Background Exposure to juvenile stress was found to have long-term effects on plasticity and the quality of associative memory in adulthood, but the underlying mechanisms are still poorly understood. Methods 3-4-week-old male Wistar rats were subjected to a three-day juvenile stress paradigm. Their electrophysiological correlates of memory using the adult hippocampal slice were inspected to detect alterations in long-term potentiation and synaptic tagging and capture model of associativity. These cellular alterations were tied in with the behavioural outcome by subjecting the rats to a step-down inhibitory avoidance paradigm to measure strength in their memory. Given the role of epigenetic response in altering plasticity as a repercussion of juvenile stress, we set forth to chart out the possible epigenetic marker and its regulation in the long-term memory mechanisms using qRT-PCR. Results We demonstrate that even long after the elimination of actual stressors, an inhibitory metaplastic state is evident, which promotes synaptic competition over synaptic co-operation and decline in latency of associative memory in the behavioural paradigm despite the exposure to novelty. Mechanistically, juvenile stress led to a heightened expression of the epigenetic marker G9a/GLP complex which is thus far ascribed to transcriptional silencing and goal directed behaviour. Conclusions The blockade of the G9a/GLP complex was found to alleviate deficits in long-term plasticity and associative memory during the adulthood of animals that were exposed to juvenile stress. Our data provides insights on the long-term effects of juvenile stress that involve epigenetic mechanisms, which directly impact long-term plasticity, synaptic tagging and capture and associative memory.

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