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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
;
Download the displayed file
/
NarayananJohnston2010
README.txt
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na3s.mod
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Fig2.hoc
Fig2A_Output.txt
Fig2B_Output.txt
mosinit.hoc
load_file("nrngui.hoc") load_file("Fig2.hoc")
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Fig 2A
Fig 2B
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