Chronic stress and lithium treatments alter hippocampal glutamate uptake and release in the rat and potentiate necrotic cellular death after oxygen and glucose deprivation
Abstract
This study was undertaken to evaluate the effects of chronic variate stress and lithium treatment on glutamatergic activity and neuronal vulnerability of rat hippocampus. Male Wistar rats were simultaneously treated with lithium and submitted to a chronic variate stress protocol during 40 days, and afterwards the hippocampal glutamatergic uptake and release, measured in slices and synaptosomes, were evaluated. We observed an increased synaptosomal [(3)H]glutamate uptake and an increase in [(3)H]glutamate stimulated release in hippocampus of lithium-treated rats. Chronic stress increased basal [(3)H]glutamate release by synaptosomes, and decreased [(3)H]glutamate uptake in hippocampal slices. When evaluating cellular vulnerability, both stress and lithium increased cellular death after oxygen and glucose deprivation (OGD). We suggest that the manipulation of glutamatergic activity induced by stress may be in part responsible for the neuroendangerment observed after stress exposure, and that, in spite of the described neuroprotective effects of lithium, it increased the neuronal vulnerability after OGD.
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Some studies report increased chronic stress-related glutamate release and receptor expression alongside reduced glutamate clearance or metabolism in the hippocampus.
“Some studies have reported enhanced chronic stress-related glutamate release and glutamate receptor expression, but reduced glutamate clearance/metabolism in the hippocampus (122,123).”
From The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology (2019) · cites this paper as [123]
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- Authors
- de Vasconcellos-Bittencourt, A. P. S., Vendite, D. A., Nassif, M., Crema, L. M., Frozza, R., Thomazi, A. P., Nieto, F. B., Wofchuk, S., Salbego, C., da Rocha, E. R., & Dalmaz, C.
- Affiliations
- Universidade Federal do Rio Grande do Sul (BR)
- Corresponding author
- Thomazi, Ana Paula
- Venue
- Neurochemical Research
- Published
- 2011-01-21
- Volume
- 36
- Issue
- 5
- Pages
- 793-800
- ISSN
- 0364-3190 (ISSN-L)
- 1573-6903
- OpenAlex
- W2040376279
- Cited by
- 36
- References
- 57
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 2 · 2023: 3 · 2022: 4 · 2021: 1 · 2019: 1 · 2018: 4 · 2017: 5 · 2015: 3 · 2014: 3 · 2013: 2 · 2012: 1
- FWCI
- 1.19
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neurochemical Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Psychiatry and Mental health › Bipolar Disorder and Treatment
- Keywords
- chronic stress, lithium, hippocampus, glutamate uptake, glutamate release, synaptosomes, oxygen-glucose deprivation, neuronal necrosis, neuroprotection, glutamatergic activity, neuronal vulnerability
- MeSH terms
- Animals, Hypoxia, Chronic Disease, Glucose, Hippocampus, L-Lactate Dehydrogenase, Male, Necrosis, Stress, Physiological, Cell Death, Rats, Wistar, Lithium Compounds, Glutamic Acid, Rats
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