Homeostatic plasticity of neuronal intrinsic excitability (HPIE) operates to maintain networks within physiological bounds in response to chronic changes in activity. Classically, this form of plasticity adjusts the output firing level of the neuron through the regulation of voltage-gated ion channels. Ion channels also determine spike timing in individual neurons by shaping subthreshold synaptic and intrinsic potentials. Thus, an intriguing hypothesis is that HPIE can also regulate network synchronization. We show here that the dendrotoxin-sensitive D-type K+ current (ID) disrupts the precision of AP generation in CA3 pyramidal neurons and may, in turn, limit network synchronization. The reduced precision is mediated by the sequence of outward ID followed by inward Na+ current. The homeostatic downregulation of ID increases both spike-time precision and the propensity for synchronization in iteratively constructed networks in vitro. Thus, network synchronization is adjusted in area CA3 through activity-dependent remodeling of ID.
ASJC Scopus subject areas