An examination of the effects of thalamic lesions on learning and memory in the rat

Hunt, Peter Richard (2000). An examination of the effects of thalamic lesions on learning and memory in the rat. PhD thesis The Open University.

Abstract

The study examined the effects of lesions of the thalamic nucleus medialis dorsalis (MD) made by neurotoxin in three cohorts ofrats to help understand the contribution of this nucleus to learning and memory. The lesions typically provided comprehensive damage to . MD, while the use of an excitotoxin helped to minimise damage to fibres of passage or adjacent fibre tracts. This excluded one confounding influence that may have been present in some previous studies. Some MD lesions also affected the anterior thalamic nuclei, and this additional damage led to spatial memory impairments, helping to confirm the value of results from rats with lesions confined to MD. Whilst the groups with MD lesions were largely unimpaired on non-spatial tests of visual recognition and discrimination, they were impaired on a configural discrimination task. The MD lesions did not impair spatial nonmatching to sample in aT-maze, nor the acquisition or performance over delay conditions of the standard radial maze task. There were impairments, however, when the radial maze was rotated during the delay, requiring a strategy shift. Similar impairment was found when a matching, rather than non-matching, strategy was required on the T-maze task and also when only some arms were rewarded on the radial arm maze task for reference memory measurement. No impairment was seen when the T-maze matching task was reversed to the non-matching variant, emphasising the lesion rats' preference for preexisting rules. In addition, some evidence was found that MD lesions brought about increased activity, but had no effect on conditioned place preference. The study concludes that MD damage in rats does not directly cause memory deficits. The influence that MD damage has on memory is, however, similar to that associated with damage to prefrontal cortex causing deficits in rule-switching ability, a higher order frontal lobe function .

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