The effects of bilateral ibotenic acid lesions of the nucleus accumbens in the rat were examined on a delayed matching to position task. The lesion induced a stable delay-dependent performance deficit suggestive of a short-term memory problem. Following analysis of the impaired performance on trials with long delays, using measures akin to signal detection indices, the deficit was interpreted as being largely due to the intrusion of a side-dependent response bias. Low-dose amphetamine (0.75 mg/kg) produced a similar disruption in the sham-operated rats, both in terms of accuracy impairment and degree of strategical bias. As well as mimicking the effects of low-dose amphetamine in sham-operated rats, the lesion also protected against the disruptive effects of the drug at low doses. Whilst exhibiting no performance deficit when the matching schedule lacked a delay component, the lesioned rats were very significantly impaired in switching their response strategies when exposed to a series of reversals. In addition, the lesioned rats were remarkably resistant to an extinction procedure. Both these findings indicate that the lesioned rats were unable to exhibit flexibility in their response patterns. These results, taken together with those of the delayed matching procedure, imply that one of the functions of the intact nucleus accumbens is to inhibit habitual responding under conditions of non-reward and low stimulus control, possibly via its connections to the dorsal striatal system.