A neural substrate of hyperactivity in Borna disease: Changes in brain dopamine receptors

被引:49
作者
Solbrig, MV
Koob, GF
Joyce, JN
Lipkin, WI
机构
[1] UNIV CALIF IRVINE, MARKEY PROGRAM HUMAN NEUROBIOL, LAB NEUROVIROL, DEPT NEUROL, IRVINE, CA 92717 USA
[2] UNIV CALIF IRVINE, MARKEY PROGRAM HUMAN NEUROBIOL, LAB NEUROVIROL, DEPT ANAT & NEUROBIOL, IRVINE, CA 92717 USA
[3] UNIV CALIF IRVINE, MARKEY PROGRAM HUMAN NEUROBIOL, LAB NEUROVIROL, DEPT MICROBIOL & MOL GENET, IRVINE, CA 92717 USA
[4] Scripps Res Inst, DEPT NEUROPHARMACOL, LA JOLLA, CA 92037 USA
[5] SUN HLTH RES INST, CHRISTOPHER PARKINSONS DIS CTR, SUN CITY, AZ 85372 USA
关键词
D O I
10.1006/viro.1996.0430
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Rats experimentally infected with the neurotropic RNA virus, Borna disease virus, have a hyperactive movement disorder. Because locomotor activity is modulated by the nucleus accumbens (N. Ace.) dopamine (DA) system, high-affinity DA uptake, DA D1, D2, and D3 receptor binding sites were examined in N. Ace. subregions of normal and infected rats by quantitative receptor autoradiography. The N. Ace. of infected rats had decreased mazindol and D2 and D3 radioligand binding in the core and decreased D3 radioligand binding in rostral subregions. The abnormalities observed in the N. Ace. DA system of infected rats may offer insights into the potential viral pathogenesis of psychiatric conditions with a dopaminergic substrate such as schizophrenia and affective disorders. (C) 1996 Academic Press, Inc.
引用
收藏
页码:332 / 338
页数:7
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