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Titolo:
TAT, A HUMAN IMMUNODEFICIENCY VIRUS-1-DERIVED PROTEIN, AUGMENTS EXCITOTOXIC HIPPOCAMPAL INJURY IN NEONATAL RATS
Autore:
WANG P; BARKS JDE; SILVERSTEIN FS;
Indirizzi:
UNIV MICHIGAN,DEPT PEDIAT ANN ARBOR MI 48109 UNIV MICHIGAN,DEPT PEDIAT ANN ARBOR MI 48109 UNIV MICHIGAN,DEPT NEUROL ANN ARBOR MI 48109
Titolo Testata:
Neuroscience
fascicolo: 2, volume: 88, anno: 1999,
pagine: 585 - 597
SICI:
0306-4522(1999)88:2<585:TAHIVP>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; METHYL-D-ASPARTATE; VIRUS TYPE-1; CELL-DEATH; HIV-1 TAT; BRAIN INJURY; PROGRESSIVE ENCEPHALOPATHY; NEURONAL INJURY; PERINATAL RATS; NMDA RECEPTOR;
Keywords:
EXCITOTOXICITY; AIDS; EXCITATORY AMINO ACIDS; NMDA; NEWBORN; BRAIN INJURY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
45
Recensione:
Indirizzi per estratti:
Citazione:
P. Wang et al., "TAT, A HUMAN IMMUNODEFICIENCY VIRUS-1-DERIVED PROTEIN, AUGMENTS EXCITOTOXIC HIPPOCAMPAL INJURY IN NEONATAL RATS", Neuroscience, 88(2), 1999, pp. 585-597

Abstract

To test the hypothesis that the human immunodeficiency virus-1-derived Tar protein may cause neuronal damage in the CNS, we evaluated the neurotoxicity of recombinant human immunodeficiency virus-1-derived Tatii vivo in seven-day-old rats. The intrinsic neurotoxicity of Tar (250 ng-l mu g) and the effects of direct intra-hippocampal co-infusion of Tat with N-methyl-D-aspartate were assessed. Extent of injury in thelesioned hippocampus was evaluated five days later, based on histopathology and morphometric measurements of hippocampal volume. To confirmthat any observed neurotoxic effects were attributable to Tat bioactivity, all experiments included controls that received equal amounts ofheat-treated (boiled) Tat. Intra-hippocampal injection of Tat, alone,elicited minimal focal tissue damage immediately adjacent to the injection track, and no hippocampal atrophy. Go-injection of Tat (500 ng) with N-methyl-D-aspartate (5 nmol, threshold excitotoxic dose) doubledthe severity of hippocampal injury, quantified by comparison of bilateral hippocampal volumes, in comparison with animals that received heat-treated Tat or saline co-injections; in animals that received injections of N-methyl-D-aspartate (5 nmol) in combination with saline, heal-treated Tat, or Tar [mean(+/- S.E.M.) % volume loss values in the lesioned hippocampus were: 11(+/-3), 11(+/-3), and 26(+/-3), respectively(P<0.002, ANOVA)I. Go-injection of 100 ng Tat with 5 nmol iv-methyl-D-aspartate exacerbated the severity of excitotoxic injury to a similarextent, whereas co-injection of 20 ng Tat had no effect on N-methyl-D-aspartate-mediated injury. Treatment with the N-methyl-D-aspartate antagonist ((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (20 mg/kg markedly attenuated hippocampal injury resulting from co-injection of 100 ng Tat with N-melhyl-D-aspartate [mean(+/-S.E.M.) % volume loss in lesioned hippocampus: 0.1(+/-2) in ((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid-treated vs 19(+/-3) in controls, P<0.001, ANOVA]. Go-injection of Tar had no effect on N-methyl-D-aspartate-mediated striatal damage or on -3-hydroxy-5-methylisoxazole-4-propionate-mediated hippocampal damage. These data support the hypothesis that locally released Tat could exert neurotoxic effects, mediated by N-methyl-D-aspartate receptor activation, in vivo in the immature brain. (C) 1998 IBRO. Published by Elsevier Science Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 18:17:17