My recent and current research has been focused on the mechanisms of social defeat stress in terms of neuroadaptive changes in the mesocorticolimbic dopaminergic system. I have studied the neuropharmacology of social stress for nearly 20 years. Social stress is a critical factor that increases the risk for drug vulnerability in humans and animal studies. Brief social defeat stress episodes cause enduring behavioral cross-sensitization to psychostimulants that persists for months. Over the evolution of my program of research, I have identified transient expression of functional µ-opioid receptors in the ventral tegmental area (VTA), which increases mesolimbic dopamine tone, and also determined the prolonged induction of brain-derived neurotrophic factor that underlies the eventual transition to long-lasting drug cross-sensitization. Now I have begun to identify the mechanisms involved in intracellular signaling in the dopamine and GABA neurons in the ventral tegmental area after social defeat stress exposure. The present work is the characterization of the role glutamate AMPA receptors expression in midbrain dopamine neurons for prolonged behavioral sensitivity to psychostimulant after exposure to social defeat stress; and assessment of the causative role of prefrontal cortex in controlling midbrain dopamine activity after stress. This research may lead us to prevent of stress-induced psychostimulant addiction.