BCM-like synaptic plasticity with conductance-based models (Narayanan Johnston, 2010)

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Accession:147538
" ... Although the BCM-like plasticity framework has been a useful formulation to understand synaptic plasticity and metaplasticity, a mechanism for the activity-dependent regulation of this modification threshold has remained an open question. In this simulation study based on CA1 pyramidal cells, we use a modification of the calcium-dependent hypothesis proposed elsewhere and show that a change in the hyperpolarization-activated, nonspecific-cation h current is capable of shifting the modification threshold. ..."
Reference:
1 . Narayanan R, Johnston D (2010) The h current is a candidate mechanism for regulating the sliding modification threshold in a BCM-like synaptic learning rule. J Neurophysiol 104:1020-33 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell; Synapse; Channel/Receptor;
Brain Region(s)/Organism: Hippocampus;
Cell Type(s): Hippocampus CA1 pyramidal GLU cell;
Channel(s): I Na,t; I A; I h; I Potassium;
Gap Junctions:
Receptor(s): AMPA; NMDA;
Gene(s):
Transmitter(s): Glutamate;
Simulation Environment: NEURON;
Model Concept(s): Active Dendrites; Synaptic Plasticity; Calcium dynamics;
Implementer(s): Narayanan, Rishikesh [rishi at iisc.ac.in];
Search NeuronDB for information about:  Hippocampus CA1 pyramidal GLU cell; AMPA; NMDA; I Na,t; I A; I h; I Potassium; Glutamate;
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