Role of the anterior cingulate cortex in the control over behavior by Pavlovian conditioned stimuli in rats.

Abstract

To investigate the contribution of the anterior cingulate cortex (ACC) to stimulus-reward learning, rats with lesions of peri- and postgenual ACC were tested on a variety of Pavlovian conditioning tasks. Lesioned rats learned to approach a food alcove during a stimulus predicting food, and responded normally for conditioned reinforcement. They also exhibited normal conditioned freezing and Pavlovian-instrumental transfer, yet were impaired at autoshaping. To resolve this apparent discrepancy, a further task was developed in which approach to the food alcove was under the control of 2 stimuli, only 1 of which was followed by reward. Lesioned rats were impaired, approaching during both stimuli. It is suggested that the ACC is not critical for stimulus-reward learning per se, but is required to discriminate multiple stimuli on the basis of their association with reward.

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

“…The CeA may mediate conditioned increases in DA measured in the NAc following the noncontingent presentation of a CS [82,141] perhaps via projections to the VTA [218] and seems to play a key role in stress-triggered relapse to cocaine-seeking behavior. Finally, the anterior cingulate cortex seems to serve as a common link in the neural circuitry underlying reinstatement of drugseeking behaviors, perhaps because the anterior cingulate cortex is critically involved in the discrimination of multiple stimuli on the basis of their association with reward [48], in shifting away from spatial locations previously associated with reward (response perseveration), attention, and the ability to adequately plan actions involved in fear responding (for a complete review, see Ref. [130]).…”

Activation in extended amygdala corresponds to altered hedonic processing during protracted morphine withdrawal

“…The BLA is known to be important for stimuluscontrolled behaviors, and lesions or chemical inactivation of this structure can result in the loss of both CPP acquisition [16,18,59] and cue-induced reinstatement of drug self-administration [17,50,57]. Lesions of the Cg do not impair reward seeking or consumption of rewards per se, but instead disrupt the ability to discriminate between a rewarded stimulus (CS+) and an unrewarded stimulus (CS-), causing an animal to approach both stimuli in an equal manner [5][6][7]43]. …”

Behavioral characteristics and neurobiological substrates shared by Pavlovian sign-tracking and drug abuse

“…Lesions of ACC also impair differential responding to CS+ and CS− in discriminative sign-tracking procedures (Bussey et al, 1997;Cardinal et al, 2002). The effects of lesions of ACC on sign-tracking are unlikely due to general impairment of cognitive or motor function, as lesions of ACC impaired sign-tracking, but had no effect on a variety of Pavlovian conditioning tasks, including goal-tracking, conditioned reinforcement, conditioned freezing and Pavlovian-Instrumental transfer (Cardinal et al, 2003).…”

“…In human cocaine addicts, imaging by positron emission tomography of synaptic activity related to addict-generated mental imagery of drug craving was associated with bilateral activation of ACC (Kilts et al, 2001), while in rats, bilateral lesions of the ACC produced a decrease in acquisition of heroin self-administration and a decrease in relapse of heroin-taking in rats (Trafton and Marquez, 1971). Lesions of ACC impair sign-tracking CR performance in rats (Bussey et al, 1997;Parkinson et al, 2000;Cardinal et al, 2002Cardinal et al, , 2003, and disconnection of the ACC from the core of the NAC also impaired the acquisition of sign-tracking CR performance (Parkinson et al, 2000). Lesions of ACC also impair differential responding to CS+ and CS− in discriminative sign-tracking procedures (Bussey et al, 1997;Cardinal et al, 2002).…”