regions such as the hippocampus and hypothalamus (Damiano et al., 2025; Dos-Santos et al., 2023; Dsouki et al., 2024; Ogiue-Ikeda et al., 2008; Pang and Han, 2012; Parent et al., 2011; Weiss, 2007).”
From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Dos-Santos et al., 2023
The Abstract passages on hippocampal spines and hypothalamic synapses describe glucocorticoid effects on dendritic spine formation, synaptic transmission, and neuronal excitability. They do not establish the claimed effects of sex steroids or thyroid hormones, or address circuit maturation. The Conclusions mention gonadal steroids only as a possible influence requiring further study; no page numbers are provided in our copy. (LLM, conf=0.88)
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Jocsak, G., Kiss, D. S., Alymbaeva, D., Diebald, A., Zsarnovszky, A., Heinzlmann, A., & Bartha, T. (2026) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2026.1821381 · Cited by 1 · see citing works
- Authors
- dos-Santos, R. C., Sweeten, B. L. W., Stelly, C. E., & Tasker, J. G.
- Affiliations
- Department of Cell and Molecular Biology and Tulane Brain Institute, Tulane University , New Orleans, LA 70118 , USA
- Tulane University (US)
- Corresponding author
- Tasker, Jeffrey G
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2023-09-23
- Volume
- 164
- Issue
- 11
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC11046011
- OpenAlex
- W4387299203
- Cited by
- 29
- References
- 18
- Citations by year
- 2026: 14 · 2025: 11 · 2024: 4
- FWCI
- 0.80
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Endocrinology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- NIH (R01 MH119283)
- Southeast Louisiana Veteran's Administration Merit (I01 BX005118)
- 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
- acute stress, synaptic plasticity, glucocorticoids, mineralocorticoid receptor, neuronal excitability, synaptic transmission, hypothalamus, hippocampus, amygdala, prefrontal cortex, neuroendocrine stress response
- MeSH terms
- Brain, Glucocorticoids, Synaptic Transmission, Neuronal Plasticity, Receptors, Glucocorticoid, Stress, Psychological, Receptors, Mineralocorticoid
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