The light spot test: Measuring anxiety in mice in an automated home-cage environment

Aarts, Emmeke; Maroteaux, Gregoire; Loos, Maarten; Koopmans, Bastijn; Kovačević, Jovana; Smit, August B.; Verhage, Matthijs; Sluis, Sophie van der

doi:10.1016/j.bbr.2015.06.011

Cited by 41 publications

(53 citation statements)

References 25 publications

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“…The DLB was the most stressful test environment compared with the OF test in which the intensity of the light was lower and therefore less stressful. Human-animal interactions in combination with heightened arousal because of novelty of the DLB, as previously discussed in Aarts et al (2015), might have made the increased anxiety response observed in mdx mice in this box more apparent compared with the habituated home-cage environment. Repeated testing for anxiety is known to reduce anxiety-related behaviors (Crawley 2007), which can be an additional factor in the absence of an anxiety phenotype in the OF.…”

Section: Discussionmentioning

confidence: 80%

“…This effect was comparable to the effect observed in the DLB, which only lasted 10 min. Human-animal interactions in combination with heightened arousal because of novelty of the DLB, as previously discussed in Aarts et al (2015), might have made the increased anxiety response observed in mdx mice in this box more apparent compared with the habituated home-cage environment. Previous reports are not conclusive about an anxiety phenotype in mdx mice.…”

Section: Discussionmentioning

confidence: 80%

“…The anxiety test in the PhenoTyper has been previously described in Aarts et al (2015). Fifteen minutes after the start of the fifth dark phase (1915 h), a bright light-emitting diode (LED) mounted in the top unit was automatically switched on (2000 lux) for the duration of 1 h. The light beam largely overlapped with the feeding station, and also illuminated the area between the feeder station and left shelter entry.…”

Section: Automated Home-cage -Anxiety Testmentioning

confidence: 99%

“…Data were log10 transformed for parameters that were not normally distributed as previously described in Loos et al (2014a). The home-cage anxiety test was analyzed using a factorial-repeated measures analysis of variance (ANOVA) as described in Aarts et al (2015). Barnes maze data, and error types during the home-cage RL task, were analyzed using factorial-repeated measures ANOVAs performed as multilevel models, where genotype and day were added as predictors.…”

Section: Statistical Analysesmentioning

confidence: 99%

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Cognitive flexibility deficits in a mouse model for the absence of full‐length dystrophin

Remmelink

Aartsma‐Rus

Smit

et al. 2016

Genes Brain and Behavior

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Duchenne muscular dystrophy (DMD) is a progressive muscle-wasting disorder, caused by mutations in the DMD gene and the resulting lack of dystrophin. The DMD gene has seven promoters, giving rise to multiple full-length and shorter isoforms. Besides the expression of dystrophin in muscles, the majority of dystrophin isoforms is expressed in brain and dystrophinopathy can lead to cognitive deficits, including intellectual impairments and deficits in executive function. In contrast to the muscle pathology, the impact of the lack of dystrophin on the brain is not very well studied. Here, we study the behavioral consequences of a lack of full-length dystrophin isoforms in mdx mice, particularly with regard to domains of executive functions and anxiety. We observed a deficit in cognitive flexibility in mdx mice in the absence of motor dysfunction or general learning impairments using two independent behavioral tests. In addition, increased anxiety was observed, but its expression depended on the context. Overall, these results suggest that the absence of full-length dystrophin in mice has specific behavioral effects that compare well to deficits observed in DMD patients.

