The DOI matches its Crossref record.
Effect of Acute Stress on Hippocampal Glutamate Levels and Spectrin Proteolysis in Young and Aged Rats
Abstract
Abstract: Aging in rats is associated with a loss of hippocampal neurons, which may contribute to age‐related cognitive deficits. Several lines of evidence suggest that stress and glucocorticoids may contribute to age‐related declines in hippocampal neuronal number. Excitatory amino acids (EAAs) have been implicated in the glucocorticoid endangerment and stress‐induced morphological changes of hippocampal neurons of young rats. Previously, we have reported that acute immobilization stress can increase extracellular concentrations of the endogenous excitatory amino acid, glutamate, in the hippocampus. The present study examined the effect of an acute bout of immobilization stress on glutamate levels in the hippocampus and medial prefrontal cortex of young (3–4‐month) and aged (22–24‐month) Fischer 344 rats. In addition, the effect of stress on spectrin proteolysis in these two brain regions was also examined. Spectrin is a cytoskeleton protein that contributes to neuronal integrity and proteolysis of this protein has been proposed as an important component of EAA‐induced neuronal death. There was no difference in basal glutamate levels between young and old rats in the hippocampus or medial prefrontal cortex. During the period of restraint stress a modest increase in glutamate levels in the hippocampus of young and aged rats was observed. After the termination of the stress procedure, hippocampal glutamate concentrations continued to rise in the aged rats, reaching a level approximately five times higher than the young rats, and remained elevated for at least 2 h after the termination of the stress. A similar pattern was also observed in the medial prefrontal cortex with an augmented post‐stress‐induced glutamate response observed in the aged rats. There was no increase in spectrin proteolysis in the hippocampus or medial prefrontal cortex of young or aged rats after stress or under basal nonstress conditions. The enhanced poststress glutamate response in the aged rats may contribute to the increased sensitivity of aged rats to neurotoxic insults.
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“In the present study, there was no evidence from TUNEL staining that IL-1β and/or acute stress elicit hippocampal cell death either in vitro or in vivo, which is consistent with previous studies (40–42), although there is one report that severe acute stress increases apoptosis (43).”
From IL-1β is an essential mediator of the antineurogenic and anhedonic effects of stress (2008) · cites this paper as [42]
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“Nitric oxide (NO) is one of the signal transmitting molecules of the central nervous system and chronic stress enhances its synthesis by increasing NOS (nitric oxide synthase) expression [6], as stress triggers the overproduction of the neurotransmitter glutamate [48].”
BackgroundMin, J. J., Bao, J., Baik, J. Y., Wen, J., Zhao, Y., Thompson, P. M., Shen, L., & Duong-Tran, D. A. (2025) · medRxiv · doi:10.1101/2025.10.26.25338821
“Repeated stress exposure induces excessive neurotransmitter release and disrupts calcium homeostasis, leading to long-term alterations in neural activity patterns in rodents [21, 22].”
Yeon, J., Yun, C., Chung, K.-J., Min, B.-J., Liu, W.-X., & Han, B. S. (2026) · Journal of Spectroscopy · doi:10.1155/jspe/8275909
Metadata
- Authors
- Lowy, M. T., Wittenberg, L., & Yamamoto, B. K.
- Affiliations
- Case Western Reserve University (US)
- Corresponding author
- Lowy, Martin T.
- ORCID
- Yamamoto, Bryan K.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 1995-07
- Volume
- 65
- Issue
- 1
- Pages
- 268-274
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2119257185
- Cited by
- 217
- References
- 0
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 4 · 2023: 5 · 2022: 3 · 2021: 8 · 2020: 5 · 2019: 7 · 2018: 6 · 2017: 3 · 2016: 5 · 2015: 3 · 2014: 4 · 2013: 10 · 2012: 9
- FWCI
- 2.64
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Drug Abuse (DA-07606, R01DA007606)
- 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, restraint stress, hippocampus, glutamate, aging, age-related cognitive decline, excitatory amino acids, neuronal cell death, medial prefrontal cortex, glucocorticoids, F344 rats
- MeSH terms
- Aging, Animals, Extracellular Space, Hippocampus, Male, Peptide Hydrolases, Rats, Inbred F344, Spectrin, Stress, Physiological, Prefrontal Cortex, Glutamic Acid, Rats
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