Optogenetic dissection of ictal propagation in the hippocampal–entorhinal cortex structures
Name
Lu-2016-Optogenetic dissection.pdf
Size
2.06 MB
Format
Adobe PDF
Checksum (MD5)
976e1f695ecc5150fce8f223170b8399
Author(s)
Lu, Yi
Zhong, Cheng
Wang, Lulu
Wei, Pengfei
He, Wei
Huang, Kang
Zhang, Yi
Zhan, Yang
Feng, Guoping
Wang, Liping
Date Issued
October 2016
Journal
Nature Communications
Publisher
Nature Publishing Group
Citation
Lu, Yi et al. “Optogenetic Dissection of Ictal Propagation in the Hippocampal–entorhinal Cortex Structures.” Nature Communications 7 (2016): 10962. © 2017 Macmillan Publishers Limited
Version
Final published version
Abstract
Temporal lobe epilepsy (TLE) is one of the most common drug-resistant forms of epilepsy in adults and usually originates in the hippocampal formations. However, both the network mechanisms that support the seizure spread and the exact directions of ictal propagation remain largely unknown. Here we report the dissection of ictal propagation in the hippocampal–entorhinal cortex (HP–EC) structures using optogenetic methods in multiple brain regions of a kainic acid-induced model of TLE in VGAT-ChR2 transgenic mice. We perform highly temporally precise cross-area analyses of epileptic neuronal networks and find a feed-forward propagation pathway of ictal discharges from the dentate gyrus/hilus (DGH) to the medial entorhinal cortex, instead of a re-entrant loop. We also demonstrate that activating DGH GABAergic interneurons can significantly inhibit the spread of ictal seizures and largely rescue behavioural deficits in kainate-exposed animals. These findings may shed light on future therapeutic treatments of TLE.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
McGovern Institute for Brain Research at MIT
Terms of Use
Creative Commons Attribution
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1038/ncomms10962
