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Full-Text Articles in Organisms

Strong Inferences About Pain In Invertebrates Require Stronger Evidence, Edgar T. Walters Jan 2022

Strong Inferences About Pain In Invertebrates Require Stronger Evidence, Edgar T. Walters

Animal Sentience

Evidence for sentience in animals distantly related to humans is often sought in observations of behavioral and neural responses to noxious stimuli that would be painful in humans. Most proposed criteria for painful sentience in “lower” animals such as decapod crustaceans have no necessary links to the affective (“suffering”) component of pain. The best evidence for painful affect in animals is learned aversion to stimuli associated with noxious experience, and conditioned preference for contexts associated with relief from aversive consequences of noxious experience, as expressed in voluntary behavior. Such evidence is currently lacking for any invertebrate except octopus.


Connecting Model Species To Nature: Predator-Induced Long-Term Sensitization In Aplysia Californica, Maria J. Mason, Amanda J. Watkins, Jordann Wakabayashi, Jennifer Buechler, Christine Pepino, Michelle Brown, William G. Wright Jan 2014

Connecting Model Species To Nature: Predator-Induced Long-Term Sensitization In Aplysia Californica, Maria J. Mason, Amanda J. Watkins, Jordann Wakabayashi, Jennifer Buechler, Christine Pepino, Michelle Brown, William G. Wright

Biology, Chemistry, and Environmental Sciences Faculty Articles and Research

Previous research on sensitization in Aplysia was based entirely on unnatural noxious stimuli, usually electric shock, until our laboratory found that a natural noxious stimulus, a single sublethal lobster attack, causes short-term sensitization. We here extend that finding by demonstrating that multiple lobster attacks induce long-term sensitization (>= 24 h) as well as similar, although not identical, neuronal correlates as observed after electric shock. Together these findings establish long-and short-term sensitization caused by sublethal predator attack as a natural equivalent to sensitization caused by artificial stimuli.