IMR Press / JIN / Volume 18 / Issue 4 / DOI: 10.31083/j.jin.2019.04.1164
Open Access Original Research
The glutamatergic system and astrocytic impairment in rat hippocampus: a comparative study of underlying etiology and pathophysiology of depression
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1 Department of Acupuncture and Moxibustion, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310000, P. R. China
2 Department of Acupuncture and Moxibustion, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310000, P. R. China
*Correspondence: (Zhong Di)
These authors contributed equally.
J. Integr. Neurosci. 2019, 18(4), 387–392;
Submitted: 26 August 2019 | Accepted: 19 November 2019 | Published: 30 December 2019
Copyright: © 2019 Jiang et al. Published by IMR Press.
This is an open access article under the CC BY 4.0 license

Correlations amongst the rat glutamatergic system, glia, and depression, as well as the underlying mechanism of astrocyte impairment, as a trigger of depression, were investigated. Rats were submitted to different durations of chronic unpredictable mild stress to induce depressive-like behavior and evaluated by weight change, sucrose preference test, open field test, and novelty suppressed feeding test. High-performance liquid chromatography was employed to detect glutamate content of hippocampal protein expression during Western blot and immunofluorescence. Results showed that 21-day chronic unpredictable mild stress was sufficient for inducing significant depressive-like behavior (reduced body weight and sucrose preference, increased feeding, and immobility time) in a model of depression. Chronic unpredictable mild stress increased the level of hippocampal glutamate, while intervention caused a considerable rise in the expression levels of Bax, caspase 3, and calcium/calmodulin-dependent protein kinase II, accompanied by a down-regulated level of B-cell lymphoma-2. Exposure to this stress model reduced hippocampal glutamate ionotropic receptor N-methyl-D-aspartic acid type subunit 2A, neuronal nuclear protein, and glial fibrillary acidic protein expression levels while it raised the level of ionotropic glutamate receptor N-methyl-D-aspartic acid type subunit 2B level. It is concluded that chronic stress induces excessive glutamate release and overstimulation of N-methyl-D-aspartic acid receptors, followed by astrocytic apoptosis. Also, in depression, calcium overload in astrocytes is attributed to an underlying mechanism of astrocyte impairment.

chronic unpredictable mild stress
rat model
Figure 1.
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