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Summary: Plasticity in the brain is ubiquitous. How do neurons and networks encode new information and simultaneously maintain homeostasis in the face of such ubiquitous plasticity? Here, we unveil a form of neuronal plasticity in rat hippocampal granule cells, which is mediated by conjunctive changes in HCN, inward-rectifier potassium, and persistent sodium channels induced by theta-modulated burst firing, a behaviorally relevant activity pattern. Cooperation and competition among these simultaneous changes resulted in a unique physiological signature: sub-threshold excitability and temporal summation were reduced without significant changes in action potential firing, together indicating a concurrent enhancement of supra-threshold excitability. This form of intrinsic plasticity was dependent on calcium influx through L-type calcium channels and inositol trisphosphate receptors. These observations demonstrate that although brain plasticity is ubiquitous, strong systemic constraints govern simultaneous plasticity in multiple components—referred here as plasticity manifolds—thereby providing a cellular substrate for concomitant encoding and homeostasis in engram cells.