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
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.