Digging and marble burying in mice: simple methods for in vivo identification of biological impacts

Deacon, Robert M. J.

doi:10.1038/nprot.2006.20

Cited by 424 publications

(379 citation statements)

References 17 publications

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“…The hippocampal formation is involved in both learning and the execution of innate routine behaviour [21][22][23]49].…”

Section: (D) the Hippocampus And Innate Routine Behaviourmentioning

confidence: 99%

“…Objects placed in the cage (like marbles) induce explorative behaviour. This includes prolonged digging eventually leading to burying of the marbles [23]. A video recorded during the 30 min of this experiment together with behaviour evaluation software (Ethovision XT, Noldus Information technology) was used to analyse differences in mouse behaviour and quantify behavioural parameters such as time spent for running, rearing and digging as well as the latency before starting these activities.…”

Section: (F ) Nest Buildingmentioning

confidence: 99%

“…(g) Explorative behaviour/marble burying Initially, we tested the performance of WT and Per1 2/2 mice in the 'marble burying' set-up, an experimental situation to test mice for their interest in 'novelty' [23,28]. It took advantage of the fact that in a fresh conventional mouse cage (Polycarbonate, type II Eurostandard 267 Â 207 Â 140 mm) filled with a 50 mm layer of litter (Lignocel, Hygienic Animal Embedding, Rettenmaier & Söhne GmbH & Co KG, Rosenberg, Germany) animals explore the cages in all three dimensions by running, rearing and digging.…”

Section: (F ) Nest Buildingmentioning

confidence: 99%

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The clock genePeriod1regulates innate routine behaviour in mice

et al. 2014

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Laboratory mice are well capable of performing innate routine behaviour programmes necessary for courtship, nest-building and exploratory activities although housed for decades in animal facilities. We found that in mice inactivation of the clock gene Period1 profoundly changes innate routine behaviour programmes like those necessary for courtship, nest building, exploration and learning. These results in wild-type and Period1 mutant mice, together with earlier findings on courtship behaviour in wild-type and period-mutant Drosophila melanogaster, suggest a conserved role of Period-genes on innate routine behaviour. Additionally, both per-mutant flies and Period1-mutant mice display spatial learning and memory deficits. The profound influence of Period1 on routine behaviour programmes in mice, including female partner choice, may be independent of its function as a circadian clock gene, since Period1-deficient mice display normal circadian behaviour.

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“…The hippocampal formation is involved in both learning and the execution of innate routine behaviour [21][22][23]49].…”

Section: (D) the Hippocampus And Innate Routine Behaviourmentioning

confidence: 99%

Section: (F ) Nest Buildingmentioning

confidence: 99%

Section: (F ) Nest Buildingmentioning

confidence: 99%

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The clock genePeriod1regulates innate routine behaviour in mice

et al. 2014

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“…Mice with AS bury fewer marbles than their wild-type controls [38]. This robust and reproducible decrease in marble burying exhibited by mice with AS may indicate abnormal repetitive, compulsive, anxiety-driven behaviors, or motor dysfunction [46]. Socially, Ube3a m-/p+ mice show reduced activity in social testing but not substantial social preference deficit [25,38].…”

Section: As Mouse Modelsmentioning

confidence: 96%

Angelman Syndrome

et al. 2015

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In this review we summarize the clinical and genetic aspects of Angelman syndrome (AS), its molecular and cellular underpinnings, and current treatment strategies. AS is a neurodevelopmental disorder characterized by severe cognitive disability, motor dysfunction, speech impairment, hyperactivity, and frequent seizures. AS is caused by disruption of the maternally expressed and paternally imprinted UBE3A, which encodes an E3 ubiquitin ligase. Four mechanisms that render the maternally inherited UBE3A nonfunctional are recognized, the most common of which is deletion of the maternal chromosomal region 15q11-q13. Remarkably, duplication of the same chromosomal region is one of the few characterized persistent genetic abnormalities associated with autistic spectrum disorder, occurring in >1-2 % of all cases of autism spectrum disorder. While the overall morphology of the brain and connectivity of neural projections appear largely normal in AS mouse models, major functional defects are detected at the level of context-dependent learning, as well as impaired maturation of hippocampal and neocortical circuits. While these findings demonstrate a crucial role for ubiquitin protein ligase E3A in synaptic development, the mechanisms by which deficiency of ubiquitin protein ligase E3A leads to AS pathophysiology in humans remain poorly understood. However, recent efforts have shown promise in restoring functions disrupted in AS mice, renewing hope that an effective treatment strategy can be found.Key Words Angelman syndrome . neurodevelopmental disorders . autism . ubiquitin ligase . Ube3a . Imprinting. Clinical OverviewIn 1965, the English physician Harry Angelman described 3 patients who presented with a stiff, jerky gait, absence of speech, excessive laughter, and seizures. The disorder that came to bear his name [Angelman syndrome (AS)] is now recognized to affect approximately 1 in 15,000 individuals and is characterized by motor dysfunction, severe intellectual disability, speech impairment, seizures, hyperactivity, and autism spectrum disorder (ASD) as a common comorbidity [1].Developmental delay in individuals with AS is usually observed within the first year of life. Though most individuals lack speech entirely, some who are mildly affected can acquire a few words. Receptive language is less impaired. Seizures occur in >80 % of patients, and onset is usually before the age of 3 years. Movement disorders include tremors, jerkiness, and ataxia. The characteristic behaviors of AS include mouthing of objects, happy demeanor with easily provoked laughter, attraction to water, hyperactivity, short attention span, and decreased sleeping (see recent reviews for more detailed description of the clinical phenotype [2][3][4]). These features of AS can be seen in other neurodevelopmental disorders, leading to a broad differential diagnosis [5], which has recently been reviewed (Table 1) [6]. Overlapping clinical features may indicate common neurophysiological pathways,

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“…Compulsive-anxiety behaviour in mice was assessed by this test (25). Eight marbles (1.5 cm diameter) were placed uniformly in a cage (45 × 28 × 20 cm) containing a constant amount of sawdust (3 cm deep).…”

Section: Marble Burying Testmentioning

confidence: 99%