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Significance Homeostatic synaptic plasticity has long been considered an anti-Hebbian mechanism that maintains the brain’s network stability, prevents aberrant Hebbian plasticity, and sustains normal cognitive functions. However, evidence supporting this hypothesis is largely lacking. Using region-specific deletions of the retinoic acid receptor RARα, a key mediator of homeostatic synaptic plasticity, we show that experience of an enriched environment (EE) engages homeostatic synaptic plasticity in hippocampal neurons in an RARα-dependent manner. EE experience in mice with deletion of RARα in the hippocampus caused runaway long-term potentiation (LTP), enhanced contextual memory, and reduced cognitive flexibility by hyperactivating mammalian target of rapamycin (mTOR) signaling. Treatment with the mTOR inhibitor rapamycin during an EE experience reversed both runaway LTP and enhanced learning, demonstrating a close functional interaction between Hebbian and homeostatic plasticity.

Synaptic retinoic acid receptor signaling mediates mTOR-dependent metaplasticity that controls hippocampal learning