Tobacco smoking is a major contributor to the burden of mental health disease worldwide. Nicotine is the primary reinforcing and main addictive component of tobacco. Nicotine addiction is a chronic relapsing disorder associated with multiple psychiatric comorbidities, and few effective interventions currently exist to curb addiction to nicotine. The neurocircuitry underlying nicotine addiction is broad, complex and depends on the stages of the disease process. It is well-acknowledged that nicotine impacts the reward system with prominent alterations of the firing properties of VTA DA neurons consequently biasing the responses to natural and addictive rewards. Yet the underlying mechanisms responsible of VTA DA alterations remain elusive. Here, we exposed mice to chronic nicotine in their drinking water to mimic the prolonged and intermittent nicotine absorption of nicotine in humans. Combining viral tracers, chemo- and optogenetic approaches, we aimed to investigate the effects of long-term nicotine intake on inputs to the reward system, establishing a parallel between circuit-based ex vivo and in vivo electrophysiological analyses and behavioural assessments in an operant conditioning task. We will present data showing that chronic nicotine consumption induces cellular alterations within inputs to the reward system that underlie changes in motivational drive for natural rewards. These changes may influence the incentive attribution process induced by drugs of abuse in the addiction process.