Single-column thalamocortical network model exhibiting gamma oscillations, sleep spindles, and epileptogenic bursts.
To better understand population phenomena in thalamocortical neuronal ensembles, we have constructed a preliminary network model with 3,560 multicompartment neurons (containing soma, branching dendrites, and a portion of axon). Types of neurons included superficial pyramids (with regular spiking [RS] and fast rhythmic bursting [FRB] firing behaviors); RS spiny stellates; fast spiking (FS) interneurons, with basket-type and axoaxonic types of connectivity, and located in superficial and deep cortical layers; low threshold spiking (LTS) interneurons, which contacted principal cell dendrites; deep pyramids, which could have RS or intrinsic bursting (IB) firing behaviors, and endowed either with nontufted apical dendrites or with long tufted apical dendrites; thalamocortical relay (TCR) cells; and nucleus reticularis (nRT) cells. To the extent possible, both electrophysiology and synaptic connectivity were based on published data, although many arbitrary choices were necessary. In addition to synaptic connectivity (by AMPA/kainate, NMDA, and GABA(A) receptors), we also included electrical coupling between dendrites of interneurons, nRT cells, and TCR cells, and--in various combinations--electrical coupling between the proximal axons of certain cortical principal neurons. Our network model replicates several observed population phenomena, including 1) persistent gamma oscillations; 2) thalamocortical sleep spindles; 3) series of synchronized population bursts, resembling electrographic seizures; 4) isolated double population bursts with superimposed very fast oscillations (>100 Hz, "VFO"); 5) spike-wave, polyspike-wave, and fast runs (about 10 Hz). We show that epileptiform bursts, including double and multiple bursts, containing VFO occur in rat auditory cortex in vitro, in the presence of kainate, when both GABA(A) and GABA(B) receptors are blocked. Electrical coupling between axons appears necessary (as reported previously) for persistent gamma and additionally plays a role in the detailed shaping of epileptogenic events. The degree of recurrent synaptic excitation between spiny stellate cells, and their tendency to fire throughout multiple bursts, also appears critical in shaping epileptogenic events.
Traub
Roger D
RD
Department of Physiology, State University of New York, Downstate Medical Center, 450 Clarkson Ave., Box 31, Brooklyn, NY 11203, USA. roger.traub@downstate.edu
Contreras
Diego
D
Cunningham
Mark O
MO
Murray
Hilary
H
LeBeau
Fiona E N
FE
Roopun
Anita
A
Bibbig
Andrea
A
Wilent
W Bryan
WB
Higley
Michael J
MJ
Whittington
Miles A
MA
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001683:Biological Clocks / Q000502:physiology*; D002540:Cerebral Cortex / Q000502:physiology*; D004827:Epilepsy / Q000503:physiopathology*; D008297:Male; D008959:Models, Neurological; D009415:Nerve Net; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D012890:Sleep / Q000502:physiology*; D013788:Thalamus / Q000502:physiology*