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Pyramidal neuron conductances state and STDP (Delgado et al. 2010)
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Neocortical neurons in vivo process each of their individual inputs in the context of ongoing synaptic background activity, produced by the thousands of presynaptic partners a typical neuron has. That background activity affects multiple aspects of neuronal and network function. However, its effect on the induction of spike-timing dependent plasticity (STDP) is not clear. Using the present biophysically-detailed computational model, it is not only able to replicate the conductance-dependent shunting of dendritic potentials (Delgado et al,2010), but show that synaptic background can truncate calcium dynamics within dendritic spines, in a way that affects potentiation more strongly than depression. This program uses a simplified layer 2/3 pyramidal neuron constructed in NEURON. It was similar to the model of Traub et al., J Neurophysiol. (2003), and consisted of a soma, an apical shaft, distal dendrites, five basal dendrites, an axon, and a single spine. The spine’s location was variable along the apical shaft (initial 50 μm) and apical. The axon contained an axon hillock region, an initial segment, segments with myelin, and nodes of Ranvier, in order to have realistic action potential generation. For more information about the model see supplemental material, Delgado et al 2010.
Delgado JY, Gómez-González JF, Desai NS (2010) Pyramidal neuron conductance state gates spike-timing-dependent plasticity.
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Neuron or other electrically excitable cell;
Neocortex L2/3 pyramidal GLU cell;
Gomez-Gonzalez, JF [jfcgomez at ull.edu.es];
Delgado JY, [jyamir at ucla.edu];
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Neocortex L2/3 pyramidal GLU cell
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//moddir mechanism/mechanism_cell1/ load_file("nrngui.hoc") chdir("experiment") load_file("run.hoc")
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