Abstract
Lesions to the CNS/PNS interface are especially severe, leading to elevated neuronal degeneration. In the present work, we establish the ventral root crush model for mice, and demonstrate the potential of such an approach, by analyzing injury evoked motoneuron loss, changes of synaptic coverage and concomitant glial responses in β2-microglobulin knockout mice (β2m KO). Young adult (8–12 weeks old) C57BL/6J (WT) and β2m KO mice were submitted to a L4–L6 ventral roots crush. Neuronal survival revealed a time-dependent motoneuron-like cell loss, both in WT and β2m KO mice. Along with neuronal loss, astrogliosis increased in WT mice, which was not observed in β2m KO mice. Microglial responses were more pronounced during the acute phase after lesion and decreased over time, in WT and KO mice. At 7 days after lesion β2m KO mice showed stronger Iba-1+ cell reaction. The synaptic inputs were reduced over time, but in β2m KO, the synaptic loss was more prominent between 7 and 28 days after lesion. Taken together, the results herein demonstrate that ventral root crushing in mice provides robust data regarding neuronal loss and glial reaction. The retrograde reactions after injury were altered in the absence of functional MHC-I surface expression.
Highlights
Compression of spinal roots is a common clinical incident, and the root axotomy is directly related to the modification in neuronal function [1]
Astrogliosis increased in WT mice, which was not observed in β2-microglobulin knockout mice (β2m KO) mice
We show the time course of neuronal degeneration, synapse retraction, and glial reaction after
Summary
Compression of spinal roots is a common clinical incident, and the root axotomy is directly related to the modification in neuronal function [1]. There are axonal changes that indicate dysfunction and degeneration happening both proximal and distal to the lesion [2]. Cell bodies of lesioned neurons undergo several morpho-functional changes that, together, are called chromatolysis. They comprise cell body hypertrophy, nucleus displacement, Nissl substance dissociation and expressive disturbance in the expression of structural molecules related to synaptic transmission [4]. The plasticity of the nervous system ensures that structural and functional circuitry remodeling occurs after injury, in particular, with the detachment of the excitatory boutons that were in apposition with the lesioned neuron, which leads to a metabolic change and a shift from the synaptic
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