Abstract
The output of a neural circuit results from an interaction between the intrinsic properties of neurons within the circuit and the features of the synaptic connections between them. The plasticity of intrinsic properties has been primarily attributed to modification of ion channel function and/or number. In this study, we demonstrate a mechanism for intrinsic plasticity in rhythmically active Drosophila neurons that is not conductance-based. Larval motor neurons show a long lasting sodium-dependent afterhyperpolarization (AHP) following bursts of action potentials that is mediated by the electrogenic activity of Na+/K+ ATPase. This AHP persists for multiple seconds following volleys of action potentials and is able to function as a pattern-insensitive integrator of spike number that is independent of external calcium. This current also interacts with endogenous Shal K+ conductances to modulate spike timing for multiple seconds following rhythmic activity, providing a cellular memory of network activity on a behaviorally relevant time scale.
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