Mouse model of voluntary movement deficits induced by needlestick injuries to the primary motor cortex
Xiao-Tian Liu1, Chang-Mei Liu2, Zhao-Qian Teng2
1State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China; Savaid Medical School, University of Chinese Academy of Sciences, Beijing 100408, China.
Background:
Motor handicap is prevalent in patients with traumatic brain injury, but currently. there is a challenging task to prevent the degeneration of motor neurons and to fully recover the. voluntary movement after injury.
New Method:
For the first time, we propose to apply needlestick injuries to the primary motor cortex to create mouse model of voluntary movement deficits. Rotarod test, cylinder test and forepaw grip strength test were used to assay motor coordination of both C57BL/6 J and the triple immunodeficient NCG mice. Immunofluorescence staining of PKC-gamma, UCHL1, GFAP, Iba1 and Fluoro-Jade C was performed to analyze the numbers of motor neurons, microglia, astrocytes and degenerating neurons.
Results:
Mice on either C57BL/6 J or immunodeficient background with the unilateral primary motor cortex injury exhibit motor neuron death, activation of glial cells and deficits in voluntary movement.
Conclusions:
The main finding of this study was that the unilateral primary motor cortex injured by needlesticks leads to reactive gliosis, motor neuron death and voluntary movement deficits in mice. This needlestick injury model of primary motor cortex might be useful for future exploration of underlying mechanisms of motor neuron degeneration and of promising treatment modalities such as cell transplantation to improve locomotor deficiency following neurotrauma.
