WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience Synaptic Systems Antibody Company
 QUICK SEARCH:   [advanced]


     
-


HOME
  |  
SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit an eLetter
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via ISI Web of Science (30)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kim, K. J.
Right arrow Articles by Rieke, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kim, K. J.
Right arrow Articles by Rieke, F.

 Previous Article  |  Next Article 

The Journal of Neuroscience, February 15, 2003, 23(4):1506

Slow Na+ Inactivation and Variance Adaptation in Salamander Retinal Ganglion Cells

Kerry J. Kim and Fred Rieke

Department of Physiology and Biophysics, University of Washington, Seattle, Washington 98195

The retina adapts to the temporal contrast of the light inputs. One component of contrast adaptation is intrinsic to retinal ganglion cells: temporal contrast affects the variance of the synaptic inputs to ganglion cells, which alters the gain of spike generation. Here we show that slow Na+ inactivation is sufficient to produce the observed variance adaptation. Slow inactivation caused the Na+ current available for spike generation to depend on the past history of activity, both action potentials and subthreshold voltage variations. Recovery from slow inactivation required several hundred milliseconds. Increased current variance caused the threshold for spike generation to increase, presumably because of the decrease in available Na+ current. Simulations indicated that slow Na+ inactivation could account for the observed decrease in excitability. This suggests a simple picture of how ganglion cells contribute to contrast adaptation: (1) increasing contrast causes an increase in input current variance that raises the spike rate, and (2) the increased spike rate reduces the available Na+ current through slow inactivation, which feeds back to reduce excitability. Cells throughout the nervous system face similar problems of accommodating a large range of input signals; furthermore, the Na+ currents of many cells exhibit slow inactivation. Thus, adaptation mediated by feedback modulation of the Na+ current through slow inactivation could serve as a general mechanism to control excitability in spiking neurons.

Key words: contrast adaptation; slow Na+ inactivation; modulation of Na+ current; retinal ganglion cell; models for spike generation; adaptation; spike-frequency adaptation; retinal signal processing


Copyright © 2003 Society for Neuroscience  0270-6474/03/2341506-11$05.00/0




-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help

-
Copyright 2008 by Society for Neuroscience ONLINE ISSN: 1529-2401
-