RT Journal Article
SR Electronic
T1 Role of inhibitory control in modulating spread of focal ictal activity
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 146407
DO 10.1101/146407
A1 Jyun-you Liou
A1 Hongtao Ma
A1 Michael Wenzel
A1 Mingrui Zhao
A1 Eliza Baird-Daniel
A1 Elliot H Smith
A1 Andy Daniel
A1 Ronald Emerson
A1 Rafael Yuste
A1 Theodore H Schwartz
A1 Catherine A Schevon
YR 2017
UL http://biorxiv.org/content/early/2017/06/26/146407.abstract
AB Focal seizure propagation is classically thought to be spatially contiguous. However, propagation through the epileptic network – a collection of disparate epileptic nodes – has been theorized. Here, we used a multielectrode array, wide field calcium imaging, and two-photon calcium imaging to study focal seizure propagation pathways in an acute rodent neocortical 4-aminopyridine model. Although ictal neuronal bursts did not propagation beyond a 2-3 mm region, they were associated with hemisphere-wide LFP fluctuations and parvalbumin-positive interneuron activity outside the seizure focus. Globally compromising this inhibitory response using bicuculline surface application resulted in classical contiguous propagation; whereas, focal bicuculline microinjection resulted in epileptic network formation with two physically disparate foci. Our study suggests both classical and epileptic network propagation could arise from inhibition defects without pre-existing pathological connectivity changes, and that preferred propagation pathways may result from variations in cortical topology.