Body wall injury in the opisthobranch mollusc Aplysia californica is associated with profound long-term alterations in the electrophysiological properties of sensory neurons

californica is associated with profound long-term alterations in the electrophysiological properties of sensory neurons innervating the injured region (Walters, 1987). Peripheral regions of sensory neurons innervating the damaged tissue exhibit a decrease in threshold and an increase in the number of action potentials evoked by a cutaneous test stimulus. An enhancement of central excitability is shown by a decrease in soma action potential threshold, a tendency for the soma to fire in regenerative bursts in response to a brief intracellular depolarizing stimulus and an enhancement of synaptic connections to identified motor neurons. This sensory plasticity appears to be mediated in part by a combination of intense spike activity in the injured sensory neuron and exposure to neuromodulators released from nearby facilitatory interneurons. Similar profound activity-dependent alterations in sensory processing are associated with primary hyperalgesia in mammalian preparations (Woolf and Walters, 1991). More recently, such long-lasting increases in the excitability of sensory neurons have been recorded following axonal crush in A. californica under anesthetic conditions where spike activity and neuromodulator release are largely blocked at the time of injury (Walters et al., 1991; Clatworthy and Walters, 1994). This injury-induced enhancement of sensory excitability is characterized by a significant decrease in spike threshold and in the amplitude of the afterhyperpolarization, a significant increase in spike duration and a significant increase in the number of action potentials evoked by a standard 1 s intracellular depolarizing pulse. Similar robust sensory plasticity has been recorded in two different populations of sensory neurons in A. californica following nerve crush, the VC pleural sensory neurons innervating the tail of the animal and the cerebral J and K sensory neurons innervating the head and mouth of the animal (Walters et al., 1991; Clatworthy and Walters, 1994). The finding that this injury-induced plasticity can be expressed when spike activity and neuromodulator release are largely blocked at the time of injury suggests that additional signals must be involved in mediating the injury-induced sensory 623 The Journal of Experimental Biology 202, 623–630 (1999) Printed in Great Britain © The Company of Biologists Limited 1999 JEB1880