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Ann Neurol. 2004 Mar;55(3):362-71.

HIV-1 Tat inhibits long-term potentiation and attenuates spatial learning [corrected].

Author information

1
Department of Physiology, Graduate School of Medicine and Dentistry, Okayama University, Shikata, Okayama, Japan. shiri-ns@umin.ac.jp

Erratum in

  • Ann Neurol. 2004 May;55(5):758.

Abstract

Although memory deficits have been clearly documented in patients with human immunodeficiency virus type-1 (HIV-1) infection, the physiological basis of this dysfunction is poorly understood. We focused on Tat, a viral protein released from HIV-1-infected cells and investigated its effect on spatial learning in adult mice. An intracerebroventricular injection of Tat leads to attenuation of spatial learning accompanied by suppression of long-term potentiation (LTP), the cellular basis of spatial learning, in hippocampal cornu ammonis 1 pyramidal neurons. Tat facilitates extrasynaptic but not synaptic N-methyl-D-aspartate (NMDA) receptor activity. Taken together, these data provide strong evidence that the Tat pathway underlies the development of memory dysfunction in patients with HIV-1 infection and suggest a causal relationship between Tat, the facilitation of extrasynaptic NMDA receptor activity, inhibition of LTP, and attenuation of spatial learning.

PMID:
14991814
DOI:
10.1002/ana.10844
[Indexed for MEDLINE]

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