Similar Neuronal Alterations Induced by Axonal Injury And Learning in Aplysia

Abstract

Learning in the marine mollusk Aplysia has been associated with enhanced sensory function, expressed in mechanosensory neurons as (i) decreases in action potential threshold, accommodation, and afterhyperpolarization, and (ii) increases in action potential duration, afterdischarge, and synaptic transmission. These alterations also occur, with a delay, after sensory axons are injured under conditions in which synaptic transmission is severely reduced. The latency and specificity of injury-induced alterations indicate that induction signals are generated at the site of injury and conveyed centrally by axonal transport. Similarities in neuronal modifications support the hypothesis that some memory mechanisms evolved from mechanisms of injury-induced sensory compensation and repair.

Recovery of tail-elicited siphon-withdrawal reflex following unilateral axonal injury is associated with ipsi- and contralateral changes in gene expression in Aplysia californica

“…It is interesting to note that increases in excitability is detected in axotomized sensory neurons located in the ipsilateral pleural ganglion but not in nonaxotomized sensory neurons in the contralateral ganglion (Walters et al, 1991). The electrophysiological and molecular data presented in this study suggest that contralateral pleural sensory neurons sprout to the injured side.…”

“…Thus, the loss of sensory neuron targets may downregulate the expression of sensorin A and FMRFamide. The decrease in expression of these inhibitory neuropeptides in the ipsilateral pleural ganglia could contribute to the increased excitability of axotomized mechanosensory neurons and increased synaptic connection with motor neurons (Walters et al, 1991;Clatworthy and Walters, 1994). …”

“…To accomplish this, we injured peripheral pedal nerves as well as the pleural-pedal connective. Surgery and injury were performed as described by Walters et al (1991) with the following modifications. The animals were anesthetized by injecting one third their body weight of cold isotonic (363 mu) MgCl, into the neck region and kept in artificial sea water maintained at 0°C for 10 min.…”

“…Due to its accessible and symmetric nervous system, Aplysia has been used as a model system to investigate behavioral, cellular and molecular changes following axonal injury (Aletta and Goldberg, 1982;Fredman 1988;Scott and Kirk, 1992). For example, injury to ventrocaudal (VC) mechanosensory neuron axons blocks the tail-elicited siphon-withdrawal reflex and leads to increased sensory neuron excitability (Walters et al, 1991). Axotomy of the giant metacerebral cell (MCC) causes changes in the rate of synthesis of specific proteins including a 60 kDa neurofilamentlike protein .…”

Synaptogenesis Regulates Axotomy-Induced Activation of c-Jun-Activator Protein-1 Transcription

“…Crushing peripheral nerves axotomizes Aplysia sensory neuron axons Steffensen et al, 1995), resulting in regenerative growth and an LTH that lasts for weeks (Billy and Walters, 1989;Walters et al, 1991;Clatworthy and Walters, 1994;Bedi et al, 1998). Because c-Jun-AP1 activities are sustained throughout (Figs.…”