Tests for Anxiety‐Related Behavior in Mice

Hölter, Sabine M.; Einicke, Jan; Sperling, Bettina; Zimprich, Annemarie; Garrett, Lillian; Fuchs, Helmut; Gailus‐Durner, Valérie; Angelis, Martin Hrabé de; Wurst, Wolfgang

doi:10.1002/9780470942390.mo150010

Cited by 37 publications

(36 citation statements)

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“…1B). In addition, 2 months after surgery, we used the elevated plus maze (EPM) and open field (OF) tests to assess anxiety-related exploratory behavior (45). SNI mice showed significantly less exploration of the open arms in the EPM (Sham: 12 ± 2.5 %, SNI: 4.2 ± 0.7 %; Fig 1C), and spent significantly less time in the center area of the OF compared to sham mice (Sham: 12.4 ± 2.3 %, SNI: 5.9 ± 1.7 %; Fig 1D).…”

Section: Resultsmentioning

confidence: 99%

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Neuropathic pain promotes adaptive changes in gene expression in brain networks involved in stress and depression

et al. 2017

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Neuropathic pain is a complex chronic condition characterized by a wide range of sensory, cognitive, and affective symptoms. A large percentage of neuropathic pain patients are also afflicted with depression and anxiety disorders – a pattern that is reliably replicated in animal models. Furthermore, clinical and preclinical studies indicate that chronic pain corresponds with adaptations in several brain networks involved in mood, motivation, and reward. Chronic stress is also a major risk factor for depression. We investigated whether chronic pain and stress affect similar mechanisms, and whether chronic pain can affect gene expression patterns known to be involved in depression. Using two mouse models for neuropathic pain and depression (spared nerve injury (SNI) and chronic unpredictable stress (CUS)) we performed next generation RNA-sequencing and pathway analysis to monitor changes in gene expression in the nucleus accumbens (NAc), the medial prefrontal cortex (mPFC), and the periaqueductal grey (PAG). These three brain regions are implicated in the pathophysiology of depression and in the modulation of pain. In addition to finding unique transcriptome profiles across the three brain regions,.we identified a substantial number of signaling pathway-associated genes with similar changes in expression in both SNI and CUS mice. Many of these genes have been implicated in depression, anxiety and chronic pain in patients. Our study provides a resource of the changes in gene expression induced by long-term neuropathic pain in three distinct brain regions and reveals molecular connections between pain and chronic stress.

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Section: Resultsmentioning

confidence: 99%

“…NSF was performed as reported previously with minor modifications (45). Briefly, mice were food deprived for 24 hours prior and habituated to the testing room for 1 hour.…”

Section: Methodsmentioning

confidence: 99%

Neuropathic pain promotes adaptive changes in gene expression in brain networks involved in stress and depression

et al. 2017

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“…The OFT was conducted as previously described [31]. Briefly, mice were placed in the centre of the OFT and the total distance the mice travelled along with the time they spent in the centre of the field within 5 min was recorded with a video tracking system.…”

Section: Open Field Test (Oft)mentioning

confidence: 99%

Faecal microbiota transplant from aged donor mice affects spatial learning and memory via modulating hippocampal synaptic plasticity- and neurotransmission-related proteins in young recipients

