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Numerous studies of learning and memory in Aplysia have focused on primary mechanosensory neurons innervating the siphon and having their somata in the left E (LE) cluster of the abdominal ganglion. Although systematic analyses have been made of the responses of these LE cells to mechanical stimulation of the tightly pinned siphon, little is known about corresponding responses when the siphon is unrestrained. The present study demonstrates that LE mechanosensory thresholds in the freely moving siphon are much higher than in the pinned siphon. Light tactile stimuli adequate to activate central neurons and reflexive siphon movements often fail to activate the LE cells when the siphon is unrestrained. Because the LE cells display increasing discharge to increasing pressures, with maximal activation by crushing or tearing stimuli that cause tissue injury, they satisfy accepted definitions of nociceptor. Indeed, they show similarities to vertebrate Adelta nociceptors, including a property apparently unique (among primary afferents) to nociceptors-sensitization by noxious stimulation of their receptive field. Either pinching or pinning the siphon decreases LE cell mechanosensory threshold and enhances soma excitability. Such stimuli reduce effective tissue compliance and cause neuromodulation that enhances sensory responsiveness. These results, and recent descriptions of predatory attacks on Aplysia, suggest that LE sensory neurons are tuned to grasping and crushing stimuli that threaten or produce bodily harm. LE cell sensitization has effects, resembling hyperalgesia and allodynia, that compensate for loss of sensory function during injury and help protect against subsequent threats.

Prior research has shown that exposure to shock can induce a decrease in pain reactivity (hypoalgesia). The present experiments show that, at the same time points that subjects are less responsive to radiant heat applied to the tail (the tail-flick test), tailshock elicits enhanced motor reactivity and vocalization. This enhanced responsiveness, or hyperalgesia, is observed with both magnitude (Experiment 1) and threshold (Experiment 2) measures and decays within 32 min (Experiment 2). Experiment 3 shows that the hyperalgesia decays irrespective of whether or not subjects remain in the shock context, which suggests that the loss of hyperalgesia does not reflect extinction of the context-shock association. Neither removing subjects from the shock context (Experiment 4) nor the presentation of a postshock distractor (Experiment 5) affected the hyperalgesia.

Prior research suggests that associative and memorial processes can modulate the activation of the endogenous antinociceptive systems. It has been generally assumed that forebrain systems play an essential role in mediating the impact of these processes. The present experiments explored whether the behavioral effects indicative of associative and memorial processes can be obtained in spinalized rats. Experiment 1 demonstrated that a conditioned nonopioid antinociception can be established after rats have experienced a spinal transection at the level of the 2nd thoracic vertebrae. Experiment 2 showed that a postshock distractor can speed the decay of shock-induced antinociception in the spinalized rat. These findings suggest that the circuitry needed to obtain associative and memorylike effects is present within the spinal cord.

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