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The Journal of Neuroscience, October 29, 2003, 23(30):9833-9841

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Behavioral/Systems/Cognitive
Lesions of Nucleus Accumbens Disrupt Learning about Aversive Outcomes

Geoffrey Schoenbaum and Barry Setlow

Department of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, Maryland 21218

Nucleus accumbens (NAcc) is critical for encoding and using information regarding the learned significance of cues predictive of reward. However, its role in processing information about cues predictive of aversive outcomes is less well studied. Here, we examined the effects of NAcc lesions in an odor-guided discrimination task in which rats use odor cues predictive of either appetitive or aversive outcomes to guide responding. Rats with sham or neurotoxic lesions of NAcc were trained on a series of two-odor discrimination problems. Performance on each problem was assessed by monitoring accuracy of choice behavior and by measuring latency to respond for fluid reinforcement after odor sampling. After acquisition of four problems, rats were trained on serial reversals of the final problem. Rats with NAcc lesions exhibited normal choice performance relative to controls on both acquisition and reversal of the discrimination problems (indeed, lesioned rats exhibited a mild facilitation on the first discrimination problem). Despite normal choice performance, however, lesioned rats failed to show normal changes in response latency during discrimination learning, particularly on trials involving the aversive outcome. These findings are consistent with a deficit in processing cue–outcome associations. These results are compared with those obtained from studies of basolateral amygdala and orbitofrontal cortex lesions in this task and suggest that NAcc integrates the motivational value of both appetitive and aversive cues to bias or modulate the vigor of subsequent responding.

Key words: accumbens; olfactory; discrimination; reversal; striatum; orbitofrontal; amgydala

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Received May 30, 2003; revised September 9, 2003; accepted September 9, 2003.

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