Cortical Consequences of HIV-1 Tat Exposure in Rats are Enhanced by Chronic Cocaine

Title:Cortical Consequences of HIV-1 Tat Exposure in Rats are Enhanced by Chronic Cocaine

Volume: 13 Issue: 1

Author(s): Wesley N. Wayman, Lihua Chen, Amanda L. Persons and T. Celeste Napier

Affiliation:

Keywords: Addiction, calcium channels, Cav1.2, neuropathogenesis, prefrontal cortex.

Abstract: The life span of individuals that are sero-positive for human immunodeficiency virus (HIV) has greatly improved; however, complications involving the central nervous system (CNS) remain a concern. While HIV does not directly infect neurons, the proteins produced by the virus, including HIV transactivator of transcription (Tat), are released from infected glia; these proteins can be neurotoxic. This neurotoxicity is thought to mediate the pathology underlying HIVassociated neurological impairments. Cocaine abuse is common among HIV infected individuals, and this abuse augments HIV-associated neurological deficits. The brain regions and pathophysiological mechanisms that are dysregulated by both chronic cocaine and Tat are the focus of the current review.

Cite this article as:

N. Wayman Wesley, Chen Lihua, L. Persons Amanda and Napier T. Celeste, Cortical Consequences of HIV-1 Tat Exposure in Rats are Enhanced by Chronic Cocaine, Current HIV Research 2015; 13 (1) . https://dx.doi.org/10.2174/0929867322666150311164504