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Low-Cost Gait Analysis for Behavioral Phenotyping of Mouse Models of Neuromuscular Disease
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Subtle gait abnormalities in Nedd4 heterozygous mice.

Daria Camera1, Natasha A Boase2, Sharad Kumar3

  • 1Health Innovations Research Institute, School of Medical Science, RMIT University, PO Box 71, Bundoora, VIC 3083, Australia.

Behavioural Brain Research
|November 28, 2013
PubMed
Summary

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Reduced Nedd4 levels in adult mice cause age-dependent gait defects, potentially linked to altered GluR1 distribution in cerebellar neurons. This study reveals Nedd4

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Nedd4 ubiquitin ligase is crucial for neuronal development but its adult brain function is poorly understood due to homozygous knockout lethality.
  • Nedd4 heterozygous mice offer a model to study Nedd4's physiological roles in the mature central nervous system.

Purpose of the Study:

  • To investigate the physiological roles of Nedd4 in adult brain function, specifically motor control and gait.
  • To determine if a partial reduction in Nedd4 levels impacts motor function and gait in adult mice.

Main Methods:

  • Utilized Nedd4 heterozygous mice, which are viable, to assess motor function and gait.
  • Analyzed Nedd4 expression patterns in the central nervous system, focusing on motor areas and the cerebellum.
  • Employed confocal immunohistochemistry to examine GluR1 expression and distribution in Purkinje neurons.
Keywords:
AMPARCerebellumE3 ubiquitin ligaseGaitGluR1

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Main Results:

  • Nedd4 heterozygous mice exhibited significant age-dependent gait abnormalities, particularly evident at 6 months of age.
  • Gait defects included an overall extension of gait, linked to pronounced Nedd4 expression in cerebellar Purkinje neurons.
  • Subtle changes in GluR1 expression and redistribution into larger puncta were observed in Purkinje neurons of 6-month-old Nedd4 heterozygous mice.

Conclusions:

  • A 50% reduction in Nedd4 levels is sufficient to cause significant gait defects in 6-month-old mice.
  • Altered distribution of GluR1 in cerebellar neurons may contribute to the observed gait abnormalities.
  • This study highlights the importance of Nedd4 in maintaining normal gait and motor function in the adult brain.