Striatal output neurons (SONs) integrate glutamatergic synaptic inputs originating from the cerebral cortex. In vivo electrophysiological data have shown that a prior depolarization of SONs induced a short-term (1 sec)increase in their membrane excitability, which facilitated the ability of corticostriatal synaptic potentials to induce firing. Here we propose, using a computational model of SONs, that the use-dependent, short-term increase in the responsiveness of SONs mainly results from the slow kinetics of a voltage-dependent, slowly inactivating potassium A-current. This mechanism confers on SONs a form of intrinsic short-term memory that optimizes the synaptic input–output relationship as a function of their past activation.
Model Type: Neuron or other electrically excitable cell
Cell Type(s): Neostriatum medium spiny direct pathway GABA cell; Abstract Wang-Buzsaki neuron
Currents: I Na,p; I Na,t; I K; I_Ks; I Krp
Model Concept(s): Action Potential Initiation; Ion Channel Kinetics; Short-term Synaptic Plasticity
Simulation Environment: NEURON
Implementer(s): Biddell, Kevin [kevin.biddell at gmail.com]
References:
Mahon S, Deniau JM, Charpier S, Delord B. (2000). Role of a striatal slowly inactivating potassium current in short-term facilitation of corticostriatal inputs: a computer simulation study. Learning & memory (Cold Spring Harbor, N.Y.). 7 [PubMed]