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Neurotrophic factor expression after CNS viral injury produces enhanced sensitivity to psychostimulants: potential mechanism for addiction vulnerability.

Author	M V Solbrig, G F Koob, L H Parsons, T Kadota, N Horscroft, T Briese, W I Lipkin
Citation Information	The Journal of neuroscience : the official journal of the Society for Neuroscience, 20:RC104 (2000)
Keywords	Animals, Blotting, Western, Borna Disease, Borna disease virus, Brain, Brain Chemistry, Central Nervous System Stimulants, Corpus Striatum, Dextroamphetamine, Disease Susceptibility, Dose-Response Relationship, Drug, Male, Motor Activity, Nerve Growth Factors, Phosphorylation, Precipitin Tests, Rats, Rats, Inbred Lew, Substance-Related Disorders, Tyrosine 3-Monooxygenase
Related Products	AB151
Pub Med ID	11050146

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.