Date of Award

Spring 2019

Document Type

Open Access Thesis



First Advisor

Rosemarie Booze


HIV-1 infection is a serious condition affecting approximately 37 million individuals. Between 30% and 60% of seropositive individuals will develop symptoms of clinical depression. These individuals are five times more likely to commit suicide than non-seropositive clinically depressed patients. Dysfunction in serotonergic and dopaminergic transmission has consistently been implicated in the pathogenesis of depression. Specifically, dysfunction in the prefrontal cortex and in the nucleus accumbens core region have been shown to be underlying factors in the trajectory of depression. Given these underlying neurological features, the present research employed behavioral testing and electrochemical recording in an attempt to elucidate the therapeutic efficacy of the SSRI escitalopram in treating HIV-1 mitigated depressive symptoms in a transgenic (Tg) rodent model of depression. The HIV-1 Tg rat contains seven of the nine genes present in the HIV viral genome and presents itself with impairments similar to those observed in human HIV-1 seropositive individuals. The HIV-1 Tg rat thus represents a non-infectious model for controlled HIV-1 exposure. Here, we report failure of the SSRI to attenuate behavioral and electrochemical alterations present in the HIV-1 Tg rat. Given the known variability of SSRI medication and previously documented individual differences to drug dosage found within the model, it is thus concluded that more research is required in order to firmly establish the global efficacy of escitalopram in treated comorbid HIV-1 clinical depression.


© 2019, Adam R. Denton