Synergistic effects of psychosocial stress and mild peripheral infection on inducing microglial activation in the hippocampal dentate gyrus and long-lasting deficits in hippocampus-related memory

Wen Yu Tzeng, Chien Chou Su, Li Han Sun, Chianfang G. Cherng, Lung Yu

Research output: Contribution to journalArticle

Abstract

Lipopolysaccharide (LPS) treatment and stress may cause immune activation in the brain, an event which has been thought to play a role in mediating stress-induced cognitive dysfunction. However, the enduring impact of psychosocial stress on brain immune activation or cognitive deficits has not been well investigated. Likewise, it remains unexplored whether there exist synergistic effects of psychosocial stress and a weak systemic LPS treatment on brain immune activation and/or cognitive function. In this work, a 10-day social defeat regimen was used to model psychosocial stress and the number and density of ionized calcium-binding adaptor molecule 1 (Iba1)-stained microglia was used to reveal brain immune activation in male Balb/C mice. The social defeat regimen did not cause observable microglial activation in dentate gyrus (DG) 24 h after the conclusion of the regimen. Microglial activation peaked in DG 24 h following a single 1 mg/kg intra-peritoneal LPS injection. At this time point, DG microglial activation was not evident providing 0.125 mg/kg or lower of LPS was used, this dose of LPS was, thus, regarded as the “sub-threshold” in this study. Twenty-four h after the conclusion of the defeat regimen, mice received a social interaction test to determine their defeat stress susceptibility and a “sub-threshold” LPS injection. DG microglial activation was observed in the defeat-stress susceptible, but not in the resilient, mice. Furthermore, the stress-susceptible mice showed impairment in object location and Y maze tasks 24 and 72 h after the “sub-threshold” LPS injection. These results suggest that psychosocial stress, when combined with a negligible peripheral infection, may induce long-lasting hippocampus-related memory deficits exclusively in subjects susceptible to psychosocial stresses.

Original languageEnglish
Pages (from-to)106-117
Number of pages12
JournalChinese Journal of Physiology
Volume61
Issue number2
DOIs
Publication statusPublished - 2018 Jan 1

Fingerprint

Parahippocampal Gyrus
Dentate Gyrus
Lipopolysaccharides
Hippocampus
Infection
Brain
Injections
Memory Disorders
Microglia
Interpersonal Relations
Cognition
Calcium
Therapeutics

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

@article{2741d7b904714a5cbe67ad0e39d51541,
title = "Synergistic effects of psychosocial stress and mild peripheral infection on inducing microglial activation in the hippocampal dentate gyrus and long-lasting deficits in hippocampus-related memory",
abstract = "Lipopolysaccharide (LPS) treatment and stress may cause immune activation in the brain, an event which has been thought to play a role in mediating stress-induced cognitive dysfunction. However, the enduring impact of psychosocial stress on brain immune activation or cognitive deficits has not been well investigated. Likewise, it remains unexplored whether there exist synergistic effects of psychosocial stress and a weak systemic LPS treatment on brain immune activation and/or cognitive function. In this work, a 10-day social defeat regimen was used to model psychosocial stress and the number and density of ionized calcium-binding adaptor molecule 1 (Iba1)-stained microglia was used to reveal brain immune activation in male Balb/C mice. The social defeat regimen did not cause observable microglial activation in dentate gyrus (DG) 24 h after the conclusion of the regimen. Microglial activation peaked in DG 24 h following a single 1 mg/kg intra-peritoneal LPS injection. At this time point, DG microglial activation was not evident providing 0.125 mg/kg or lower of LPS was used, this dose of LPS was, thus, regarded as the “sub-threshold” in this study. Twenty-four h after the conclusion of the defeat regimen, mice received a social interaction test to determine their defeat stress susceptibility and a “sub-threshold” LPS injection. DG microglial activation was observed in the defeat-stress susceptible, but not in the resilient, mice. Furthermore, the stress-susceptible mice showed impairment in object location and Y maze tasks 24 and 72 h after the “sub-threshold” LPS injection. These results suggest that psychosocial stress, when combined with a negligible peripheral infection, may induce long-lasting hippocampus-related memory deficits exclusively in subjects susceptible to psychosocial stresses.",
author = "Tzeng, {Wen Yu} and Su, {Chien Chou} and Sun, {Li Han} and Cherng, {Chianfang G.} and Lung Yu",
year = "2018",
month = "1",
day = "1",
doi = "10.4077/CJP.2018.BAG569",
language = "English",
volume = "61",
pages = "106--117",
journal = "Chinese Journal of Physiology",
issn = "0304-4920",
publisher = "Chinese Physiological Society",
number = "2",

}

Synergistic effects of psychosocial stress and mild peripheral infection on inducing microglial activation in the hippocampal dentate gyrus and long-lasting deficits in hippocampus-related memory. / Tzeng, Wen Yu; Su, Chien Chou; Sun, Li Han; Cherng, Chianfang G.; Yu, Lung.

