Abstract
Rats rely on communication between the basolateral amygdala (BLA) and nucleus accumbens (NAc) to express lever directed approach in a Pavlovian lever autoshaping (PLA) task that distinguishes sign- and goal-tracking rats. During PLA, sign-tracking rats preferentially approach an insertable lever cue, while goal-tracking rats approach a foodcup where rewards are delivered. While sign-tracking rats inflexibly respond to cues even after the associated reward is devalued, goal-tracking rats flexibly reduce responding to cues during outcome devaluation. Here, we sought to determine whether BLA–NAc communication, which is necessary for sign, but not goal-tracking, drives a rigid appetitive approach of sign-tracking rats that are insensitive to manipulations of outcome value. Using a contralateral chemogenetic inactivation design, we injected contralateral BLA and NAc core with inhibitory DREADD (hm4Di-mCherry) or control (mCherry) constructs. To determine sign- and goal-tracking groups, we trained rats in five PLA sessions in which brief lever insertion predicts food pellet delivery. We sated rats on training pellets (devalued condition) or chow (valued condition) before systemic clozapine injections (0.1 mg/kg) to inactivate BLA and contralateral NAc during two outcome devaluation probe tests, in which we measured lever and foodcup approach. Contralateral BLA–NAc chemogenetic inactivation promoted a flexible lever approach in sign-tracking rats but disrupted the flexible foodcup approach in goal-tracking rats. Consistent with a prior BLA–NAc disconnection lesion study, we find contralateral chemogenetic inactivation of BLA and NAc core reduces lever, but not the foodcup approach in PLA. Together these findings suggest rigid appetitive associative encoding in BLA–NAc of sign-tracking rats hinders the expression of flexible behavior when outcome value changes.
Highlights
A body of evidence suggests that sign- and goal-tracking differences predict vulnerability to Substance Use Disorder (SUD; Tomie et al, 2008; Flagel et al, 2009; Saunders and Robinson, 2010; Saunders et al, 2013; Yager et al, 2015; Kawa et al, 2016; Villaruel and Chaudhri, 2016)
We hypothesized that ST rats rely on basolateral amygdala (BLA)–nucleus accumbens (NAc) core to drive rigid appetitive approach. To test this a priori hypothesis, we examined the extent to which BLA–NAc core contralateral chemogenetic inactivation altered the preferred response of ST rats during satiety devaluation tests
We examined the effect of contralaterally inactivating BLA and NAc core on devaluation sensitivity in sign- and goal-tracking rats
Summary
A body of evidence suggests that sign- and goal-tracking differences predict vulnerability to Substance Use Disorder (SUD; Tomie et al, 2008; Flagel et al, 2009; Saunders and Robinson, 2010; Saunders et al, 2013; Yager et al, 2015; Kawa et al, 2016; Villaruel and Chaudhri, 2016). Reward predictive cues acquire appetitive motivational properties; a psychological process often referred to as incentive salience that is postulated to drive SUD vulnerability (Berridge, 1996; Robinson and Berridge, 1993; Berridge and Robinson, 2016). Sign-tracking (ST) and goal-tracking (GT) individual differences during a Pavlovian lever autoshaping (PLA) task capture the degree to which reward predictive cues acquire incentive salience (Flagel et al, 2009; Pitchers et al, 2015; Flagel and Robinson, 2017) and predict heightened drug-cue induced relapse despite negative consequences (Saunders and Robinson, 2010; Saunders et al, 2013). We aim to determine the extent to which the incentive salience process supported by BLA–NAc core communication interferes with the expression of devaluation sensitivity in ST rats
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