Hypoalgesia Induced by Reward Devaluation in Rats

Abstract

Reduced sensitivity to physical pain (hypoalgesia) has been reported after events involving reward devaluation. Reward devaluation was implemented in a consummatory successive negative contrast (cSNC) task. Food-deprived Wistar rats had access to 32% sucrose during 16 sessions followed by access to 4% sucrose during 3 additional sessions. An unshifted control group had access to 4% sucrose throughout the 19 sessions. Pain sensitivity was measured using von Frey filaments (Experiment 1) and Hargreaves thermal stimuli (Experiment 2) in pretraining baseline, 5 min, and 300 min after either the first (session 17) or second (session 18) devaluation session in the cSNC situation. Sucrose consumption was lower in downshifted groups relative to unshifted groups during postshift sessions—the cSNC effect. Hypoalgesia was observed in downshifted groups relative to unshifted controls when pain sensitivity was assessed 5 min after either the first or second devaluation session, regardless of the pain sensitivity test used. Both pain sensitivity tests yielded evidence of hypoalgesia 300 min after the second downshift session, but not 300 min after the first devaluation session. Whereas hypoalgesia was previously shown only after the second devaluation session, here we report evidence of hypoalgesia after both the first and second devaluation sessions using mechanical and thermal nociceptive stimuli. Moreover, the hypoalgesia observed 300 min after the second devaluation session in both experiments provides unique evidence of the effects of reward loss on sensitivity to physical pain 5 hours after the loss episode. The underlying neurobehavioral mechanisms remain to be identified.

Within-session decrement of the emission of licking bursts following reward devaluation in rats licking for sucrose

“…The failure to observe the contrast effect more robustly might depend on the sucrose concentrations used in our experiments. Indeed, most experiments on successive negative contrast with sucrose use 32% as the high concentration and 4% as the low concentration [ 29 , 30 ], or 1M vs 0.1M [ 28 ], alternatively. With these concentrations one obtains a higher degree of dilution (1/8-1/10) compared to our experiment (1/5), providing a stronger reward devaluation, and a more concentrated low concentration solution, which might support a higher response level in the low concentration group.…”

Reward shifts in forced-choice and free-choice autoshaping with rats.

“…Reward downshift leads to transient response suppression (Flaherty, 1996) and it has consequences that implicate negative emotion (Amsel, 1992; Papini & Dudley, 1997; Papini et al, 2015). For example, response suppression is correlated with elevated corticosterone levels (Mitchell & Flaherty, 1998; Pecoraro, de Jong, & Dallman, 2009), fever (Pecoraro, Ginsberg, Akana, & Dallman, 2007), and reduction in sensitivity to physical pain (Jiménez-García et al, 2016; Mustaca & Papini, 2005); it is reduced by benzodiazepine anxiolytics (Flaherty, Coppotelli, & Potaki, 1996; Flaherty, Grigson, & Rowan, 1986), ethanol (Becker & Flaherty, 1982; Kamenetzky, Mustaca, & Papini, 2008), and cannabinoid agonists (Genn, Tucci, Parikh, & File, 2004); and it is modulated by opioids (Pellegrini, Wood, Daniel, & Papini, 2005; Wood, Daniel, & Papini, 2005; Wood, Norris, Daniel, & Papini, 2008). Response suppression after reward downshift is also attenuated by amygdala disruption (Kawasaki, Annicchiarico, Glueck, Morón, & Papini, 2017; Kawasaki, Glueck, Annicchiarico, & Papini, 2015).…”

Reward devaluation disrupts latent inhibition in fear conditioning

“…It is possible that by the time animals were exposed to the shock, the hypoalgesic response was sufficiently attenuated to make little difference. There is evidence of such time decay after a single exposure to reward devaluation (Jiménez-García et al, 2016). The connection between reward devaluation and fear conditioning also deserves additional study.…”

“…The basic assumption is that these two forms of pain share some fundamental mechanisms at the neurochemical and neural levels that allow them to interact in selective ways. For example, exposure to reward devaluation, which is known to induce the release of endogenous opioids (Pellegrini, Wood, Daniel, & Papini, 2005), leads to reduced sensitivity to peripheral physical pain (Jiménez-García et al, 2016;Mustaca & Papini, 2005). Such hypoalgesia could interfere with fear conditioning by reducing the subjective intensity of the electric shock.…”