A model of spike initiation in neocortical pyramidal neurons. Export

@article{Mainen_1995_model, abstract = {Neocortical pyramidal cells possess voltage-dependent dendritic sodium channels that promote propagation of action potentials into the dendritic tree but paradoxically may fail to originate dendritic spikes. A biophysical model was constructed to reconcile these observations with known anatomical and physiological properties. When dendritic and somatic sodium channel densities compatible with electrophysiological measurements were combined with much higher densities in the axon initial segment then, regardless of the site of stimulation, spikes initiated at the initial segment and subsequently invaded the dendrites. The lower initial segment threshold arose from high current density and electrical isolation from the soma. Failure of dendritic channels to initiate spikes was due to inactivation and source-load considerations, which were more favorable for conduction of back-propagated spikes.}, address = {Howard Hughes Medical Institute, Computational Neurobiology Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA.}, author = {Mainen, Z. F. and Joerges, J. and Huguenard, J. R. and Sejnowski, T. J.}, citeulike-article-id = {1123275}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/8845165}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=8845165}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/8845165}, issn = {0896-6273}, journal = {Neuron}, keywords = {apinit, model}, month = {December}, number = {6}, pages = {1427--1439}, pdf = {mainen\_95\_model.pdf}, posted-at = {2008-06-30 13:07:58}, priority = {2}, title = {A model of spike initiation in neocortical pyramidal neurons.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/8845165}, volume = {15}, year = {1995} }

TY - JOUR ID - Mainen_1995_model L3 - citeulike-article-id:1123275 N2 - Neocortical pyramidal cells possess voltage-dependent dendritic sodium channels that promote propagation of action potentials into the dendritic tree but paradoxically may fail to originate dendritic spikes. A biophysical model was constructed to reconcile these observations with known anatomical and physiological properties. When dendritic and somatic sodium channel densities compatible with electrophysiological measurements were combined with much higher densities in the axon initial segment then, regardless of the site of stimulation, spikes initiated at the initial segment and subsequently invaded the dendrites. The lower initial segment threshold arose from high current density and electrical isolation from the soma. Failure of dendritic channels to initiate spikes was due to inactivation and source-load considerations, which were more favorable for conduction of back-propagated spikes. IS - 6 JF - Neuron SN - 0896-6273 AD - Howard Hughes Medical Institute, Computational Neurobiology Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA. EP - 1439 TI - A model of spike initiation in neocortical pyramidal neurons. VL - 15 SP - 1427 KW - apinit KW - model AU - Mainen, ZF AU - Joerges, J AU - Huguenard, JR AU - Sejnowski, TJ PY - 1995/December// UR - http://view.ncbi.nlm.nih.gov/pubmed/8845165 ER -