A Review on HIV's Effects on Exploratory Activity, Motor Functions, and Learning in Animals

Infection with the human immunodeficiency virus (HIV) causes human neuropsychological disorders, such as apathy and hypokinesia, as well as deficits in motor skills, selective attention, and learning. Based on findings from multiple studies, similar signs have been reproduced in animal models following intracerebral injections of HIV-infected human monocytes or monocyte-derived macrophages, or exposure to gp120, Tat, or Nef. These include learning deficits in Morris, radial arm, and Barnes mazes; impairments in novel object place and shape recognition; motor coordination deficits on stationary and mobile beams; and hypoactivity. Relative to non-transgenic controls, deficits in most tests have also been reproduced in transgenic mice or rats expressing HIV-1 or related proteins. There is evidence that corticosterone contributes to these behavioral abnormalities, which may have implications for treating AIDS dementia complex, given its ability to exacerbate the neurotoxic effects of gp120 in tissue cultures. Possible mechanisms include corticosterone-induced worsening of lipid peroxidation, inhibition of aspartate uptake, increased calcium mobilization, and reduced ATP levels.