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Journal of Neuroscience, Vol 7, 400-407, Copyright © 1987 by Society for Neuroscience
Site-specific sensitization of defensive reflexes in Aplysia: a simple model of long-term hyperalgesia
ET Walters
Brief, noxious, electrical or mechanical stimulation of the skin of Aplysia
produces enhancement of defensive reflexes triggered at the same site for
at least a week after the noxious stimulation. This site- specific
behavioral sensitization can be expressed as an increase in duration of the
siphon-withdrawal reflex and as an increase in magnitude of the
tail-withdrawal reflex. It is unlikely that peripheral factors play a
predominant role in the long-term memory. First, long- term enhancement is
blocked when the CNS is disconnected from the noxious stimulation site by
nerve transection. Second, long-term enhancement is blocked by preventing
neural activation at the noxious stimulation site, indicating that
persistent physical damage alone is insufficient to cause the enhancement.
A role for activity-dependent extrinsic modulation (ADEM) of mechanosensory
neurons is suggested by similar site-specific enhancement produced when
weak sensory activation is paired with general modulation elicited by
strong stimulation of a distant site. Because this pairing represents a
form of classical conditioning, site-specific sensitization and cutaneous
classical conditioning appear to be closely related in this system. These
findings suggest that site-specific sensitization reflects, at least in
part, a central, long-term memory of injury. This form of memory may be
phylogenetically widespread, and functionally similar to aspects of
hyperalgesia. In addition, the close relationship between site-specific
sensitization and cutaneous classical conditioning supports the hypothesis
that some forms of classical conditioning evolved from mechanisms of
sensitization.
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