D’Amato

Cesare-Mannelli

Lucarini

et al. 2019

Preprint

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Background. The gut-brain axis and the intestinal microbiota are emerging as key players in health and disease. Shifts in intestinal microbiota composition affect a variety of systems, however, evidence of their direct impact on cognitive functions is still lacking. We tested whether faecal microbiota transplant (FMT) from aged donor mice into young adult recipients affected the hippocampus, an area of the central nervous system (CNS) known to be affected by the ageing process, and related functions. Methods and Findings.Young adult mice were transplanted with the microbiota from either aged or age-matched donor mice. Following transplantation, characterization of the microbiotas and metabolomics profiles along with a battery of cognitive and behavioural tests were performed. Label-free quantitative proteomics was employed to monitor protein expression in the hippocampus of the recipients. Gut permeability, levels of circulating cytokines and expression of markers of microglia cells were also assessed. FMT from aged donors led to impaired spatial learning and memory in young adult recipients, whereas anxiety, explorative behaviour and locomotor activity remained unaffected. This was paralleled by altered expression of proteins involved in synaptic plasticity and neurotransmission in the hippocampus. Also, a strong reduction of bacteria associated with short-chain fatty acids (SCFAs) production (Lachnospiraceae, Faecalibaculum, and Ruminococcaceae) and disorders of the CNS (Prevotellaceae and Ruminococcaceae) was observed. Finally, microglia cells of the hippocampus fimbria, acquired an ageing-like phenotype, while gut permeability and levels of circulating cytokines remained unaffected. Conclusions.These results demonstrate a direct effect of the age-associated shifts of the microbiota on protein expression and key functions of the central nervous system. Furthermore, these results additionally highlight the paramount importance of the gut-brain axis in ageing and provide a strong rationale to devise therapies aiming to restore a younglike microbiota to improve cognitive functions in the elderly.

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“…Animals from each experimental group were put into an open field arena (50 x 50 x 30 cm) (Holter et al, 2015;Kaushik et al, 2018) and allowed to freely move for 10 minutes while being recorded by an overhead camera. The arena was predefined into two parts, the central area (30 x 30 cm) and a peripheral area (the 10 cm area adjacent to the wall of recording chamber).…”

Section: Open Fieldmentioning

confidence: 99%

Epigenetic mechanism of carbohydrate sulfotransferase 3 (CHST3) downregulation in the aging brain

Baidoe-Ansah

Sakib

Jia

et al. 2019

Preprint

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Neural extracellular matrix (ECM) is a complex molecular meshwork surrounding neurons and glial cells in the extracellular space. Structural and functional state of ECM in the brain is tightly regulated by various components of neural ECM such as hyaluronic acid, chondroitin sulfate proteoglycans, link proteins, tenascins, various matrix-modifying enzymes such as chondroitin sulfate synthases and carbohydrate sulfotransferase together with matrix-degrading enzymes. Agedependent accumulation of ECM molecules is implicated in the age-associated decline in synaptic and cognitive functions. Understanding age-associated changes in the expression of genes involved in regulating various components of ECM can provide an insight into the role of ECM in the aging brain. Hence, in this study, we compared the expression levels of ECM regulating genes in three groups of mice: 2-3 months old mice (2-3M), 22-to 26-month-old mice (22-26M) and more than 30-month-old mice (>30M). Using qPCR, we discovered that in the hippocampus of >30M old mice, the majority of ECM related genes are downregulated, while genes related to neuroinflammation are highly upregulated. This pattern was accompanied by a decrease in cognitive performance of the >30M old mice and was most correlated among ECM-related genes with the downregulation of carbohydrate sulfotransferase 3 (CHST3) gene expression. Interestingly, in 24-26M mice, no general decrease in the expression of ECM related genes was observed, although we still found the upregulation in neuroinflammatory genes and downregulation of CHST3. Further analysis of epigenetic mechanisms revealed a decrease in H3K4me3, three methyl groups at the lysine 4 on the histone H3 proteins, associated with the promoter region of CHST3 gene in non-neuronal (NeuN-negative) but not in neuronal (NeuNpositive) cells. We conclude that in 22-26 M old brains there are minor changes in expression of the studied bona fide neural ECM genes but there is a prominent epigenetic dysregulation of the CHST3 gene responsible for 6-sulfation of chondroitin sulfates, which may lead to impaired brain plasticity and cognitive decline.

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Tests for Anxiety‐Related Behavior in Mice

Cited by 37 publications

References 36 publications

Neuropathic pain promotes adaptive changes in gene expression in brain networks involved in stress and depression

Neuropathic pain promotes adaptive changes in gene expression in brain networks involved in stress and depression

Faecal microbiota transplant from aged donor mice affects spatial learning and memory via modulating hippocampal synaptic plasticity- and neurotransmission-related proteins in young recipients

Epigenetic mechanism of carbohydrate sulfotransferase 3 (CHST3) downregulation in the aging brain

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