A novel visuospatial priming task for rats with relevance to Tourette syndrome and modulation of dopamine levels

Individuals with Tourette syndrome (TS) exhibit deficits in inhibitory information processing which may reflect impaired neural mechanisms underlying symptoms and which can be detected using a negative priming (NP) task. NP is the normal reduction of performance when identifying target stimuli that...

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Veröffentlicht in:Neuroscience and biobehavioral reviews 2013-07, Vol.37 (6), p.1139-1149
Hauptverfasser: Amitai, Nurith, Weber, Martin, Swerdlow, Neal R, Sharp, Richard F, Breier, Michelle R, Halberstadt, Adam L, Young, Jared W
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Sprache:eng
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Zusammenfassung:Individuals with Tourette syndrome (TS) exhibit deficits in inhibitory information processing which may reflect impaired neural mechanisms underlying symptoms and which can be detected using a negative priming (NP) task. NP is the normal reduction of performance when identifying target stimuli that appear where non-target stimuli appeared previously. TS subjects exhibit diminished NP and their NP levels predict their response to behavioral therapy. Here we review relevant literature on this issue and also report a novel rat NP task. In the latter, rats respond to target stimuli (continuous light) while ignoring non-target stimuli (blinking light). Each trial was preceded by a prime in which target and non-target stimuli were briefly presented. Performance was challenged by shortening prime duration and by administering amphetamine. During the short prime challenge, rats exhibited lower accuracy in NP vs. baseline trials, indicative of inhibitory information processing. Modulation by amphetamine administration indicates that this drug had rate-dependent effects. Evidence is provided of individual differences in NP and response to the drug, with priming being reduced in high NP rats, while it was increased in low NP subjects. The rat NP task represents a novel and suitable tool for investigating the neural bases of inhibitory information processing and its dysfunction in TS.
ISSN:0149-7634
1873-7528
DOI:10.1016/j.neubiorev.2012.09.007