AXOPLASM ENRICHED IN A PROTEIN MOBILIZED BY NERVE INJURY INDUCES MEMORY-LIKE ALTERATIONS IN APLYSIA NEURONS

Citation
Rt. Ambron et al., AXOPLASM ENRICHED IN A PROTEIN MOBILIZED BY NERVE INJURY INDUCES MEMORY-LIKE ALTERATIONS IN APLYSIA NEURONS, The Journal of neuroscience, 15(5), 1995, pp. 3440-3446
Citations number
53
Categorie Soggetti
Neurosciences,Neurosciences
Journal title
ISSN journal
02706474
Volume
15
Issue
5
Year of publication
1995
Part
1
Pages
3440 - 3446
Database
ISI
SICI code
0270-6474(1995)15:5<3440:AEIAPM>2.0.ZU;2-8
Abstract
Axon regeneration after injury and long-term alterations associated wi th learning both require protein synthesis in the neuronal cell body, but the signals that initiate these changes are largely unknown. Direc t evidence that axonal injury activates molecular signals in the axon was obtained by injecting axoplasm from crushed or uncrushed nerves in to somata of sensory neurons with uncrushed axons, Those injected with crush axoplasm behaved as if their axons had been crushed, exhibiting increases in both repetitive firing and spike duration, and a decreas e in spike afterhyperpolarization 1 d after injection, Because similar changes occur in the same cells after learning, these data suggest th at some of the long-lasting adaptive changes that occur after injury a nd learning may be induced by common axoplasmic signals, Since the sig nals in axoplasm must be conveyed to the cell soma, we have begun to t est the hypothesis that at least some of these signals are proteins co ntaining a nuclear localization signal (NLS), Axoplasmic proteins at t he crush site and those that accumulated at a ligation proximal to the crush were probed with an antibody to an amino acid sequence (sp) con taining a NLS that provides access to the retrograde transport/nuclear import pathway, One protein, sp97, displayed properties expected of a n axonal injury signal: it responded to injury by undergoing an antero grade-to-retrograde change in movement acid, when the ligation was omi tted, it was transported to the cell bodies of the injured neurons.