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Early life stress increases sensitivity to stress later in life, which may be at the root of increased risk for mental health disorders. Our work seeks to understand the mechanistic underpinnings of this heightened stress sensitivity. Using transgenic mice to label and capture experience-actiated neurons, we show that neurons active during early life stress are more likely to be reactivated during adult stress experience, and that chemogenetically inhibiting these neurons rescues behavioral changes. Heightened cellular reactivity may be due to long-lasting changes in the epigenome that leave chromatin more open and transcriptionally reactive to additional stimuli, particularly in stress-activated neurons. Together, this work supports a biological model in which stress alters chromatin development, leading to increased cellular reactivity and ultimately behavioral sensitivity to future stress.