BRAIN DOPAMINE-RECEPTOR PLASTICITY - TESTING A DIATHESIS-STRESS HYPOTHESIS IN AN ANIMAL-MODEL

A wealth of clinical data supports a major role of genetic liability a s well as of altered brain dopamine (DA) functioning in different type s of behavioural disturbances. Genetic influence on behaviour involves multiple genes, rather than one or two major genes, as well as non-ge netic sources of variance. Thus, in recent years, increasing attention has been devoted to the involvement of stressful experiences (life ev ents) in the development and expression of psychopathology. Moreover, a diathesis-stress hypothesis has been proposed, which suggests that t he environmental factors (stress) are not specific for a given patholo gy, whereas genetic factors (diathesis) are. Results obtained in an an imal model offer support to this hypothesis. Indeed, mice of the C57BL /6 and DBA/2 inbred strains are equally susceptible to stress but deve lop different behavioural disturbances related to different alteration s of brain DA receptors. Moreover, quantitative trait loci (QTL) assoc iations in the C57 (B) x DBA (D) recombinant inbred (RI) strains indic ate a number of provisional QTLs influencing the behavioural effect of stress. Finally, the results of this analysis suggest the involvement of regulatory factors related to stress response and neural or synapt ic plasticity in the control of brain DA receptor plasticity.