Application of hairless mouse strain to bioluminescence imaging of Arc expression in mouse brain

Izumi, Hironori; Ishimoto, Tetsuya; Yamamoto, Hiroshi; Mori, Hisashi

doi:10.1186/s12868-017-0335-6

Cited by 8 publications

(4 citation statements)

References 29 publications

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“…Future studies to address this may include crossing transgenes onto an albino background as we have done here to avoid the pigmentation and avoid the need for shaving. A hairless mouse might provide optimal background (Collaco and Geusz, 2003; Izumi et al, 2017) although hairless mice might still have skin pigmentation and can show other alterations in their phenotype (Hoshino et al, 2017). Moreover, there are sex differences in the optical properties of murine skin to be considered in experimental design.…”

Section: Discussionmentioning

confidence: 99%

Methods for Detecting PER2:LUCIFERASE Bioluminescence Rhythms in Freely Moving Mice

et al. 2021

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Circadian rhythms are driven by daily oscillations of gene expression. An important tool for studying cellular and tissue circadian rhythms is the use of a gene reporter, such as bioluminescence from the reporter gene luciferase controlled by a rhythmically expressed gene of interest. Here we describe methods that allow measurement of circadian bioluminescence from a freely moving mouse housed in a standard cage. Using a LumiCycle In Vivo (Actimetrics), we determined conditions that allow detection of circadian rhythms of bioluminescence from the PER2 reporter, PER2::LUC, in freely behaving mice. The LumiCycle In Vivo applies a background subtraction that corrects for effects of room temperature on photomultiplier tube (PMT) output. We tested delivery of d-luciferin via a subcutaneous minipump and in the drinking water. We demonstrate spikes in bioluminescence associated with drinking bouts. Further, we demonstrate that a synthetic luciferase substrate, CycLuc1, can support circadian rhythms of bioluminescence, even when delivered at a lower concentration than d-luciferin, and can support longer-term studies. A small difference in phase of the PER2::LUC bioluminescence rhythms, with females phase leading males, can be detected with this technique. We share our analysis scripts and suggestions for further improvements in this method. This approach will be straightforward to apply to mice with tissue-specific reporters, allowing insights into responses of specific peripheral clocks to perturbations such as environmental or pharmacological manipulations.

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Section: Discussionmentioning

confidence: 99%

Methods for Detecting PER2:LUCIFERASE Bioluminescence Rhythms in Freely Moving Mice

et al. 2021

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“…Further investigations are necessary to identify the bioluminescence signals from peripheral tissues. A hairless mouse strain [ 31 ] would help us further examine peripheral Bdnf expression by in vivo BLI. In contrast, TokeOni produced signals in the brain, reflecting the high expression levels of endogenous BDNF in the brain.…”

Section: Discussionmentioning

confidence: 99%

“…After BLI, the mice were housed in the dark for a further 2 days, and then the mice were exposed to light for 1 h. After light exposure, the mice were housed in the dark for 5 h, and then in vivo BLI was performed again. Region of interest (ROI) analysis was performed according to previous reports [ 30 , 31 ] with modifications. Briefly, the region of the cerebral cortex was estimated by the bioluminescence signal image (Supplementary Fig.…”

Section: Methodsmentioning

confidence: 99%

Visualization of activity-regulated BDNF expression in the living mouse brain using non-invasive near-infrared bioluminescence imaging

et al. 2020

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Altered levels of brain-derived neurotrophic factor (BDNF) have been reported in neurologically diseased human brains. Therefore, it is important to understand how the expression of BDNF is controlled under pathophysiological as well as physiological conditions. Here, we report a method to visualize changes in BDNF expression in the living mouse brain using bioluminescence imaging (BLI). We previously generated a novel transgenic mouse strain, Bdnf-Luciferase (Luc), to monitor changes in Bdnf expression; however, it was difficult to detect brain-derived signals in the strain using BLI with d-luciferin, probably because of incomplete substrate distribution and light penetration. We demonstrate that TokeOni, which uniformly distributes throughout the whole mouse body after systematic injection and produces a near-infrared bioluminescence light, was suitable for detecting signals from the brain of the Bdnf-Luc mouse. We clearly detected brain-derived bioluminescence signals that crossed the skin and skull after intraperitoneal injection of TokeOni. However, repeated BLI using TokeOni should be limited, because repeated injection of TokeOni on the same day reduced the bioluminescence signal, presumably by product inhibition. We successfully visualized kainic acid-induced Bdnf expression in the hippocampus and sensory stimulation-induced Bdnf expression in the visual cortex. Taken together, non-invasive near-infrared BLI using Bdnf-Luc mice with TokeOni allowed us to evaluate alterations in BDNF levels in the living mouse brain. This will enable better understanding of the involvement of BDNF expression in the pathogenesis and pathophysiology of neurological diseases.

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“…Maternally exposed GLA is reported to cause reduced locomotor activity, impaired memory formation, and an autism-like behavior in offspring in mice ( Laugeray et al, 2014 ; Dong et al, 2020 ; Oummadi et al, 2023 ). Previously, we established a novel transgenic (Tg) mouse strain termed Arc-Luc Tg to visualize neuronal activity-dependent Arc expression in vivo ( Izumi et al, 2017 ). Arc is one of the molecules responsible for synaptic regulation among neurons, and its expression is induced in a neuronal activity-dependent manner ( Okuno et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Developmental synapse pathology triggered by maternal exposure to the herbicide glufosinate ammonium

Izumi,

Demura,

Imai

et al. 2023

Front. Mol. Neurosci.

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Environmental and genetic factors influence synapse formation. Numerous animal experiments have revealed that pesticides, including herbicides, can disturb normal intracellular signals, gene expression, and individual animal behaviors. However, the mechanism underlying the adverse outcomes of pesticide exposure remains elusive. Herein, we investigated the effect of maternal exposure to the herbicide glufosinate ammonium (GLA) on offspring neuronal synapse formation in vitro. Cultured cerebral cortical neurons prepared from mouse embryos with maternal GLA exposure demonstrated impaired synapse formation induced by synaptic organizer neuroligin 1 (NLGN1)–coated beads. Conversely, the direct administration of GLA to the neuronal cultures exhibited negligible effect on the NLGN1-induced synapse formation. The comparison of the transcriptomes of cultured neurons from embryos treated with maternal GLA or vehicle and a subsequent bioinformatics analysis of differentially expressed genes (DEGs) identified “nervous system development,” including “synapse,” as the top-ranking process for downregulated DEGs in the GLA group. In addition, we detected lower densities of parvalbumin (Pvalb)-positive neurons at the postnatal developmental stage in the medial prefrontal cortex (mPFC) of offspring born to GLA–exposed dams. These results suggest that maternal GLA exposure induces synapse pathology, with alterations in the expression of genes that regulate synaptic development via an indirect pathway distinct from the effect of direct GLA action on neurons.

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Application of hairless mouse strain to bioluminescence imaging of Arc expression in mouse brain

Cited by 8 publications

References 29 publications

Methods for Detecting PER2:LUCIFERASE Bioluminescence Rhythms in Freely Moving Mice

Methods for Detecting PER2:LUCIFERASE Bioluminescence Rhythms in Freely Moving Mice

Visualization of activity-regulated BDNF expression in the living mouse brain using non-invasive near-infrared bioluminescence imaging

Developmental synapse pathology triggered by maternal exposure to the herbicide glufosinate ammonium

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