Rebound Relays and Inhibitory Vetoes Stabilize Sparse Sequential Activity in HVC

Abstract Brains build behavior by chaining actions and perceptions into precisely timed sequences, an ability central to speech, skilled movement, and memory, yet the circuit logic that propagates sequences remains unclear. Songbird HVC captures this problem: premotor HVC RA neurons burst once per motif, while basal ganglia-projecting HVC X neurons burst 2-4 times across the same motif. We developed a biophysically grounded HVC network as linked microcircuits encoding sub-syllabic segments. The model highlights inhibition not merely as suppressive but actively structuring sequence propagation and fidelity. Tonic inhibitory epochs prime HVC X by deinactivating T-type Ca 2+ channels and recruiting I h , so that release elicits precisely timed rebound bursts that recruit the next HVC RA ensemble. A complementary phasic inhibitory veto suppresses off-time activation, preventing pathological restarts while preserving HVC RA single-burst sparseness. More broadly, inhibitory timing can serve as the brain’s internal “clocked handshake,” converting suppression into forward drive to advance sequences while enforcing error-corrected precision.