Human immunodeficiency virus (HIV)-associated dementia (HAD) has been detec
ted in 20-30% of patients suffering AIDS. The envelope glycoprotein 120 (gp
720) derived from HIV seems to play a critical role in the pathophysiology
of this dementia. Likewise, the feline immunodeficiency virus (FIV)-derived
gp120 causes neurological and electrophysiological abnormalitites in cats.
We have studied the effects of gp120 derived from HIV or FIV on learning a
nd memory processing, hippocampal long-term potentiation (LTP), hippocampal
neuronal cAMP production, the sleep-waking cycle, and locomotor activity a
nd equilibrium in rats. Results showed that while both HIV- and FIV-gp120 i
mpaired the mt's performance in the Barnes maze task, only HIVgp120 impaire
d the induction and maintenance of LTP. However, both glycoproteins induced
a significant decrease in the posttetanic potentiation. HIVgp120 also caus
ed a significant reduction in cAMP production in the hippocampus. Regarding
the sleep-waking cycle, HIV- and FIV-gp120 increased the waking state and
slow-wave sleep 1 (SWS1), while decreasing both SWS2 and REM sleep. Locomot
or activity and equilibrium were significantly altered by these glycoprotei
ns. These results suggest that HIVgp120 causes neurophysiological abnormali
ties and therefore may facilitate HAD development in AIDS patients. (C) 200
0 Academic Press.