In: Chinese Journal of Physiology, Vol. 61, No. 2, 01.01.2018, p. 106-117.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Synergistic effects of psychosocial stress and mild peripheral infection on inducing microglial activation in the hippocampal dentate gyrus and long-lasting deficits in hippocampus-related memory

AU - Tzeng, Wen Yu

AU - Su, Chien Chou

AU - Sun, Li Han

AU - Cherng, Chianfang G.

AU - Yu, Lung

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Lipopolysaccharide (LPS) treatment and stress may cause immune activation in the brain, an event which has been thought to play a role in mediating stress-induced cognitive dysfunction. However, the enduring impact of psychosocial stress on brain immune activation or cognitive deficits has not been well investigated. Likewise, it remains unexplored whether there exist synergistic effects of psychosocial stress and a weak systemic LPS treatment on brain immune activation and/or cognitive function. In this work, a 10-day social defeat regimen was used to model psychosocial stress and the number and density of ionized calcium-binding adaptor molecule 1 (Iba1)-stained microglia was used to reveal brain immune activation in male Balb/C mice. The social defeat regimen did not cause observable microglial activation in dentate gyrus (DG) 24 h after the conclusion of the regimen. Microglial activation peaked in DG 24 h following a single 1 mg/kg intra-peritoneal LPS injection. At this time point, DG microglial activation was not evident providing 0.125 mg/kg or lower of LPS was used, this dose of LPS was, thus, regarded as the “sub-threshold” in this study. Twenty-four h after the conclusion of the defeat regimen, mice received a social interaction test to determine their defeat stress susceptibility and a “sub-threshold” LPS injection. DG microglial activation was observed in the defeat-stress susceptible, but not in the resilient, mice. Furthermore, the stress-susceptible mice showed impairment in object location and Y maze tasks 24 and 72 h after the “sub-threshold” LPS injection. These results suggest that psychosocial stress, when combined with a negligible peripheral infection, may induce long-lasting hippocampus-related memory deficits exclusively in subjects susceptible to psychosocial stresses.

AB - Lipopolysaccharide (LPS) treatment and stress may cause immune activation in the brain, an event which has been thought to play a role in mediating stress-induced cognitive dysfunction. However, the enduring impact of psychosocial stress on brain immune activation or cognitive deficits has not been well investigated. Likewise, it remains unexplored whether there exist synergistic effects of psychosocial stress and a weak systemic LPS treatment on brain immune activation and/or cognitive function. In this work, a 10-day social defeat regimen was used to model psychosocial stress and the number and density of ionized calcium-binding adaptor molecule 1 (Iba1)-stained microglia was used to reveal brain immune activation in male Balb/C mice. The social defeat regimen did not cause observable microglial activation in dentate gyrus (DG) 24 h after the conclusion of the regimen. Microglial activation peaked in DG 24 h following a single 1 mg/kg intra-peritoneal LPS injection. At this time point, DG microglial activation was not evident providing 0.125 mg/kg or lower of LPS was used, this dose of LPS was, thus, regarded as the “sub-threshold” in this study. Twenty-four h after the conclusion of the defeat regimen, mice received a social interaction test to determine their defeat stress susceptibility and a “sub-threshold” LPS injection. DG microglial activation was observed in the defeat-stress susceptible, but not in the resilient, mice. Furthermore, the stress-susceptible mice showed impairment in object location and Y maze tasks 24 and 72 h after the “sub-threshold” LPS injection. These results suggest that psychosocial stress, when combined with a negligible peripheral infection, may induce long-lasting hippocampus-related memory deficits exclusively in subjects susceptible to psychosocial stresses.

UR - http://www.scopus.com/inward/record.url?scp=85046652731&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85046652731&partnerID=8YFLogxK

U2 - 10.4077/CJP.2018.BAG569

DO - 10.4077/CJP.2018.BAG569

M3 - Article

VL - 61

SP - 106

EP - 117

JO - Chinese Journal of Physiology

JF - Chinese Journal of Physiology

SN - 0304-4920

IS - 2

ER -