As animals learn novel behavioural responses, performance is maintained by two dissociable influences. Initial responding is goal-directed and under voluntary control, but overtraining of the same response routine leads to behavioural autonomy and the development of habits that are no longer voluntary or goal-directed. Rats normally show goal-directed performance after limited training, indexed by sensitivity to changes in the value of reward, but this sensitivity to goal value is lost with extended training. Rats with selective lesions of the prelimbic medial prefrontal cortex showed no sensitivity to goal value after either limited or extended training, whereas rats with lesions of the infralimbic region of the medial prefrontal cortex showed the opposite pattern of deficit, a marked sensitivity to goal value after both limited and extended training. This double-dissociation suggests that the prelimbic region is responsible for voluntary response performance and the infralimbic cortex mediates the incremental ability of extended training to override this goal-directed behaviour.
The amygdala has long been thought to be involved in emotional behaviour, and its role in anxiety and conditioned fear has been highlighted. Individual amygdaloid nuclei have been shown to project to various cortical and subcortical regions implicated in affective processing. Here we show that some of these nuclei have separate roles in distinct mechanisms underlying conditioned fear responses. Rats with lesions of the central nucleus exhibited reduction in the suppression of behaviour elicited by a conditioned fear stimulus, but were simultaneously able to direct their actions to avoid further presentations of this aversive stimulus. In contrast, animals with lesions of the basolateral amygdala were unable to avoid the conditioned aversive stimulus by their choice behaviour, but exhibited normal conditioned suppression to this stimulus. This double dissociation demonstrates that distinct neural systems involving separate amygdaloid nuclei mediate different types of conditioned fear behaviour. We suggest that theories of amygdala function should take into account the roles of discrete amygdala subsystems in controlling different components of integrated emotional responses.
Performance of instrumental actions in rats is initially sensitive to postconditioning changes in reward value, but after more extended training, behavior comes to be controlled by stimulus-response (S-R) habits that are no longer goal directed. To examine whether sensitization of dopaminergic systems leads to a more rapid transition from action-outcome processes to S-R habits, we examined performance of amphetamine-sensitized rats in an instrumental devaluation task. Animals were either sensitized (7 d, 2 mg/kg/d) before training (experiment 1) or sensitized between training and testing (experiment 2). Rats were trained to press a lever for a reward (three sessions) and were then given a test of goal sensitivity by devaluation of the instrumental outcome before testing in extinction. Control animals showed selective sensitivity to devaluation of the instrumental outcome. However, amphetamine sensitization administered before training caused the animals' responding to persist despite the changed value of the reinforcer. This deficit resulted from an inability to use representations of the outcome to guide behavior, because a reacquisition test confirmed that all of the animals had acquired an aversion to the reinforcer. In experiment 2, post-training sensitization did not disrupt normal goal-directed behavior. These findings indicate that amphetamine sensitization leads to a rapid progression from goal-directed to habit-based responding but does not affect the performance of established goal-directed actions.
In three experiments, we assessed the effect of lesions of the amygdala basolateral complex (BLA) on instrumental conditioning in rats. In experiment 1, the lesion had no effect on the acquisition of either lever pressing or chain pulling in food-deprived rats whether these actions earned food pellets or a maltodextrin solution. The lesion did attenuate, however, the impact of outcome devaluation, induced by sensory-specific satiety, on instrumental performance both when assessed in extinction and when reward was delivered contingent on instrumental performance. In experiment 2, evidence was found to suggest that the lesioned rats differed from shams in their ability to encode the specific action-outcome contingencies to which they were exposed during training: lesioned rats failed to adjust their performance appropriately when the action-outcome contingency was degraded. These effects were not caused by an inability of BLA lesioned rats to discriminate the two instrumental actions; these rats were similar to shams in their acquisition of a heterogeneous instrumental chain involving lever pressing and chain pulling (experiment 3). In experiment 4, however, lesions of the BLA were found to produce a deficit in the ability of rats to use the specific properties of the instrumental outcomes used in the previous experiments to discriminate rewarded from unrewarded actions in a free operant discrimination situation. Together these results suggest that in instrumental conditioning, the BLA mediates outcome encoding, specifically relating the sensory features of nutritive commodities to the emotional consequences induced by their consumption.
The incidence of obesity in middle age is increasing markedly, and in parallel the prevalence of metabolic disorders including cardiovascular disease and type II diabetes is also rising. Numerous studies have demonstrated that both obesity and metabolic disorders are associated with poorer cognitive performance, cognitive decline, and dementia. In this review we discuss the effects of obesity on cognitive performance, including both clinical and preclinical observations, and discuss some of the potential mechanisms involved, namely inflammation and vascular and metabolic alterations.
The amygdala is known to play a role in learning about motivationally significant events. We investigated this role further by examining the effects of excitotoxic lesions of the basolateral amygdala on the ability of rats to use instrumental outcomes to direct responding (the differential outcomes effect) and on the ability of Pavlovian cues to modulate instrumental performance based on shared outcomes (reinforcer-selective Pavlovian-toinstrumental transfer). We found that basolateral amygdala (BLA) lesions did not affect the ability of rats to learn a basic instrumental conditional discrimination, but did disrupt the ability of differential outcomes to facilitate acquisition. In Pavlovianto-instrumental transfer, BLA lesions did not disrupt the basic enhancement of instrumental performance but did abolish the reinforcer specificity of that enhancement. These results suggest that the BLA is involved in the representation of the sensory aspects of motivationally significant events.Key words: appetitive conditioning; basolateral amygdala; reward; reinforcement; Pavlovian; instrumental Many studies have demonstrated that lesions of the basolateral amygdala (BLA) impair a range of forms of learning about motivationally significant events. In fear conditioning, BLA lesions produce deficits in freezing to an aversive context (Phillips and LeDoux, 1992), freezing to a specific cue that has been paired with a shock (LeDoux, 2000), conditioned punishment (Killcross et al., 1997), and fear-potentiated startle (Davis, 1992(Davis, , 2000. However, despite the well defined role of the amygdala in aversive learning, its role in appetitive tasks is much less clear. BLA lesions have no effect on many simple appetitive Pavlovian conditioning tasks, including autoshaping (Willoughby and Killcross, 1998;Parkinson et al., 2000), conditioned orienting (Holland, 1997), and conditioned magazine approach (Hatfield et al., 1996;Willoughby and Killcross, 2000). Similarly BLA lesions do not influence simple instrumental conditioning (B.W. Balleine, S. Killcross, and A. Dickinson, unpublished observations) or the nonspecific modulatory influence of Pavlovian stimuli on instrumental performance . However, in some circumstances BLA lesions do influence aspects of appetitive learning. Specifically, Hatfield et al. (1996) report a deficit in appetitive Pavlovian second-order conditioning. Although firstorder conditioning proceeded normally, the first-order conditional stimulus (CS 1 ) failed to act as a reinforcer when it is subsequently paired with a second stimulus (CS 2 ). Parallel deficits have been reported in conditioned reinforcement Burns et al., 1993). Here, BLA-lesioned and shamlesioned rats received first-order appetitive Pavlovian conditioning and then were allowed to make instrumental responses that were reinforced by presentation of the first-order CS. Sham-, but not BLA-lesioned rats came to respond more on a lever that resulted in the presentation of this CS than on a control lever.Although BLA lesions do not affect acquisitio...
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