Background

There is experimental evidence that emotional states (e.g., anxiety or frustration) influence sensitivity to physical pain and correlate with the consumption of psychoactive substances like alcohol (Wiech and Tracey, 2008; Xie et al., 2012; Manzo et al., 2015). Reward devaluation is a viable strategy to induce a negative emotion such as anxiety (see Flaherty, 1996; Papini et al., 2015). Reward devaluation can be implemented in different procedures, including appetitive extinction, partial reinforcement, and successive negative contrast (SNC). All of them imply unexpected changes in reward magnitude or quality. In appetitive extinction, the reward is withheld altogether, while for partial reinforcement the reward is withheld on some random number of trials. SNC implies not the elimination, but a devaluation of the magnitude or quality of the reward. In the consummatory successive negative contrast (cSNC) task, one type of SNC procedure, animals receive free access for 5 min to a high-value sucrose solution (usually 32% sucrose) during several daily sessions, followed by several sessions of access to a low-value sucrose solution (usually 4% sucrose) (Jiménez-García et al., 2016). Performance of downshifted animals is compared to the consummatory behavior of animals that have always received access to 4% sucrose (unshifted controls). The cSNC effect involves a suppression of consummatory behavior after the 32%-4% sucrose downshift followed by a recovery to the level of unshifted controls. The initial suppression (typically observed during the first devaluation session) and the recovery that follows (normally starting during the second devaluation session) are dissociable stages of the cSNC effect (Flaherty, 1996).

Several sources of evidence suggest that cSNC modulates and is also modulated by physical pain (Jiménez-García et al., 2016). Papini et al. (2015) suggested a connection between physical pain (tissue damage) and psychological pain (reward loss) that invites further comparisons between these two sets of phenomena. For example, opioid ligands known to modulate physical pain also modulate cSNC, either during the first downshift session ([D-Pen2,D-Pen5]enkephalin, a selective delta-receptor agonist; Wood et al., 2005), during the second downshift session (U50,488H, a selective kappa-receptor agonist; Wood et al., 2008), or during both sessions (morphine; Rowan and Flaherty, 1987). Two opioid-receptor antagonists enhance the cSNC effect either selectively during the first downshift session (naltrindole, a selective delta receptor antagonist) or during both the first and second downshift sessions (naloxone, a nonselective opioid receptor antagonist; Pellegrini et al., 2005). Similarly, lesions of brain areas involved in pain processing, such as the anterior cingulate cortex, also affect recovery from reward downshift from the second downshift session onward (Ortega et al., 2011).

Likewise, ethanol consumption is increased by cSNC. Reward devaluation produces an anxious state (frustration) that can be mitigated by the anxiolytic effects of ethanol. Manzo et al. (2015) showed an increase in ethanol consumption after reward devaluation (post-shift sessions).