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Journal of Neuroscience, Vol 15, 3440-3446, Copyright © 1995 by Society for Neuroscience
Axoplasm enriched in a protein mobilized by nerve injury induces memory- like alterations in Aplysia neurons
RT Ambron, MF Dulin, XP Zhang, R Schmied and ET Walters
Department of Anatomy, Columbia University, New York, New York 10032, USA.
Axon regeneration after injury and long-term alterations associated with
learning both require protein synthesis in the neuronal cell body, but the
signals that initiate these changes are largely unknown. Direct evidence
that axonal injury activates molecular signals in the axon was obtained by
injecting axoplasm from crushed or uncrushed nerves into 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 decrease in spike afterhyperpolarization 1
d after injection. Because similar changes occur in the same cells after
learning, these data suggest that some of the long-lasting adaptive changes
that occur after injury and learning may be induced by common axoplasmic
signals. Since the signals in axoplasm must be conveyed to the cell soma,
we have begun to test the hypothesis that at least some of these signals
are proteins containing a nuclear localization signal (NLS). Axoplasmic
proteins at the crush site and those that accumulated at a ligation
proximal to the crush were probed with an antibody to an amino acid
sequence (sp) containing a NLS that provides access to the retrograde
transport/nuclear import pathway. One protein, sp97, displayed properties
expected of an axonal injury signal: it responded to injury by undergoing
an anterograde-to-retrograde change in movement and, when the ligation was
omitted, it was transported to the cell bodies of the injured neurons.
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