Cited by 262Stress Responses and CortisolNeuroscience and Neuropharmacology ResearchMemory and Neural Mechanisms

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Experimental diabetes in rats causes hippocampal dendritic and synaptic reorganization and increased glucocorticoid reactivity to stress

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Magariños, Ana María, McEwen, Bruce S.·2000·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.97.20.11056PMC PMC27147

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Abstract

We report that 9 d of uncontrolled experimental diabetes induced by streptozotocin (STZ) in rats is an endogenous chronic stressor that produces retraction and simplification of apical dendrites of hippocampal CA3 pyramidal neurons, an effect also observed in nondiabetic rats after 21 d of repeated restraint stress or chronic corticosterone (Cort) treatment. Diabetes also induces morphological changes in the presynaptic mossy fiber terminals (MFT) that form excitatory synaptic contacts with the proximal CA3 apical dendrites. One effect, synaptic vesicle depletion, occurs in diabetes as well as after repeated stress and Cort treatment. However, diabetes produced other MFT structural changes that differ qualitatively and quantitatively from other treatments. Furthermore, whereas 7 d of repeated stress was insufficient to produce dendritic or synaptic remodeling in nondiabetic rats, it potentiated both dendritic atrophy and MFT synaptic vesicle depletion in STZ rats. These changes occurred in concert with adrenal hypertrophy and elevated basal Cort release as well as hypersensitivity and defective shutoff of Cort secretion after stress. Thus, as an endogenous stressor, STZ diabetes not only accelerates the effects of exogenous stress to alter hippocampal morphology; it also produces structural changes that overlap only partially with those produced by stress and Cort in the nondiabetic state.

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Authors: Magariños, A. M., & McEwen, B. S.
Affiliations: The Rockefeller University, 1230 York Avenue, New York, NY 10021
Rockefeller University (US)
ORCID: McEwen, Bruce S.
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2000-09-26
Volume: 97
Issue: 20
Pages: 11056-11061
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.97.20.11056
PMC: PMC27147
OpenAlex: W2116721266
Cited by: 262
References: 62
Citations by year: 2026: 3 · 2024: 7 · 2023: 6 · 2022: 6 · 2021: 5 · 2020: 8 · 2019: 8 · 2018: 15 · 2017: 9 · 2016: 11 · 2015: 18 · 2014: 13 · 2013: 17 · 2012: 13
FWCI: 2.72
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of Mental Health (MH-41256, R37MH041256, R01MH041256)
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: experimental diabetes, streptozotocin-induced diabetes, hippocampus, CA3 pyramidal cells, dendritic reorganization, mossy fiber terminals, synaptic vesicle depletion, chronic stress, restraint stress, corticosterone, adrenal hypertrophy, glucocorticoid secretion, hippocampal synaptic plasticity
MeSH terms: Animals, Anti-Bacterial Agents, Corticosterone, Dendrites, Diabetes Mellitus, Experimental, Hippocampus, Male, Streptozocin, Stress, Physiological, Synapses, Rats, Sprague-Dawley, Rats

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Experimental diabetes in rats causes hippocampal dendritic and synaptic reorganization and increased glucocorticoid reactivity to stress

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