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Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 80%

Section: Automated Home-cage -Anxiety Testmentioning

confidence: 99%

Section: Statistical Analysesmentioning

confidence: 99%

See 2 more Smart Citations

Cognitive flexibility deficits in a mouse model for the absence of full‐length dystrophin

Remmelink

Aartsma‐Rus

Smit

et al. 2016

Genes Brain and Behavior

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“…The analysis of behavioral rhythmicity has led to the development of specialized hardware and software for a variety of different applications, with target organisms ranging from fruit flies to humans, and data acquisition based on methods including infrared (IR) sensors, accelerometers, and radioand video-tracking [3][4][5][6][7][8]. Associated with these systems, a range of commercially available analysis packages have been developed to run on Windows or MacOS operating systems [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Monitoring and Analyzing of Circadian and Ultradian Locomotor Activity Based on Raspberry-Pi

et al. 2016

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Abstract:A new device based on the Raspberry-Pi to monitor the locomotion of Arctic marine invertebrates and to analyze chronobiologic data has been made, tested and deployed. The device uses infrared sensors to monitor and record the locomotor activity of the animals, which is later analyzed. The software package consists of two separate scripts: the first designed to manage the acquisition and the evolution of the experiment, the second designed to generate actograms and perform various analyses to detect periodicity in the data (e.g., Fourier power spectra, chi-squared periodograms, and Lomb-Scargle periodograms). The data acquisition hardware and the software has been previously tested during an Arctic mission with an arctic marine invertebrate.

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Clinicopathologic Dissociation: Robust Lafora Body Accumulation in Malin KO Mice Without Observable Changes in Home‐Cage Behavior

Krishnan,

Wu,

Mazumder

et al. 2024

J of Comparative Neurology

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Lafora disease (LD) is a syndrome of progressive myoclonic epilepsy and cumulative neurocognitive deterioration caused by recessively inherited genetic lesions of EPM2A (laforin) or NHLRC1 (malin). Neuropsychiatric symptomatology in LD is thought to be directly downstream of neuronal and astrocytic polyglucosan aggregates, termed Lafora bodies (LBs), which faithfully accumulate in an age‐dependent manner in all mouse models of LD. In this study, we applied home‐cage monitoring to examine the extent of neurobehavioral deterioration in a model of malin‐deficient LD as a means to identify robust preclinical endpoints that may guide the selection of novel genetic treatments. At 6 weeks, ∼6–7 months, and ∼12 months of age, malin‐deficient mice (“KO”) and wild‐type (WT) littermates underwent a standardized home‐cage behavioral assessment designed to non‐obtrusively appraise features of rest/arousal, consumptive behaviors, risk aversion, and voluntary wheel‐running. At all timepoints, and over a range of metrics that we report transparently, WT and KO mice were essentially indistinguishable. In contrast, within WT mice compared across the same timepoints, we identified age‐related nocturnal hypoactivity, diminished sucrose preference, and reduced wheel‐running. Neuropathological examinations in subsets of the same mice revealed expected age‐dependent LB accumulation, gliosis, and microglial activation in cortical and subcortical brain regions. At 12 months of age, despite the burden of neocortical LBs, we did not identify spontaneous seizures during an electroencephalographic (EEG) survey, and KO and WT mice exhibited similar spectral EEG features. However, in an in vitro assay of neocortical function, paroxysmal bursts of network activity (UP states) in KO slices were more prolonged at 3 and 6 months of age, but similar to WT at 12 months. KO mice displayed a distinct response to pentylenetetrazole, with a greater incidence of clonic seizures and a more pronounced postictal suppression of movement, feeding, and drinking behavior. Together, these results highlight the clinicopathologic dissociation in a mouse model of LD, where the accrual of LBs may latently modify cortical circuit function and seizure threshold without clinically meaningful changes in home‐cage behavior. Our findings allude to a delay between LB accumulation and neurobehavioral decline in LD: one that may provide a window for treatment, and whose precise duration may be difficult to ascertain within the typical lifespan of a laboratory mouse.

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The light spot test: Measuring anxiety in mice in an automated home-cage environment

Cited by 41 publications

References 25 publications

Cognitive flexibility deficits in a mouse model for the absence of full‐length dystrophin

Cognitive flexibility deficits in a mouse model for the absence of full‐length dystrophin

Monitoring and Analyzing of Circadian and Ultradian Locomotor Activity Based on Raspberry-Pi

Clinicopathologic Dissociation: Robust Lafora Body Accumulation in Malin KO Mice Without Observable Changes in Home‐Cage Behavior

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