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

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

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 3,4-Dihydroxyphenylacetic Acid / metabolism
  • Animals
  • Autoradiography
  • Borna Disease / physiopathology*
  • Borna disease virus / genetics
  • Brain Mapping
  • Dopamine / physiology
  • Gene Expression Regulation, Viral / physiology
  • Male
  • Motor Activity / physiology
  • Neurocognitive Disorders / physiopathology*
  • Prefrontal Cortex / physiopathology*
  • RNA Probes
  • Rats
  • Rats, Inbred Lew
  • Receptors, Dopamine D1 / physiology*
  • Receptors, Dopamine D2 / physiology*
  • Stereotyped Behavior / physiology

Substances

  • RNA Probes
  • Receptors, Dopamine D1
  • Receptors, Dopamine D2
  • 3,4-Dihydroxyphenylacetic Acid
  • Dopamine