Tau Gene Deletion does not Influence Axonal Regeneration and Retinal Neuron Survival in the Injured Mouse Visual System.

Léa Rodriguez,Vincent Pernet,Julius Baya Mdzomba,Sandrine Joly

doi:10.3390/ijms21114100

Abstract

In the present study, we hypothesized that the microtubule-associated protein Tau may influence retinal neuron survival and axonal regeneration after optic nerve injury. To test this hypothesis, the density of retinal ganglion cells was evaluated by immunostaining retinal flat-mounts for RNA-binding protein with multiple splicing (RBPMS) two weeks after optic nerve micro-crush lesion in Tau-deprived (Tau knock-out (KO)) and wild-type (WT) mice. Axon growth was determined on longitudinal sections of optic nerves after anterograde tracing. Our results showed that the number of surviving retinal ganglion cells and growing axons did not significantly vary between WT and Tau KO animals. Moreover, sustained activation of the neuronal growth program with ciliary neurotrophic factor (CNTF) resulted in a similar increase in surviving neurons and in growing axons in WT and Tau KO mice. Taken together, our data suggest that Tau does not influence axonal regeneration or neuronal survival.

Highlights

Traumatic injuries in the adult central nervous system (CNS) are often associated with permanent neurological impairments
A role for Tau has been established in retinal ganglion cell death, its influence in axonal regeneration remains unclear. To clarify this in the present study, we examined the effect of Tau deletion on retinal ganglion cell axon regeneration after mouse optic nerve crush with or without ciliary neurotrophic factor (CNTF) stimulation
Using the classical model of mouse optic nerve injury, we observed that the level of Tau decreased after massive retinal ganglion cells (RGCs) loss, suggesting that RGCs are an important source of Tau in the retina

Summary

Introduction

Traumatic injuries in the adult central nervous system (CNS) are often associated with permanent neurological impairments This is mainly due to the limited capacity of adult axons to regenerate and to the irreversible loss of neuronal cells [1,2]. Microtubule polymerization is sufficient to enable axonal extension from the lesion site. Topic application of the microtubule-stabilizing agent Paclitaxel (Taxol) on the injured optic nerve increased axonal growth and facilitated inflammation-induced axonal regeneration [9,10]. It has been proposed that microtubule-associated protein 1 B (MAP1B) and collapsin response mediator protein-2 (CRMP2) activity could be modulated to stimulate axonal regeneration in the optic nerve [12].

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Conclusion