PREFRONTAL CORTEX DYSFUNCTION IN BORNA-DISEASE VIRUS (BDV)-INFECTED RATS

Viruses have been proposed to play a role in the pathogenesis of schiz ophrenia; however the mechanisms by which infection could cause the af fective, cognitive, and movement disorders of schizophrenia ave not un derstood. The neurotropic RNA virus, Borna disease (BD) virus, linked to schizophrenia by serologic studies, causes movement and behavior di sorders in a wide variety of mammalian and bird hosts. BD rats have hy peractivity and stereotyped behaviors similar to those that follow neu rotoxic 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 bindin g of D1 or D2 receptor radioligands in PFC. Since frontal lobe dysfunc tion is frequently reported in schizophrenia, the BD vat model may pro vide insights into pathogenesis and management of this debilitating ps ychiatric disease.