| Literature DB >> 31907437 |
Tristan Shuman1,2, Daniel Aharoni3,4, Denise J Cai5,6, Christopher R Lee5,3, Spyridon Chavlis7, Lucia Page-Harley5, Lauren M Vetere5, Yu Feng5, Chen Yi Yang3, Irene Mollinedo-Gajate3, Lingxuan Chen5, Zachary T Pennington5, Jiannis Taxidis3, Sergio E Flores3, Kevin Cheng3, Milad Javaherian3, Christina C Kaba3, Naina Rao3, Mimi La-Vu6, Ioanna Pandi7,8, Matthew Shtrahman9, Konstantin I Bakhurin6, Sotiris C Masmanidis6, Baljit S Khakh10, Panayiota Poirazi11, Alcino J Silva4,6,12,13, Peyman Golshani14,15,16,17,18,19.
Abstract
Temporal lobe epilepsy causes severe cognitive deficits, but the circuit mechanisms remain unknown. Interneuron death and reorganization during epileptogenesis may disrupt the synchrony of hippocampal inhibition. To test this, we simultaneously recorded from the CA1 and dentate gyrus in pilocarpine-treated epileptic mice with silicon probes during head-fixed virtual navigation. We found desynchronized interneuron firing between the CA1 and dentate gyrus in epileptic mice. Since hippocampal interneurons control information processing, we tested whether CA1 spatial coding was altered in this desynchronized circuit, using a novel wire-free miniscope. We found that CA1 place cells in epileptic mice were unstable and completely remapped across a week. This spatial instability emerged around 6 weeks after status epilepticus, well after the onset of chronic seizures and interneuron death. Finally, CA1 network modeling showed that desynchronized inputs can impair the precision and stability of CA1 place cells. Together, these results demonstrate that temporally precise intrahippocampal communication is critical for spatial processing.Entities:
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Year: 2020 PMID： 31907437 PMCID： PMC7259114 DOI： 10.1038/s41593-019-0559-0
Source DB: PubMed Journal: Nat Neurosci ISSN： 1097-6256 Impact factor: 24.884