Normal development of spinal axons in early embryo stages and posterior locomotor function is independent of GAL-1

PASQUINI JM, BARRANTES FJ, QUINTÁ HR

JOURNAL OF COMPARATIVE NEUROLOGY

WILEY-LISS, DIV JOHN WILEY & SONS INC

Lugar: New York; Año: 2017 vol. 525 p. 2861 - 2875

0021-9967

It was recently described that Galectin-1 (Gal-1) promotes axonal growth after spinal cord injury.This effect depends on protein dimerization, since monomeric Gal-1 fails to stimulate axonal regrowth.Gal-1 is expressed in vivo at concentrations that favor the monomeric species. The aim ofthe present study is to investigate whether endogenous Gal-1 is required for spinal axon developmentand normal locomotor behavior in mice. In order to characterize axonal development, weused a novel combination of 3-DISCO technique with 1-photon microscopy and epifluorescencemicroscopy under high power LED illumination, followed by serial image section deconvolutionand 3-D reconstruction. Cleared whole lgals-1-/- embryos were used to analyze the 3-D cytoarchitectureof motor, commissural, and sensory axons. This approach allowed us to evaluate axonaldevelopment, including the number of fibers, fluorescence density of the fiber tracts, fiber lengthas well as the morphology of axonal sprouting, deep within the tissue. Gal-1 deficient embryos didnot show morphological/anatomical alterations in any of the axonal populations and parametersanalyzed. In addition, specific guidance receptor PlexinA4 did not change its axonal localization inthe absence of Gal-1. Finally, Gal-1 deficiency did not change normal locomotor activity in postnatalanimals. Taken together, our results show that development of spinal axons as well as thelocomotor abilities observed in adult mice are independent of Gal-1. Supporting our previousobservations, the present study further validates the use of lgals-1-/- mice to develop spinal cordortraumatic brain injury models for the evaluation of the regenerative action of Gal-1.