International Journal of Comparative Psychology

The sensory component of chronic pain is amenable to comparative study and evolutionaryinterpretations. Pain is usually initiated by activation of nociceptors, which detect damaging stimuli.A comparison of rats and a marine snail, Aplysia, shows that nociceptors in each group satisfy thesame functional definition and exhibit similar functional alterations, including persistenthyperexcitability and synaptic potentiation following noxious stimulation. These alterations are alsoassociated with conventional learning and memory. Because of the ancient divergence of theselineages, some similarities probably reflect independent evolution. However, the molecular signalslinked thus far to known forms of long-term neuronal plasticity represent homologous processes thatare found in all metazoan cells. Persistent plasticity mechanisms now used for chronic pain andmemory may have evolved originally in the earliest neurons by selective recruitment of core cellsignaling and effector systems for neuronal repair, sensory compensation, and protective functionsrelated to peripheral injury.

Honey bees were trained in a proboscis extension response procedure on a high quality reward to one of two odors under one of two contexts and then on a lower quality reward under the alternative context to the alternative odor. The performance decrement induced by the reduced reward, revealed by comparisons with subjects trained continually on the lower reward, was independent of odor context combinations or the order of experience with stimuli. In a second experiment subjects were forward or backward conditioned to a high quality reward or fed unconditionally and then trained ona low reward in a novel context to a novel odor. The observed performance decrement depended only on exposure to the high quality reward. These results suggest that incentive contrast effects arise from a simple mechanism—the comparison of a current incentive with experienced incentives— that is effectively independent of cues that signal a reward.

The endogenous opioid peptides and their receptors play important roles in Pavlovian fear conditioning in many species, including mice, rats, and humans. These roles are best viewed as regulating the conditions for fear learning by determining the actions of predictive error on association formation. Evidence will be reviewed showing such roles for opioid receptors in ventrolateral quadrant of the midbrain periaqueductal gray (vlPAG). These roles are shared across mammalian species because many of the effects of opioid receptor manipulations on fear learning first reported in rodents have now been documented in humans.

A downshift from a more preferred to a less preferred incentive leads to a transient rejection of the lower incentive. This phenomenon, known as successive negative contrast (SNC), has been reported in studies with mammals, but not with fish, amphibians, or reptiles, all showing gradual adjustments to the new incentive conditions. It is assumed that an understanding of the brain systems involved in the onset of SNC in mammals will suggest likely brain areas for a comparative analysis in non mammalian vertebrates. Studies reviewed in this article show that opioid receptors are normally engaged during SNC, participate in the detection of the incentive downshift, play a role in SNC onset (delta receptors), and modulate recovery from SNC (kappa receptors). However, opioid receptors do not seem to be involved in the consolidation of the downshift memory. These results suggest a relationship between the evolution of the opioid system and the evolution of learning mechanisms involved in the adjustment to incentive downshifts in vertebrates.