Network bistability mediates spontaneous transitions between normal and pathological brain states.
Little is known about how cortical networks support the emergence of remarkably different activity patterns. Physiological activity interspersed with epochs of pathological hyperactivity in the epileptic brain represents a clinically relevant yet poorly understood case of such rich dynamic repertoire. Using a realistic computational model, we demonstrate that physiological sparse and pathological tonic-clonic activity may coexist in the same cortical network for identical afferent input level. Transient perturbations in the afferent input were sufficient to switch the network between these two stable states. The effectiveness of the potassium regulatory apparatus determined the stability of the physiological state and the threshold for seizure initiation. Our findings contrast with the common notions of (1) pathological brain activity representing dynamic instabilities and (2) necessary adjustments of experimental conditions to elicit different network states. Rather, we propose that the rich dynamic repertoire of cortical networks may be based on multistabilities intrinsic to the network.
Fröhlich
Flavio
F
Computational Neurobiology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.
Sejnowski
Terrence J
TJ
Bazhenov
Maxim
M
D000200:Action Potentials / Q000502:physiology; D001921:Brain / Q000473:pathology*; D003198:Computer Simulation; D006801:Humans; D008959:Models, Neurological; D009415:Nerve Net / Q000503:physiopathology*; D009434:Neural Pathways / Q000503:physiopathology*; D009457:Neuroglia / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D017711:Nonlinear Dynamics; D011188:Potassium / Q000378:metabolism; D012640:Seizures / Q000473:pathology / Q000503:physiopathology
D011188:Potassium