title: Cortical consequences of HIV-1 Tat exposure in rats are enhanced by chronic cocaine.
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.
authors.affiliation: Department of Pharmacology, Rush University Medical Center, 1735 W. Harrison Street, Cohn Research Building, Rm. 463, Chicago, IL 60612, USA. wesley_n_wayman@rush.edu.
authors.forename: Wesley N
authors.initials: WN
authors.lastname: Wayman
authors.forename: Lihua
authors.initials: L
authors.lastname: Chen
authors.forename: Amanda L
authors.initials: AL
authors.lastname: Persons
authors.forename: T Celeste
authors.initials: TC
authors.lastname: Napier
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects*; D002540:Cerebral Cortex / Q000187:drug effects* / Q000503:physiopathology; D003042:Cocaine / Q000009:adverse effects*; D019970:Cocaine-Related Disorders / Q000150:complications*; D004195:Disease Models, Animal; D015658:HIV Infections / Q000150:complications*; D015497:HIV-1; D019965:Neurocognitive Disorders / Q000209:etiology* / Q000503:physiopathology; D051381:Rats; D054322:tat Gene Products, Human Immunodeficiency Virus / Q000502:physiology*
chemical_list: D054322:tat Gene Products, Human Immunodeficiency Virus; D003042:Cocaine