Bilateral striatal lesions disrupt performance in an operant delayed reinforcement task in rats

Abstract

In order to provide an animal model of the impulsivity observed in Huntington's disease, the effects of bilateral neostriatal lesions in rats were evaluated in an operant delayed reinforcement task. When given a choice between responding to one lever for a small but immediate reward and a second lever for a larger delayed reward, normal rats exhibit a marked preference for responding to the high reward lever when the imposed delay is short, but progressively choose the lever associated with immediate small reward as the delays increase. Following striatal lesions, the animals continue to express similar preferences, but the lesions initially impose a distinct flattening of the delay-preference function, suggesting a relative insensitivity to the increasing delay parameter in making their response choices. However, this deficit declines with extend retraining on the task, such that 1-2 months after lesion the delay-dependent shift of preference from the delayed to the immediate lever as the delays lengthened was comparable in lesion and sham animals. Amphetamine further disinhibited all animals, apparent as a further increase in the number and reduction of the latencies of responses made to the lever associated with immediate reward. Striatal lesions had little influence on the effects of amphetamine on task performance, other than the increase in the numbers of omissions of lever and panel responses induced by the drug was more marked in the lesion than sham animals, and the lesioned animals exhibited less delay-dependency than the controls in their preference for responding to the lever associated with the larger delayed reinforcement at the highest (1.5 mg/kg) dose tested. The present results indicate small but clear effects of dorsal striatal lesions in an operant delayed reinforcement task, suggestive of an initial impairment in response selection and a reduction in their sensitivity to the delay interval itself. This deficit recovered with further training, which may be dependent upon relearning choice response procedures disrupted by the lesion, but might be reinstated by treatment with stimulant drugs. This article is part of a special issue entitled 'Behavioural, Anatomical, and Genetic Characterisation of Mouse and Rat Models of Huntington's Disease.'