Pre-weaning Sensorial and Motor Development in Mice Transpolygenic for the Critical Region of Trisomy 21

Roubertoux, Pierre L.; Bichler, Zoë; Pinoteau, Walter; Jamon, Marc; Sérégaza, Zohra; Smith, Desmond J.; Rubin, Edward; Migliore‐Samour, Danièle

doi:10.1007/s10519-006-9073-8

Cited by 2 publications

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“…Ts65Dn mice also have a greater latency for homing test. In a mouse model for partial trisomy 21, the onset of specific motor and sensorial neonatal behaviors was altered in transgenic mice (Roubertoux et al, 2006). TgDyrk1A mice, another model for Down syndrome, have delayed responses to walking and homing (Altafaj et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Abnormal motor phenotype in the SMNΔ7 mouse model of spinal muscular atrophy

Butchbach

Edwards

Burghes

2007

Neurobiology of Disease

123

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Spinal muscular atrophy (SMA) is recessive motor neuron disease that affects motor neurons in the anterior horn of the spinal cord. SMA results from the reduction of SMN (survival motor neuron) protein. Even though SMN is ubiquitously expressed, motor neurons are more sensitive to the reduction in SMN than other cell types. We have previously generated mouse models of SMA with varying degrees of clinical severity. So as to more clearly understand the pathogenesis of motor neuron degeneration in SMA, we have characterized the phenotype of the SMNΔ7 SMA mouse which normally lives for 13.6 ± 0.7 days. These mice are smaller than their non-SMA littermates and begin to lose body mass at 10.4 ± 0.4 days. SMNΔ7 SMA mice exhibit impaired responses to surface righting, negative geotaxis and cliff aversion but not to tactile stimulation. Spontaneous motor activity and grip strength are also significantly impaired in SMNΔ7 SMA mice. In summary, we have demonstrated an impairment of neonatal motor responses in SMNΔ7 SMA mice. This phenotype characterization could be used to assess the effectiveness of potential therapies for SMA.

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Section: Discussionmentioning

confidence: 99%

Abnormal motor phenotype in the SMNΔ7 mouse model of spinal muscular atrophy

Butchbach

Edwards

Burghes

2007

Neurobiology of Disease

123

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“…The early‐development battery showed a differential developmental delay among the four strains. Figure shows that the mice with the 152F7 extra fragment were more generally impacted, but that the three other trisomic strains were not healthy (Roubertoux et al., ). As expected from these results, we observed in adults a large effect size of impairment of forepaw strength and of hind paw incoordination with 152F7, and an effect in the other strains (Roubertoux et al., ).…”

Section: Commentarymentioning

confidence: 99%

Measuring Preweaning Sensorial and Motor Development in the Mouse

2018

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The immaturity at birth and the slowness of ontogenic processes in mice provide the opportunity to measure rates of development. We describe here 18 measures covering the sensorial and motor onset from birth to weaning. The measures are non-invasive, making a follow-up strategy possible. The first basic protocol indicates how to produce mice with known conceptional or chronological age, as the control of the age is a prerequisite to compare rates of development in groups of mice. The second basic protocol describes a set of methods for identifying the pups during a follow-up study. A third basic protocol describes testing newborn mice for the appearance of sensorial and motor abilities in a follow-up design. Taken together, the three protocols make possible the validation of potential murine models of interest for understanding human developmental disorders. © 2018 by John Wiley & Sons, Inc.

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Pre-weaning Sensorial and Motor Development in Mice Transpolygenic for the Critical Region of Trisomy 21

Cited by 2 publications

References 0 publications

Abnormal motor phenotype in the SMNΔ7 mouse model of spinal muscular atrophy

Abnormal motor phenotype in the SMNΔ7 mouse model of spinal muscular atrophy

Measuring Preweaning Sensorial and Motor Development in the Mouse

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