博尔纳病病毒（BDV）感染大鼠的前额叶皮质功能障碍

Prefrontal cortex dysfunction in Borna disease virus (BDV)--infected rats.

作者信息

Solbrig M V, Koob G F, Fallon J H, Reid S, Lipkin W I

机构信息

Department of Neurology, University of California, Irvine 92717-4290, USA.

出版信息

Biol Psychiatry. 1996 Oct 1;40(7):629-36. doi: 10.1016/0006-3223(95)00480-7.

DOI:10.1016/0006-3223(95)00480-7

PMID:8886296

Abstract

Viruses have been proposed to play a role in the pathogenesis of schizophrenia; however, the mechanisms by which infection could cause the affective, cognitive, and movement disorders of schizophrenia are not understood. The neurotropic RNA virus, Borna disease (BD) virus, linked to schizophrenia by serologic studies, causes movement and behavior disorders in a wide variety of mammalian and bird hosts. BD rats have hyperactivity and stereotyped behaviors similar to those that follow neurotoxic or electrolytic lesions in frontal cortex or its catecholamine afferents in rats. BD rats have high levels of viral nucleic acid in the prefrontal cortex (PFC), abnormal mesocortical dopamine activity (elevated levels of DOPAC in PFC), yet no alteration in specific binding of D1 or D2 receptor radioligands in PFC. Since frontal lobe dysfunction is frequently reported in schizophrenia, the BD rat model may provide insights into pathogenesis and management of this debilitating psychiatric disease.

摘要

病毒被认为在精神分裂症的发病机制中起作用；然而，感染导致精神分裂症的情感、认知和运动障碍的机制尚不清楚。嗜神经性RNA病毒，博尔纳病（BD）病毒，通过血清学研究与精神分裂症相关，可在多种哺乳动物和鸟类宿主中引起运动和行为障碍。BD大鼠具有多动和刻板行为，类似于大鼠额叶皮质或其儿茶酚胺传入神经发生神经毒性或电解损伤后的行为。BD大鼠前额叶皮质（PFC）中病毒核酸水平较高，中皮质多巴胺活性异常（PFC中DOPAC水平升高），但PFC中D1或D2受体放射性配体的特异性结合没有改变。由于精神分裂症患者经常报告有额叶功能障碍，BD大鼠模型可能为这种使人衰弱的精神疾病的发病机制和治疗提供见解。