Functional-anatomical changes in reward related brain circuits are described in chronic pain patients who report anhedonia or depressed mood. In pre-clinical rodent models of neuropathic pain there are varying reports of the effects of nerve injury on the motivation to consume sucrose, although hedonic responses to sucrose appear unchanged. These observations are derived from brief periods of exposure to sucrose. When sucrose is available ad libitum over a period of 21 days, there are marked individual differences in consumption. The motivation for, and hedonic experience of, drinking sucrose is mediated in part by dopamine-D2 and µ-opioid receptors in the nucleus accumbens (NAc). This study investigated the effects of chronic constriction injury (CCI) on ad libitum sucrose consumption in male Sprague Dawley rats and the expression of accumbal dopamine D2 and µ-opioid receptors. Nerve injury reduced sucrose drinking predominantly in rats with the highest pre-injury consumption levels. Despite these reductions in consumption, sucrose preferences were stable. In the NAc of rats whose sucrose consumption was affected by CCI, immunohistochemical analyses revealed bilateral reductions of dopamine D2-receptor expression in the core and shell; and a lateralised reduction of µ-opioid receptor expression in the core and dorsomedial shell of the right NAc. These alterations in receptor expression are located in regions which have been identified as hedonic hot and coldspots along an affective-motivational keyboard which directs behaviours either towards, or away from salient stimuli. These changes likely underlie the reduction in sucrose consumption observed in a subgroup of rats following nerve injury.