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HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 COAT PROTEIN NEUROTOXICITY MEDIATED BY NITRIC-OXIDE IN PRIMARY CORTICAL CULTURES

被引：335
作者：
DAWSON, VL
DAWSON, TM
UHL, GR
SNYDER, SH
机构：
[1] JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,725 N WOLFE ST,BALTIMORE,MD 21205
[2] NIDA,ADDICT RES CTR,BALTIMORE,MD 21224
[3] JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205
[4] JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL & MOLEC SCI,BALTIMORE,MD 21205
[5] JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205
来源：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1993年 / 90卷 / 08期
关键词：
GP120; AIDS; GLUTAMATE; N-METHYL-D-ASPARTATE; MICROGLIA;
D O I：
10.1073/pnas.90.8.3256
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
The human immunodeficiency virus type 1 coat protein, gp120, kills neurons in primary cortical cultures at low picomolar concentrations. The toxicity requires external glutamate and calcium and is blocked by glutamate receptor antagonists. Nitric oxide (NO) contributes to gp120 toxicity, since nitroarginine, an inhibitor of NO synthase, prevents toxicity as does deletion of arginine from the incubation medium and hemoglobin, which binds NO. Superoxide dismutase also attenuates toxicity, implying a role for superoxide anions.
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收藏
页码：3256 / 3259
页数：4
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