We have developed a mouse model in which dopamine neurons lack the ability to synthesize BDNF (BDNF knockout mice), by expressing Cre recombinase through the dopamine transporter locus in a BDNF loxP transgenic mouse. This mouse model provides a tool to determine how BDNF synthesized exclusively in DA neurons contributes to the shaping and function of the dopaminergic system. BDNF is highly expressed in midbrain DA neurons, and as a secreted molecule it could act on DA neurons, as a paracrine factor, or have an effect on surrounding neurons and in target areas by anterograde transport. We intend to utilize the BDNF knockout mouse model to determine how the ablation of BDNF in DA neurons affects the state of midbrain dopaminergic neurotransmission during development and in adult animals. In addition, as expression of BDNF in DA neurons has been shown to shape the neuro-plasticity observed during learning and reward, we intend to define how the lack of BDNF exclusively in DA neurons may affect behavioral outputs related to the reward system, and to define what cellular mechanisms and pathways intrinsic to DA neurons may be directly affected by BDNF expression.