AN EVALUATION OF COGNITIVE DEFICITS IN A RAT - MODEL OF HUNTINTONS'S DISEASE
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Author
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Department of Psychology
Abstract
The purpose of this thesis was to develop methodology by which treatments for the
cognitive impairments in Huntington\\\'s disease (HD) could be tested. As such, the thesis focused
mainly on evaluating rats with quinolinic acid (QA) lesions of the striatum, as this manipulation
mimics some aspects of the neural damage in Huntington\\\'s disease, to try to identify cognitive
deficits of HD resulting from cell loss in the striatum.
In the first part (Chapters 3-5), the role of the striatum in implicit memory was
investigated. Chapter 3 compared the performance of rats and humans on a reaction time task
that evaluated implicit memory by presenting visual stimuli with differing probabilities which
change over time. Although rats made higher percentage of incorrect responses and late errors,
both groups showed a similar pattern of reaction times. Chapter 4 investigated whether implicit
memory (the computation of probabilities to predict the location of a stimulus) was affected by
selective blockade of dopaminergic transmission at the D1 or D2 receptors by SCH-23390 and
raclopride, respectively. Reaction times were slower with SCH-23390 and raclopride, but only
SCH-23390 reduced errors to the least probable target location. Chapter 5 used the same task to
evaluate implicit memory in rats with QA lesions of the dorsomedial striatum (DMS). Implicit
memory was not affected by lesions of the DMS, which suggested that once a task that requires
implicit memory has been learned, the DMS was not involved in sustaining the performance of
the task. The second part of this thesis (Chapter 6), explored the contribution of the DMS in
habit formation. DMS lesioned rats did not show habitual responding, and were not impaired in
learning a new goal-directed behaviour. The third part (Chapters 7 and 8), investigated the role
of the dorsal striatum in reversal learning, attentional set-formation, and set-shifting. Dorsal
striatum lesioned rats were not impaired in reversal learning, but had a diminished shift-cost,
which suggested that dorsal striatum lesions disrupted the formation of attentional sets.
These results showed that although QA lesions of the dorsal striatum mimic some aspects
of the neural damage in HD, they did not result in the same cognitive deficits observed in
patients with HD, at least using the tasks presented in this thesis. However, other animal models
of HD could be evaluated using the different tasks presented in this thesis to continue the search
of a reliable animal model of HD in which treatments for the disease could be evaluated.
Table of Contents
Abstract . . . . . . . . . . . . . . . . v
Acknowledgements . . . . . . . . . . . . . .. vii
Chapter 1
General Introduction . . . . . . . . . . . . . 15
Huntington\\\'s disease. . . . . . . . . . . . . 17
1.1 Introduction . . . . . . . . . . . . . .. 17
1.2 Epidemiology. . . . . . . . . . . . . 17
1.3 Genetics . . . . . . . . . . . . . .
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