We have shown that adolescent rats consumed less alcohol than adults, when assessed across an intermittent and chronic two-bottle choice test, and exhibited a progressive increase in alcohol intake and preference, whereas adults exhibited a stable pattern. Despite drinking less alcohol, adolescent consumption was associated with greater ΔFosB expression in several areas of mesocorticolimbic pathway. ΔFosB is an early transcription factor, that regulates gene expression and accumulates after chronic exposure to drugs. Here, we assessed if ΔFosB induction is dependent on an escalating pattern of alcohol exposure, rather than in the volume of exposure. Adolescent or adult rats were intermittently administrated vehicle, escalating (0.5- 2.5 g/kg) or high, constant (2.0 g/kg) doses of intragastric alcohol, across 18 sessions. Seventy-two hours after the last administration, ΔFosB was quantified in Prelimbic Cortex, Nucleus Accumbens, Striatum, Basolateral Amygdala and Central Nucleus of Amygdala, by immunohistochemistry. We found that both patterns of alcohol exposure increased ΔFosB levels, equally in adolescent and adult rats. The constant doses exacerbated ΔFosB in all brain areas but in Central Nucleus of Amygdala, whereas the escalating doses induced ΔFosB expression in Prelimbic Cortex and Basolateral Amygdala. The study further confirmed that chronic and passive alcohol exposure induces ΔFosB in brain areas involved in reward processing, in adolescent and adults.