Abstract
Animals respond to the threat of predation with a number of defensive behaviors, including: flight, immobilization or ‘freezing’, risk assessment, increased wariness and the suppression of non-defensive behaviors (Blanchard et al. 1990). It has become evident that a reduction in nociceptive and pain sensitivity (antinociception or analgesia, respectively) is a also a major correlate of predator exposure. Activation of endogenous analgesic mechanisms has been demonstrated in laboratory mice and rats exposed to a cat (Lester and Fanselow, 1985; Lichtman and Fanselow, 1990; Kavaliers and Colwell, 1991, 1992), deer mice and white-footed mice exposed to a weasel (Kavaliers, 1988, 1990), and laboratory mice exposed to the calls of avian predators (Hendrie, 1991). There is mounting evidence that these analgesic responses are an important component of an animal’s defense repertoire. Defensive systems that are activated by either innate or learned danger stimuli, such as that of predators, may inhibit nociceptive and pain sensivitity (i.e. induce analgesia) associated with either the perception of, defense against, and/or recuperatio;l from the danger stimuli (Bolles and Fanselow, 1980). As such, analgesia is advantageous in predator exposure, in which responding to noxious stimulation might compete with and/or disrupt effective defensive behaviors.
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Kavaliers, M., Innes, D., Ossenkopp, KP. (1992). Predator-Odor Analgesia in Deer Mice: Neuromodulatory Mechanisms and Sex Differences. In: Doty, R.L., Müller-Schwarze, D. (eds) Chemical Signals in Vertebrates 6. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9655-1_81
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DOI: https://doi.org/10.1007/978-1-4757-9655-1_81
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