The Human Immunodeficiency Virus-1 Protein Tat and Its Discrete Fragments Evoke Selective Release of Acetylcholine from Human and Rat Cerebrocortial Terminals through Species-Specific Mechanisms.

Investigates the effect of the human immunodeficiency virus-1 protein Tat on neurotransmitter release from human and rat cortical nerve endings. Status of the protein in human nerve terminals; Failure of Tat to affect the release of several neurotransmitters; Factor that sustains the occurrence of neurotoxic events.