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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
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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];
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Neostriatum medium spiny direct pathway GABA cell
;
I Na,p
;
I Na,t
;
I K
;
I_Ks
;
I Krp
;
/
MahonEtAl2000
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