No abstract

For the past 35 years, learning theorists have been providing models that depend on mental representations, even in their most simple, deterministic, and mechanistic approaches. Hence, cognitive involvement (typically thought of as expectancy) is assumed for most instances of classical and operant conditioning, with current theoretical differences concerning the level of cognition that is involved (e.g., simple association vs. rule learning), rather than its presence. Nevertheless, many psychologists not in the mainstream of learning theory continue to think of cognitive and conditioning theories as rival families of hypotheses. In this article, the data pertaining to the role of higher-order cognition in conditioning is reviewed, and a theoretical synthesis is proposed that provides a role for both automatic and cognitively mediated processes.

HIV-1 infection of the central nervous system impairs neural, cognitive, and behavioral functioning in patients despite antiretroviral therapy. However, studying mechanisms underlying HIV-1-related neurological and cognitive dysfunction has been limited without an adequate animal model. A novel, noninfectious HIV-1 transgenic (HIV-1Tg) rat model was recently created that expresses an HIV-1 provirus with a deletion of functional gag and pol genes. This HIV-1Tg rat reportedly develops clinical manifestations of human HIV disease and thus appears to mimic the persistent infection that results from the presence of HIV viral proteins in the host. We evaluated the HIV-1Tg rat model using the Morris water maze, a popular paradigm for testing learning and memory deficits in rodents. Because of congenital cataracts in HIV-1Tg rats, however, the traditional use of visual navigational cues in this paradigm were precluded. We first designed a modified Morris water maze and demonstrated that neurologically intact rats can effectively learn the water maze in the absence of visual cues and in the presence of non-visual navigation cues. We then tested HIV-1Tg rats in this modified Morris water maze. These HIV-1Tg rats showed a deficit in learning how to swim to the location of the hidden platform but did not show a deficit in their memory of the general location of the hidden platform. These results suggest that the noninfectious HIV-1Tg rat can be a valid model for the behavioral studies of HIV-related neurological dysfunction.

Despite the ability of current combination anti-retroviral therapy (cART) to limit the progression of HIV-1 to AIDS, HIV-positive individuals continue to experience neuroHIV in the form of HIV-associated neurological disorders (HAND), which can range from subtle to substantial neurocognitive impairment. NeuroHIV may also influence substance use, abuse, and dependence in HIV-positive individuals. Because of the nature of the virus, variables such as mental health co-morbidities make it difficult to study the interaction between HIV and substance abuse in human populations. Several rodent models have been developed in an attempt to study the transmission and pathogenesis of the HIV-1 virus. The HIV-1 transgenic (HIV-1Tg) rat is a reliable model of neuroHIV because it mimics the condition of HIV-infected patients on cART. Research using this model supports the hypothesis that the presence of HIV-1 viral proteins in the central nervous system increases the sensitivity and susceptibility of HIV-positive individuals to substance abuse.

Human immunodeficiency virus (HIV)-associated dementia (HAD) encompasses a spectrum of cognitive and motor deficits resulting from the progression of central nervous system abnormalities caused by the HIV-1 virus. With the advent of highly active antiretroviral therapy (HAART), these deficits have become milder, but more prevalent as the population of HIV-positive individuals ages. Mild impairment in cognition has also been identified in asymptomatic HIV-1 patients. The noninfectious HIV-1 transgenic (Tg) rat recently developed to study the pathogenesis of acquired immunodeficiency syndrome (AIDS) may also be useful for the study of the early and chronic effects of HIV-1 on learning and cognition. In a previous study, we demonstrated that HIV-1Tg rats show a deficit in learning how to swim to a hidden platform in a modified water maze task compared to normal and transgenic controls. In the present study, we replicate this result and demonstrate that HIV-1Tg rats also show a significant deficit in reversal learning and new strategy learning. These results indicate that the HIV-1Tg rat is a promising model in which to study the neuropathogenic mechanisms that can cause cognitive deficits in patients with HAD as well as asymptomatic HIV-positive individuals.