The Journal of Neuroscience, June 7, 2006, 26(23):6153-6162; doi:10.1523/JNEUROSCI.5509-05.2006
Previous Article | Next Article 
Behavioral/Systems/Cognitive
Slow State Transitions of Sustained Neural Oscillations by Activity-Dependent Modulation of Intrinsic Excitability
Flavio Fröhlich,1,2
Maxim Bazhenov,1
Igor Timofeev,3
Mircea Steriade,3 and
Terrence J. Sejnowski1,2
1The Salk Institute for Biological Studies, Computational Neurobiology Laboratory and Howard Hughes Medical Institute, La Jolla, California 92037, 2Division of Biological Sciences, Section of Neurobiology, University of California San Diego, La Jolla, California 92093, and 3Laboratory of Neurophysiology, School of Medicine, Laval University, Quebec, Canada G1K 7P4
Correspondence should be addressed to Dr. Maxim Bazhenov, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037. Email: bazhenov{at}salk.edu
Little is known about the dynamics and mechanisms of transitions between tonic firing and bursting in cortical networks. Here, we use a computational model of a neocortical circuit with extracellular potassium dynamics to show that activity-dependent modulation of intrinsic excitability can lead to sustained oscillations with slow transitions between two distinct firing modes: fast run (tonic spiking or fast bursts with few spikes) and slow bursting. These transitions are caused by a bistability with hysteresis in a pyramidal cell model. Balanced excitation and inhibition stabilizes a network of pyramidal cells and inhibitory interneurons in the bistable region and causes sustained periodic alternations between distinct oscillatory states. During spike-wave seizures, neocortical paroxysmal activity exhibits qualitatively similar slow transitions between fast run and bursting. We therefore predict that extracellular potassium dynamics can cause alternating episodes of fast and slow oscillatory states in both normal and epileptic neocortical networks.
Key words: neocortex; computational model; bistability; hysteresis; extracellular potassium concentration; paroxysmal activity
Received Dec. 22, 2005;
revised April 14, 2006;
accepted April 21, 2006.
Correspondence should be addressed to Dr. Maxim Bazhenov, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037. Email: bazhenov{at}salk.edu
This article has been cited by other articles:

|
 |

|
 |
 
F. Frohlich, M. Bazhenov, V. Iragui-Madoz, and T. J. Sejnowski
Potassium Dynamics in the Epileptic Cortex: New Insights on an Old Topic
Neuroscientist,
October 1, 2008;
14(5):
422 - 433.
[Abstract]
[PDF]
|
 |
|

|
 |

|
 |
 
F. Frohlich, M. Bazhenov, and T. J. Sejnowski
Pathological Effect of Homeostatic Synaptic Scaling on Network Dynamics in Diseases of the Cortex
J. Neurosci.,
February 13, 2008;
28(7):
1709 - 1720.
[Abstract]
[Full Text]
[PDF]
|
 |
|