| pubmed-article:17067274 | pubmed:abstractText | NeuroAIDS, the neurological, motor, and cognitive impairments that occur in acquired immunodeficiency syndrome (AIDS) patients, is characterized by compromised function in frontal cortical and subcortical brain regions including impairments in motor control, reaction time, and executive functions. Executive function is a cognitive domain involving the regulation of behavior, including inhibitory control. The present study evaluated the effects of simian immunodeficiency virus (SIV) infection on the object retrieval detour (ORD) task to assess inhibitory control. The ORD task measures the ability to inhibit the prepotent response of reaching directly toward a food reinforcer placed in a transparent box. The box has one open side, and the animal must inhibit the initial reaching response and look to see which side is open. Subjects were 12 experimentally naive pigtailed macaques; six monkeys were infected with SIV. Baseline performance was compared to performance under "terminal" conditions (the week prior to the scheduled euthanasia) to determine if progression of SIV disease led to decreased ORD performance. SIV-infected monkeys acquired ORD performance at the same levels as uninfected control monkeys, and had similar latencies and error rates. However, in the terminal week there was a significant difference between the groups in the number of barrier reach errors (touching the side of the transparent box). Three individual SIV-infected monkeys were impaired on ORD performance both in terms of errors and speed of performance. Given the sensitivity of ORD performance to dopaminergic dysfunction, these results further implicate dopaminergic dysfunction as a mechanism of cognitive and motor impairments in NeuroAIDS. | lld:pubmed |
