Restraint stress differentially regulates inflammation and glutamate receptor gene expression in the hippocampus of C57BL/6 and BALB/c mice

Sathyanesan, Monica; Haiar, Jacob; Watt, Michael J.; Newton, Samuel S.

doi:10.1080/10253890.2017.1298587

Cited by 46 publications

(35 citation statements)

References 36 publications

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“…We hypothesize the stress of restraint and i.p. injection may alter the expression of TLR pathways due to the link between stress and immune response (Bollinger et al, 2017;Malki et al, 2015;Sathyanesan et al, 2017). Taken together, the shorter inflammatory response to poly(I:C) in B6N mice suggests that the longer-lasting changes in gene expression that occur in B6J mice may be crucial to how poly(I:C) increases EtOH intake.…”

Section: B6n Mice Have a Shorter Immune Response Compared With B6j Micementioning

confidence: 99%

Inbred Substrain Differences Influence Neuroimmune Response and Drinking Behavior

Warden

DaCosta

Mason

et al. 2020

Alcoholism Clin & Exp Res

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Background The inbred mouse strain C57BL/6 is widely used in both models of addiction and immunological disease. However, there are pronounced phenotypic differences in ethanol (EtOH) consumption and innate immune response between C57BL/6 substrains. The focus of this study was to examine the effects of substrain on innate immune response and neuroimmune‐induced escalation of voluntary EtOH consumption. The main goal was to identify whether substrain differences in immune response can account for differences in EtOH behavior. Methods We compared acute innate immune response with a viral dsRNA mimic, polyinosinic:polycytidylic acid (poly(I:C)), in brain using qRT‐PCR in both C57BL/6N and C57BL/6J mice. Next, we used a neuroimmune model of escalation using poly(I:C) to compare drinking behavior between substrains. Finally, we compared brain neuroimmune response with both EtOH and repeated poly(I:C) in both substrains as a way to account for differences in EtOH behavior. Results We found that C57BL/6 substrains have differing immune response and drinking behaviors. C57BL/6N mice have a shorter but more robust inflammatory response to acute poly(I:C). In contrast, C57BL/6J mice have a smaller but longer‐lasting acute immune response to poly(I:C). In our neuroimmune‐induced escalation model, C57BL/6J mice but not C57BL/6N mice escalate EtOH intake after poly(I:C). Finally, only C57BL/6J mice show enhanced proinflammatory transcript abundance after poly(I:C) and EtOH, suggesting that longer‐lasting immune responses are critical to neuroimmune drinking phenotypes. Conclusions Altogether, this work has elucidated additional influences that substrain has on both innate immune response and drinking phenotypes. Our observations highlight the importance of considering and reporting the source and background used for production of transgenic and knockout mice. These data provide further evidence that genetic background must be carefully considered when investigating the role of neuroimmune signaling in EtOH abuse.

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Section: B6n Mice Have a Shorter Immune Response Compared With B6j Micementioning

confidence: 99%

Inbred Substrain Differences Influence Neuroimmune Response and Drinking Behavior

Warden

DaCosta

Mason

et al. 2020

Alcoholism Clin & Exp Res

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“…Maternal separation induces increased expression of GluN2A (but not GluN2B) subunit of NMDARs in the hippocampus of adult rats [ 205 ]. Chronic restraint stress significantly elevated GRIN2a (GluN2A) and GRIN2b (GluN2B) subunit genes in BALB/c mice, but not in C57BL/6 mice [ 206 ]. Chronic restraint stress also increased the levels of GRIN1 mRNA, along with a reduction in protein levels in dorsal hippocampus [ 207 ].…”

Section: Nmda Receptors In Depressionmentioning

confidence: 99%

Brain NMDA Receptors in Schizophrenia and Depression

Adell

2020

Biomolecules

151

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N-methyl-D-aspartate (NMDA) receptor antagonists such as phencyclidine (PCP), dizocilpine (MK-801) and ketamine have long been considered a model of schizophrenia, both in animals and humans. However, ketamine has been recently approved for treatment-resistant depression, although with severe restrictions. Interestingly, the dosage in both conditions is similar, and positive symptoms of schizophrenia appear before antidepressant effects emerge. Here, we describe the temporal mechanisms implicated in schizophrenia-like and antidepressant-like effects of NMDA blockade in rats, and postulate that such effects may indicate that NMDA receptor antagonists induce similar mechanistic effects, and only the basal pre-drug state of the organism delimitates the overall outcome. Hence, blockade of NMDA receptors in depressive-like status can lead to amelioration or remission of symptoms, whereas healthy individuals develop psychotic symptoms and schizophrenia patients show an exacerbation of these symptoms after the administration of NMDA receptor antagonists.

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“…It is likely that LPS-induced peripheral inflammation may cause neuroinflammatory reaction in the cortex via MCP1/CCR2 pathway, what can lead to an apoptosis (Bidzhekov et al 2006;Zhou et al 2006). It is interesting that the IMO induces the same effect (Sathyanesan et al 2017). We found an increase of MCP1 gene expression without any changes in the gene expression of its receptor CCR2 in the cortex of IMO mice (Figure 4).…”

Section: Discussionmentioning

confidence: 79%

“…-body weight. mation-related genes in the hippocampus in both BABLB/c and C57BL/6 mice (Sathyanesan et al 2017).…”

Section: Discussionmentioning

confidence: 98%

Exposure to a single immobilization or lipopolysaccharide challenge increases expression of genes implicated in the development of Alzheimer’s disease in the mice brain cortex

Padová

Rokytova

Mravec

et al. 2019

Endocrine Regulations

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Objectives. Despite extensive research efforts, mechanisms participating on development of Alzheimer’s disease (AD) are covered only partially. Data from the last decades indicate that various stressors, as etiological factors, may play a role of in the AD. Therefore, we investigated the effect of two acute stressors, immobilization (IMO) and lipopolysaccharide (LPS), on the AD-related neuropathology.Methods. Adult C57BL/6J mice males were exposed to a single IMO stress or a single intraperitoneal injection of LPS (250 µg/kg body weight). After terminating the experiments, the brains were removed and their cortices isolated. Gene expression of pro-inflammatory cytokines, as well as expression of genes implicated in the AD neuropathology were determined. In addition, mediators related to the activation of the microglia, monocytes, and perivascular macrophages were determined in brain cortices, as well.Results. In comparison with the control animals, we found increased gene expression of proinflammatory mediators in mice brain cortex in both IMO and LPS groups. In stressed animals, we also showed an increased expression of genes related to the AD neuropathology, as well as positive correlations between genes implicated in AD development and associated neuroinflammation.Conclusions. Our data indicate that acute exposure to a strong IMO stressor, composed of the combined physical and psychological challenges, induces similar inflammatory and other ADrelated neuropathological changes as the immune LPS treatment. Our data also indicate that cytokines are most likely released from the peripheral immune cells, as we detected myeloid cells activity, without any microglia response. We hypothesize that stress induces innate immune response in the brain that consequently potentiate the expression of genes implicated in the AD-related neuropathology.

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Restraint stress differentially regulates inflammation and glutamate receptor gene expression in the hippocampus of C57BL/6 and BALB/c mice

Cited by 46 publications

References 36 publications

Inbred Substrain Differences Influence Neuroimmune Response and Drinking Behavior

Inbred Substrain Differences Influence Neuroimmune Response and Drinking Behavior

Brain NMDA Receptors in Schizophrenia and Depression

Exposure to a single immobilization or lipopolysaccharide challenge increases expression of genes implicated in the development of Alzheimer’s disease in the mice brain cortex

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