Memantine prevents HIV coat protein-induced neuronal injury in vitro.
Studies with in vitro model systems suggest that at least part of the neurologic deficits of human immunodeficiency virus (HIV)-1-associated cognitive/motor complex may stem from neuronal injury mediated by the HIV-1 coat protein gp120. Concurrent activation of N-methyl-D-aspartate (NMDA) receptors is also necessary for gp120 to induce neuronal damage. We studied memantine, a drug that blocks NMDA receptor-operated ion channels, for possible protective effects from gp120-induced neuronal injury. In identified rat retinal ganglion cells in culture, we found that 2 microM memantine completely prevented the injury engendered by 20 pM gp120. These data suggest that memantine has therapeutic potential as an NMDA antagonist capable of ameliorating neuronal damage associated with gp120.
Lipton
S A
SA
Laboratory of Cellular and Molecular Neuroscience, Children's Hospital, Boston, MA.
D000818:Animals; D002478:Cells, Cultured; D015699:HIV Envelope Protein gp120 / Q000187:drug effects*; D008559:Memantine / Q000494:pharmacology*; D016202:N-Methylaspartate / Q000037:antagonists & inhibitors; D009474:Neurons / Q000187:drug effects*; D051381:Rats; D012165:Retinal Ganglion Cells / Q000187:drug effects
D015699:HIV Envelope Protein gp120; D016202:N-Methylaspartate; D008559:Memantine