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However, several studies strongly suggest that secretory viral and immune products from infected brain macrophages and microglia affect the onset and tempo of disease. One critical neurotoxin among these secretory products is the HIV\u20101 envelope glycoprotein gp120. To better understand how HIV\u20101 gp120 may affect cognitive function, we studied its effects on long\u2010term potentiation (LTP) in the CA1 region of rat hippocampus, the brain region best linked to learning and memory. Although no effects were observed on basal synaptic transmission, HIV\u20101 gp120 inhibited LTP in a concentration\u2010dependent manner in the presence of \u03b3\u2010aminobutyric acid type A (GABA<jats:sub>A<\/jats:sub>) receptor antagonist. Heat\u2010inactivated gp120 failed to block LTP. The HIV\u20101 gp120\u2010mediated LTP inhibition was blocked by T140, a chemokine receptor CXCR4 antagonist, demonstrating gp120 inhibition of LTP via CXCR4. HIV\u20101 gp120 V3 loop peptides mimicked the inhibitory effects of HIV\u20101 gp120 protein on LTP. Monoclonal antibodies against the V3 loop epitope KRIHI eliminated the HIV\u20101 gp120 effects on LTP. These results further underscore the importance of HIV\u20101 gp120 in the pathogenesis of HIV\u20101\u2010associated cognitive impairments seen during progressive viral infection. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.20745","type":"journal-article","created":{"date-parts":[[2006,1,9]],"date-time":"2006-01-09T20:09:49Z","timestamp":1136837389000},"page":"489-496","source":"Crossref","is-referenced-by-count":23,"title":["Human immunodeficiency virus type 1 gp120 inhibits long\u2010term potentiation via chemokine receptor CXCR4 in rat hippocampal 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