|Sodium currents activate without a Hodgkin-and-Huxley-type delay in central mammalian neurons.|
|PMID: 16407565 Owner: NLM Status: MEDLINE|
|Hodgkin and Huxley established that sodium currents in the squid giant axons activate after a delay, which is explained by the model of a channel with three identical independent gates that all have to open before the channel can pass current (the HH model). It is assumed that this model can adequately describe the sodium current activation time course in all mammalian central neurons, although there is no experimental evidence to support such a conjecture. We performed high temporal resolution studies of sodium currents gating in three types of central neurons. The results show that, within the tested voltage range from -55 to -35 mV, in all of these neurons, the activation time course of the current could be fit, after a brief delay, with a monoexponential function. The duration of delay from the start of the voltage command to the start of the extrapolated monoexponential fit was much smaller than predicted by the HH model. For example, in prefrontal cortex pyramidal neurons, at -46 mV and 12 degrees C, the observed average delay was 140 micros versus the 740 micros predicted by the two-gate HH model and the 1180 micros predicted by the three-gate HH model. These results can be explained by a model with two closed states and one open state. In this model, the transition between two closed states is approximately five times faster than the transition between the second closed state and the open state. This model captures all major properties of the sodium current activation. In addition, the proposed model reproduces the observed action potential shape more accurately than the traditional HH model.|
|Gytis Baranauskas; Marco Martina|
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|Type: Comparative Study; In Vitro; Journal Article; Research Support, Non-U.S. Gov't|
|Title: The Journal of neuroscience : the official journal of the Society for Neuroscience Volume: 26 ISSN: 1529-2401 ISO Abbreviation: J. Neurosci. Publication Date: 2006 Jan|
|Created Date: 2006-01-12 Completed Date: 2006-03-17 Revised Date: 2007-11-15|
Medline Journal Info:
|Nlm Unique ID: 8102140 Medline TA: J Neurosci Country: United States|
|Languages: eng Pagination: 671-84 Citation Subset: IM|
|Psychiatric Institute, University of Illinois, Chicago, Illinois 60612, USA. firstname.lastname@example.org|
|APA/MLA Format Download EndNote Download BibTex|
Axons / metabolism
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Calcium-Calmodulin-Dependent Protein Kinases / biosynthesis, genetics
Dendrites / metabolism
Dentate Gyrus / cytology
Glutamate Decarboxylase / biosynthesis, genetics
Hippocampus / cytology
Ion Channel Gating / physiology*
Ion Transport / physiology
Isoenzymes / biosynthesis, genetics
Neurons / classification, physiology*
Prefrontal Cortex / cytology
Pyramidal Cells / physiology
RNA, Messenger / biosynthesis
Reverse Transcriptase Polymerase Chain Reaction
Sodium / metabolism*
Sodium Channel Blockers / pharmacology
Sodium Channels / physiology*
Tetrodotoxin / pharmacology
|0/Isoenzymes; 0/RNA, Messenger; 0/Sodium Channel Blockers; 0/Sodium Channels; 4368-28-9/Tetrodotoxin; 7440-23-5/Sodium; EC 126.96.36.199/Calcium-Calmodulin-Dependent Protein Kinase Type 2; EC 188.8.131.52/Calcium-Calmodulin-Dependent Protein Kinases; EC 184.108.40.206/Glutamate Decarboxylase; EC 220.127.116.11/glutamate decarboxylase 1|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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