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The Journal of Neuroscience, 0000, 20:RC104:1-5

RAPID COMMUNICATION
Neurotrophic Factor Expression After CNS Viral Injury Produces Enhanced Sensitivity to Psychostimulants: Potential Mechanism for Addiction Vulnerability

Marylou V. Solbrig¹, George F. Koob², Loren H. Parsons², Tomoko Kadota³, Nigel Horscroft¹, Thomas Briese¹, and W. Ian Lipkin¹

¹ Departments of Neurology, Microbiology, and Molecular Genetics, University of California-Irvine, Irvine, California 92697-4292, ² Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California 92037, and ³ Department of Anatomy, Chiba University School of Medicine, Chiba 260, Japan

Hypothesized risk factors for psychostimulant, amphetamine, and cocaine abuse include dopamine (DA) receptor polymorphisms, HIV infection, schizophrenia, drug-induced paranoias, and movement disorders; however, the molecular, cellular, and biochemical mechanisms that predispose to drug sensitivity or drive the development of addiction are incompletely understood. Using the Borna disease rat, an animal model of viral-induced encephalopathy wherein sensitivity to the locomotor and stereotypic behavioral effects of D-amphetamine and cocaine is enhanced (Solbrig et al., 1994, 1998), we identify a specific neurotrophin expression pattern triggered by striatal viral injury that increases tyrosine hydroxylase activity, an early step in DA synthesis, to produce a phenotype of enhanced amphetamine sensitivity. The reactive neurotrophin pattern provides a molecular framework for understanding how CNS viral injury, as well as other CNS adaptations producing similar growth factor activation profiles, may influence psychostimulant sensitivity.

Key words: virus; encephalitis; neurotrophin; Borna disease; rat; cocaine; amphetamine; dopamine

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