Striatal Output Neuron (Mahon, Deniau, Charpier, Delord 2000)

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Accession:150621
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.
Reference:
1 . 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. Learn Mem 7:357-62 [PubMed]
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Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism:
Cell Type(s): Neostriatum medium spiny direct pathway GABA cell; Abstract Wang-Buzsaki neuron;
Channel(s): I Na,p; I Na,t; I K; I_Ks; I Krp;
Gap Junctions:
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Action Potential Initiation; Ion Channel Kinetics; Short-term Synaptic Plasticity;
Implementer(s): Biddell, Kevin [kevin.biddell at gmail.com];
Search NeuronDB for information about:  Neostriatum medium spiny direct pathway GABA cell; I Na,p; I Na,t; I K; I_Ks; I Krp;
 
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