Nicotine use during adolescence (ADO) constitutes a risk factor to later develop mood disorders. Yet, the mechanisms underlying the enduring effects of adolescent nicotine exposure remain poorly elucidated. During ADO, the cognitive and goal-directed behaviors are refined in parallel to the development of dopamine (DA) circuitry, and both are uniquely sensitive to disruption by environmental influence during this time. Prolonged nicotine exposure in adult mice favors the appearance of depressive-like symptoms by altering the activity of ventral tegmental area (VTA) DA neurons and nicotinic pathways. Also, withdrawal from prolonged nicotine intake triggers an aversive abstinent state that is a deterrent to quit smoking. Hence, understanding the molecular mechanisms underlying the impact of protracted nicotine exposure is key to developing and optimizing novel aids for smoking cessation treatment. In this project, ADO and adulthood (ADU) mice were exposure to nicotine (diluted in a saccharin solution) during 1 week via their drinking water in their home cage. After 4 weeks, spontaneous excitatory postsynaptic currents (sEPSCs) induced by puffing nicotine onto VTA DA cells were measured, as well as analyses of AMPA/NMDA ratio as an index of synaptic adaptations. Here, we show that the DA system was primarily affected by nicotine exposure during ADO but not ADU. Our results support that short-term nicotine exposure during the critical period of ADO triggers long-term plastic changes in the DA cells of VTA that could contribute to the high prevalence of nicotine addiction in the ADU, as well as the risk of developing psychiatric disorders