Intra-Accumbens Amphetamine Increases the Conditioned Incentive Salience of Sucrose Reward: Enhancement of Reward “Wanting” without Enhanced “Liking” or Response Reinforcement

Abstract

Amphetamine microinjection into the nucleus accumbens shell enhanced the ability of a Pavlovian reward cue to trigger increased instrumental performance for sucrose reward in a pure conditioned incentive paradigm. Rats were first trained to press one of two levers to obtain sucrose pellets. They were separately conditioned to associate a Pavlovian cue (30 sec light) with free sucrose pellets. On test days, the rats received bilateral microinjection of intra-accumbens vehicle or amphetamine (0.0, 2.0, 10.0, or 20.0 g/0.5 l), and lever pressing was tested in the absence of any reinforcement contingency, while the Pavlovian cue alone was freely presented at intervals throughout the session. Amphetamine microinjection selectively potentiated the cue-elicited increase in sucrose-associated lever pressing, although instrumental responding was not reinforced by either sucrose or the cue during the test. Intra-accumbens amphetamine can therefore potentiate cue-triggered incentive motivation for reward in the absence of primary or secondary reinforcement. Using the taste reactivity measure of hedonic impact, it was shown that intra-accumbens amphetamine failed to increase positive hedonic reaction patterns elicited by sucrose (i.e., sucrose "liking") at doses that effectively increase sucrose "wanting." We conclude that nucleus accumbens dopamine specifically mediates the ability of reward cues to trigger "wanting" (incentive salience) for their associated rewards, independent of both hedonic impact and response reinforcement.

Tryptophan Depletion Disrupts the Motivational Guidance of Goal-Directed Behavior as a Function of Trait Impulsivity

“…The discrepancy between the Crean et al study and our study may relate to the difference in sample size (n ¼ 20 in their study vs n ¼ 11 in our study) or the different dose: Crean et al administered 100 mg drinks, associated with an average 84% reduction of TRPÀ levels relative to baseline, while we administered 75 mg drinks, which reduced TRPÀ levels by 61% relative to baseline. Nevertheless, the differential sensitivity of the two measures observed here might be interesting in the context of their association with dissociable underlying corticostriatal circuitries (Taylor and Robbins, 1986;Jentsch and Taylor, 1999;Wyvell and Berridge, 2000;Eagle and Robbins, 2003a, b;Aron et al, 2003;Robbins, 2000).…”

The role of central dopamine D3 receptors in drug addiction: a review of pharmacological evidence

“…For example, the presentation of a drug-associated CS to animals can induce large conditioned increases in NAc DA [82,141], suggesting that DA in the NAc is involved in cue-controlled drug seeking [308] through interactions with limbic afferents to the NAc [81,83]. Cue incentive properties [24,242] appear mediated by hippocampal and amygdaloid mechanisms [55,152,196].…”

The role of learning-related dopamine signals in addiction vulnerability

“…Interpreted in the RL framework, this suggests that the opportunity cost might be preferentially mediated via tonic dopamine in those animals that rely on model-free learning whereas the timing and vigour of model-based choices might be more directly linked to the anticipated outcome, and hence less sensitive to such tonic dopaminergic mechanisms. Indeed, interference with DA by pharmacological means or by VTA inactivation abolish the ability of Pavlovian CSs to motivate approach and produce PIT (Wassum et al, 2011;Murschall and Hauber, 2006;Lex and Hauber, 2008), and DA stimulation promotes it (Wyvell and Berridge, 2000); whereas model-based behaviour is often rather more resilient to DA manipulations (e.g. Wassum et al 2011; though see Wunderlich et al 2012b;Guitart-Masip et al 2013).…”

“…Furthermore, drug-craving is correlated with the reduction in D 2 receptors . It is conceivable that reductions in presynaptic D 2 receptors might also affect tonic dopamine signals (Martinez et al, 2005(Martinez et al, , 2009 and that this relates to the effects of dopamine and cached values on Pavlovian-instrumental transfer (Murschall and Hauber, 2006;Wyvell and Berridge, 2000) and sign-tracking . There is also evidence that the link between dopamine synthesis and phasic prediction errors is altered by addiction, and this might be mediated by a failure of the presynaptic D 2 control (Schlagenhauf et al, 2013;Deserno et al, 2013).…”