Searching the Resource Information Network

Our searching services are busy right now. Please try again later

  • Register
X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X

Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.

No
Yes

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

Juana M Pasquini | Francisco J Barrantes | Héctor R Quintá
The Journal of comparative neurology | 2017

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 re-growth. Gal-1 is expressed in vivo at concentrations that favor the monomeric species. The aim of the present study is to investigate whether endogenous Gal-1 is required for spinal axon development and normal locomotor behavior in mice. In order to characterize axonal development, we used a novel combination of 3-DISCO technique with 1-photon microscopy and epifluorescence microscopy under high power LED illumination, followed by serial image section deconvolution and 3-D reconstruction. Cleared whole lgals-1-/- embryos were used to analyze the 3-D cytoarchitecture of motor, commissural, and sensory axons. This approach allowed us to evaluate axonal development, including the number of fibers, fluorescence density of the fiber tracts, fiber length as well as the morphology of axonal sprouting, deep within the tissue. Gal-1 deficient embryos did not show morphological/anatomical alterations in any of the axonal populations and parameters analyzed. In addition, specific guidance receptor PlexinA4 did not change its axonal localization in the absence of Gal-1. Finally, Gal-1 deficiency did not change normal locomotor activity in post-natal animals. Taken together, our results show that development of spinal axons as well as the locomotor abilities observed in adult mice are independent of Gal-1. Supporting our previous observations, the present study further validates the use of lgals-1-/- mice to develop spinal cord- or traumatic brain injury models for the evaluation of the regenerative action of Gal-1.

Pubmed ID: 28512739

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

This is a list of tools and resources that we have found mentioned in this publication.


Anti-Peripherin, clone 8G2 (antibody)

RRID:AB_2284441

This monoclonal targets Prph

View all literature mentions

galectin-1 (H-45) (antibody)

RRID:AB_640838

This polyclonal targets LGALS1

View all literature mentions

Anti-Peripherin, clone 8G2 (antibody)

RRID:AB_2284441

This monoclonal targets Prph

View all literature mentions

Anti-Peripherin, clone 8G2 (antibody)

RRID:AB_2284441

This monoclonal targets Prph

View all literature mentions

galectin-1 (H-45) (antibody)

RRID:AB_640838

This polyclonal targets LGALS1

View all literature mentions

galectin-1 (H-45) (antibody)

RRID:AB_640838

This polyclonal targets LGALS1

View all literature mentions