Nitric oxide is an activity-dependent regulator of target neuron intrinsic excitability.

ABSTRACT: Activity-dependent changes in synaptic strength are well established as mediating long-term plasticity underlying learning and memory, but modulation of target neuron excitability could complement changes in synaptic strength and regulate network activity. It is thought that homeostatic mechanisms match intrinsic excitability to the incoming synaptic drive, but evidence for involvement of voltage-gated conductances is sparse. Here, we show that glutamatergic synaptic activity modulates target neuron excitability and switches the basis of action potential repolarization from Kv3 to Kv2 potassium channel dominance, thereby adjusting neuronal signaling between low and high activity states, respectively. This nitric oxide-mediated signaling dramatically increases Kv2 currents in both the audit

SUBMITTER: Steinert JR 

PROVIDER: S-EPMC3245892 | biostudies-literature | 2011 Jul

REPOSITORIES: biostudies-literature