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NGF-REGULATES SEMAPHORIN3A CHEMOREPULSION OF PRIMARY NOCICEPTIVE AFFERENT in vitro AND IN THE ADULT SPINAL CORD



NGF-REGULATES SEMAPHORIN3A CHEMOREPULSION OF PRIMARY NOCICEPTIVE AFFERENT in vitro AND IN THE ADULT SPINAL CORD



Society for Neuroscience Abstract Viewer & Itinerary Planner : Abstract No 27 6



We previously demonstrated NGF/Adenovirus (Ad) injections into adult spinal cords induced robust regeneration of CGRP(+) axons. During spinal cord development Sema3A is thought to play an important role in targeting CGRP(+) fiber growth to lamina I & II. To examine if over-expression of sema3A could restrict regeneration of these afferents to lamina I & II, we constructed an adenovirus encoding semaphorin3A (Sema/Ad) displaying excellent functional expression. To examine efficacy on sprouting, Sema3/Ad or GFP/Ad were co-injected into adult rat spinal cords with NGF/Ad at either a high or low concentration. We found extensive sprouting of CGRP(+) fibers after co-injections of GFP/Ad with either NGF/Ad dose. However, Sema3A only demonstrated statistically significant reductions when co-injected with the lower concentration of NGF/Ad. The failure of sema3A to elicit chemorepulsion at high NGF concentration indicates NGF can neutralize this growth inhibition. To further identify the mechanism, in vitro experiment using combinations of Sema/Ad, NGF/Ad or GFP/Ad infected U373 cell aggregates and a E10 chicken DRG co-culture system are being examined. Infection with Sema/Ad, but not NGF/Ad or GFP/Ad, leads to extensive neurite repulsion away from U373 aggregates. Co-infection of Sema/Ad with NGF/Ad showed reduced repulsion with increased concentrations of NGF/Ad. Co-infection with equal concentrations of NGF/Ad and Sema/Ad completely abolished the repulsive effect of Sema3A. This study demonstrates that the chemorepulsive effect of Sema3A can be reduced or inhibited by increasing doses of NGF both in vitro and in vivo, and might aid in enhancing regeneration after CNS injury.

Accession: 035365437

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