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Cited by 172Tryptophan and brain disordersNeuroinflammation and Neurodegeneration MechanismsStress Responses and Cortisol

The DOI matches its Crossref record; 64 of the 64 references it cites were found in a registry or an index.

Minocycline ameliorates depressive behaviors and neuro-immune dysfunction induced by chronic unpredictable mild stress in the rat

Zhang, Cai, Zhang, Yong-Ping, Li, Yu-Yu, Liu, Bai-Ping, Wang, Hao-Yin, Li, Kang-Wei, Zhao, Shannon, Song, Cai·2019·Behavioural Brain Research
DOI 10.1016/j.bbr.2018.07.001
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Abstract

Activated microglia-induced neuroinflammation can stimulate the hypothalamic- pituitary-adrenal (HPA) axis to release glucocorticoids and suppress astrocyte functions, such as reducing neurotrophin production, which occur in depression. However, the balance between M1 (pro-inflammation) and M2 (anti-inflammation) microglial phenotypes and the interaction between these two glial cells are unclear in the depression. Hence, the chronic unpredictable mild stress (CUMS)-induced depression model was chosen to study depression- and anxiety-like behaviors, the concentration of corticosterone and relevant hippocampal cytokines, mRNA and protein expressions of microglial and astrocyte markers. To demonstrate the role of M1 phenotype activation in depression, the effect of microglial inhibitor minocycline on these aspects was also evaluated. Six weeks after CUMS exposure, behaviors were tested. Compared to the control group, CUMS increased serum corticosterone concentration and depression-like behaviors, like anhedonia, helplessness and anxiety. Moreover, CUMS increased microglia M1 marker CD11b expression and tumor necrosis factor (TNF)-α, interferon (INF)-γ, interleukin (IL)-1β and IL-17 concentrations, but decreased the concentration of M2 cytokines, IL-4, IL-10 and IL-13. Meanwhile, CUMS inhibited the expressions of astrocyte marker glial fibrillary acidic protein (GFAP), brain-derived neurotrophic factor (BDNF) and TrKB. Minocycline (40 mg/kg, 45 days) treatment significantly attenuated CUMS-induced behavioral abnormalities, which were associated with the suppressed M1 response, restored GFAP, BDNF and its receptor expression. In conclusion, CUMS-induced depression- and anxiety-like behavior may result from an imbalance between M1 and M2 and suppressed astrocyte function. Minocycline treatment reversed M1 response, which was associated with behavioral normalization.

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Metadata

Authors
Zhang, C., Zhang, Y.-P., Li, Y.-Y., Liu, B.-P., Wang, H.-Y., Li, K.-W., Zhao, S., & Song, C.
Affiliations
  • Guangdong Ocean University (CN)
  • University of Southern California (US)
Corresponding author
Song, Cai
ORCID
Venue
Behavioural Brain Research
Publisher
Elsevier BV
Published
2019-01
Volume
356
Pages
348-357
ISSN
0166-4328 (ISSN-L)
DOI
10.1016/j.bbr.2018.07.001
OpenAlex
W2871444027
Cited by
172
References
64
Citations by year
2026: 17 · 2025: 15 · 2024: 22 · 2023: 22 · 2022: 25 · 2021: 29 · 2020: 25 · 2019: 13
FWCI
5.42
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Behavioural Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Natural Science Foundation of China (81471223, 81171118)
  • Project of Enhancing School with Innovation of Guangdong Ocean University (GDOU2013050110)
  • Guangdong Provincial Science and Technology Planning Project of Guangdong Province, China (2016A020215153, 2016B020235001)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
minocycline, depression, chronic unpredictable mild stress, neuroinflammation, astrocyte dysfunction, hippocampus, corticosterone, hypothalamic-pituitary-adrenal axis, brain-derived neurotrophic factor, glial fibrillary acidic protein, cytokines, anxiety-like behavior
MeSH terms
Animals, Antidepressive Agents, Anxiety Disorders, Behavior, Animal, Depression, Disease Models, Animal, Female, Hypothalamo-Hypophyseal System, Minocycline, Pituitary-Adrenal System, Stress, Psychological, Rats, Sprague-Dawley, Brain-Derived Neurotrophic Factor

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