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Journal of Neuroscience, Vol 15, 439-448, Copyright © 1995 by Society for Neuroscience
Retrograde transport of plasticity signals in Aplysia sensory neurons following axonal injury
JD Gunstream, GA Castro and ET Walters
Department of Physiology and Cell Biology, University of Texas-Houston Medical School 77225.
Following injury to their peripheral branches, mechanosensory neurons in
Aplysia display long-term plasticity that is expressed as soma
hyperexcitability, synaptic facilitation, and neurite outgrowth. To
investigate the nature of signals that convey information about distant
axonal injury, we have investigated the development of injury-induced soma
hyperexcitability in two in vitro preparations. In isolated ganglia,
proximal nerve crush caused hyperexcitability to appear sooner than did
distal crush, and the difference in development of hyperexcitability
indicated that the injury signal moved at a rate (36 mm/d) similar to
previously reported rates of retrograde axonal transport in this animal.
This hyperexcitability was not due to interruption of continuous retrograde
transport of trophic substances (a negative signal) because inhibitors of
axonal transport applied to uncrushed nerve segments did not induce
hyperexcitability. Indeed, inhibitors of axonal transport blocked
crush-induced hyperexcitability, indicating that positive injury signals
are involved. Crush-induced hyperexcitability was unaffected by bathing the
nerve in tetrodotoxin or the ganglion in Cd2+, suggesting that the
retrograde signals depend upon neither spike activity in the nerve nor
synaptic transmission in the ganglion. Close excision of sensory neuron
somata (which largely eliminated delays attributable to axonal transport)
produced soma hyperexcitability that was expressed after 10 hr and lasted
at least 17 d. These data indicate that axonal injury mobilizes signal
molecules that are conveyed by retrograde axonal transport into the soma
and possibly the nucleus, where they induce long-term plasticity similar to
that expressed by these cells during learning and memory.
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