摘要：SummaryPlasticity 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 throughL-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 asplasticity manifolds—thereby providing a cellular substrate for concomitant encoding and homeostasis in engram cells.Graphical abstractDisplay OmittedHighlights•Theta-burst firing induces intrinsic plasticity in dentate gyrus granule cells•Changes in HCN, inward-rectifier K+, and persistent Na+channels mediate plasticity•Ca2+influx throughL-type Ca2+channels and InsP3receptors governs plasticity•Intrinsic plasticity could drive encoding and homeostasis in engram cellsBiological sciences; Molecular physiology; Molecular neuroscience; Cellular neuroscience
