Slow state transitions of sustained neural oscillations by activity-dependent modulation of intrinsic excitability.
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.
Fröhlich
Flavio
F
The Salk Institute for Biological Studies, Computational Neurobiology Laboratory, Howard Hughes Medical Institute, La Jolla, California 92037, USA.
Bazhenov
Maxim
M
Timofeev
Igor
I
Steriade
Mircea
M
Sejnowski
Terrence J
TJ
D000818:Animals; D002415:Cats; D004553:Electric Conductivity; D004594:Electrophysiology; D045604:Extracellular Fluid / Q000378:metabolism; D006801:Humans; D008959:Models, Neurological; D019579:Neocortex / Q000166:cytology / Q000502:physiology*; D009415:Nerve Net / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D009991:Oscillometry; D011188:Potassium / Q000378:metabolism; D011930:Reaction Time; D013569:Synapses / Q000502:physiology
D011188:Potassium