Rapid glucocorticoid effects on excitatory amino acid levels in the hippocampus: a microdialysis study in freely moving rats
Abstract
Glucocorticoids can rapidly affect neuronal function and behaviour in mammals. Several studies have suggested the possible existence of rapid, non-genomic effects of glucocorticoids in the hippocampus. To investigate whether glucocorticoids could affect neurotransmission in the hippocampus through rapid, non-genomic mechanisms, we studied the effects of acute glucocorticoid administration on extracellular amino acid levels in the CA1 area of the hippocampus. By means of microdialysis on freely moving rats, we observed that an intraperitoneal injection of corticosterone (2.5 mg/kg) induced a rapid (within 15 min) and transient (returning to basal levels by 35-45 min) increase in extracellular aspartate and glutamate levels ( approximately 155-160%), both in sham-operated and adrenalectomized rats. These effects occurred in parallel with a rise in corticosterone concentration, also detected by microdialysis, in this hippocampal area. Intrahippocampal perfusion of corticosterone by retrodialysis also produced the same fast and reversible effects on excitatory amino acid (EAA) levels. Extracellular concentrations of taurine and gamma-aminobutyric acid (GABA) were unchanged after intrahippocampal glucocorticoid administration. This corticosterone-mediated rise in EAA levels was not inhibited by the presence of specific antagonists for the two types of intracellular corticosteroid receptors, nor by a protein synthesis inhibitor, anisomycin. Perfusion of dexamethasone, a synthetic glucocorticoid, elicited a similar effect to that observed with corticosterone treatment in all studied cases. However, non-glucocorticoid steroids did not affect amino acid transmission in this hippocampal area. These results indicate that glucocorticoids induce a rapid and transient increase in hippocampal EAA levels in vivo that might be exerted through a novel non-genomic mechanism of action.
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Activation of the HPA axis is known to induce glutamatergic strengthening.
“Consistent with the correlation between FM and acute or chronic stress, the activation of the HPA axis is known to induce glutamatergic strengthening [59–61].”
From Fibromyalgia pathogenesis explained by a neuroendocrine multistable model (2024) · cites this paper as [61]
The activational period involves a stress-induced increase in glutamatergic transmission and activation of AMPA and NMDA receptors.
“The activational period, identified by the “1A” and “1B” in Figure 3, involves a stress-induced increase in glutamatergic transmission and activation of AMPA and NMDA receptors (Bagley and Moghaddam [243]; Venero and Borrell [244]; McEwen et al. [245]; Kole et al. [246]).”
From The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law (2007) · cites this paper as Venero and Borrell [244]
Glucocorticoid enhancement of extracellular levels of glutamate plays an important role in both modulatory and excitotoxic effects of glucocorticoids.
“a phenomenon that involved glucocorticoid enhancement of extracellular levels of glutamate (Venero and Borrell, 1999) that plays an important role in both modulatory and excitotoxic effects of glucocorticoids”
From Central effects of stress hormones in health and disease: understanding the protective and damaging effects of stress and stress mediators (2008) · cites this paper as Venero and Borrell, 1999
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- Authors
- Venero, C., & Borrell, J.
- Affiliations
- Instituto Cajal (ES)
- Venue
- European Journal of Neuroscience
- Publisher
- Wiley
- Published
- 1999-07
- Volume
- 11
- Issue
- 7
- Pages
- 2465-2473
- ISSN
- 0953-816X (ISSN-L)
- 1460-9568
- OpenAlex
- W1979948882
- Cited by
- 277
- References
- 56
- Citations by year
- 2025: 2 · 2024: 5 · 2023: 6 · 2022: 3 · 2021: 7 · 2020: 5 · 2019: 8 · 2018: 7 · 2017: 10 · 2016: 8 · 2015: 13 · 2014: 19 · 2013: 13 · 2012: 16
- FWCI
- 3.57
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Journal of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- 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
- glucocorticoids, non-genomic steroid action, excitatory amino acids, hippocampus, corticosterone, glutamate, aspartic acid, CA1, neurotransmission, dexamethasone, adrenalectomy, freely moving rats
- MeSH terms
- Adrenalectomy, Mineralocorticoid Receptor Antagonists, Animals, Calcium, Corticosterone, Dexamethasone, Glucocorticoids, Hippocampus, Injections, Injections, Intraperitoneal, Male, Mineralocorticoids, Protein Synthesis Inhibitors, Receptors, Glucocorticoid, Rats, Wistar, Microdialysis, Excitatory Amino Acids, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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