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Abstract :
[en] Brain is a complex organ composed of neurons in a highly. To perform properly their function,
neurons interact with the brain extracellular matrix and are interconnected with other neurons
and glial cells. During head shocks or violent acceleration neurons can be severely damaged,
see their function impaired and their interactions highly modified [1]. Due to the natural
complexity of the neural networks, cellular and molecular mechanism of traumatic brain
injuries (TBI) as well as the propagation of forces is not well understood. Based on the
assumption that cell deformation is the initiating event of TBI [2], we investigate the
mechanical properties of neuronal cells at the sub-cellular level (soma vs axon).
In this way, we developed a new method to control and tune separately matrix stiffness, cell
shape and protein type and density, which are major environment factors that play a role in
neuron function and mechanotransduction [3]. In addition, we developed a magnetic tweezers
set-up to probe the neuron mechanical behaviour in response to a strain exerted at the subcellular
level (axon vs soma).
Taking advantage of both techniques, we studied how the neuron matrix stiffness impacts the
mechanical behaviour of neurons. Cryogenic primary neuron cells were grown on laminincoated
lines deposited on soft polyacrylamide gels with a stiffness ranging from 3 kPa to 500
kPa. By using magnetic tweezers, we probed the mechanosensitivity of soma and axon
structures to determine the mechanical vulnerability of both sub-cellular components. Based
on viscoelastic models and immunostaining experiments, our results show that the cytoskeletal
composition of soma and neurite compartment can explain diffuse axonal injury observed in
TBI.
[1] A.Maas, N. Stocchetti and R. Bullock, Lancet Neurology, 7, 728, 2008.
[2] O. Farkas, J. Povlishok, Prog in Brain Res, 161, 43, 2007.
[3] R. Frischknecht, M. Heine, D. Perrais et al., Nat Neurosc, 12, 897, 2009.
