Publication Abstract Display
Type: Published Manuscript
Title: Behavioral effects of chronic methamphetamine treatment in HIV-1 gp120 transgenic mice.
Authors: Henry BL, Geyer MA, Buell MR, Perry W, Young JW, Minassian A
Year: 2013
Publication: Behavioural Brain Research
Volume: 236 Issue: 1 Pages: 210-220
Abstract:HIV infection and Methamphetamine (METH) represent significant and overlapping threats to public health. METH use is associated with a higher risk of viral infection and more severe cognitive and neuropathological dysfunction in HIV-infected individuals. Both disorders are characterized by inhibitory deficits, which may manifest as increased motor activity, inappropriate perseverative behavior, and elevated exploratory responses to novel stimuli, but the effect of combined METH exposure and HIV infection is not well understood. In this study, we administered a chronic escalation/binge regimen of METH or vehicle treatment to wildtype (WT) or transgenic (tg) mice expressing the HIV-1 gp120 envelope protein and quantified disinhibition during the 7 days following drug withdrawal. We hypothesized that METH-treated gp120tg mice would exhibit inhibitory deficits compared to vehicle-treated WT animals, corresponding to evidence of increased neurocognitive impairment in individuals with comorbid METH dependence and HIV infection. Our results showed that METH treatment alone increased novel object interaction while female METH-treated gp120tg mice exhibited the highest level of exploration (holepoking) compared to other female mice. Transgenic mice exhibited fewer rears relative to WT and slightly less locomotion, and also demonstrated a trend towards more perseverative motor patterns. In summary, both METH treatment and gp120 expression may modify inhibition, but such effects are selective and dependent upon variations in age and sex that could impact dopamine and frontostriatal function. Cross-species translational studies with human and rodent open-field paradigms will enable improved characterization of the underlying neuropathology and facilitate improved treatment methods for comorbid disease and drug dependence.

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