Gamma oscillatory activity in vitro: a model system to assess pathophysiological mechanisms of comorbidity between autism and epilepsy.

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State: Public
Version: Final published version
Serval ID
serval:BIB_C1071CD33539
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Gamma oscillatory activity in vitro: a model system to assess pathophysiological mechanisms of comorbidity between autism and epilepsy.
Journal
Translational psychiatry
Author(s)
Subramanian D., Pralong E., Daniel R.T., Chacko A.G., Stoop R., Babu K.S.
ISSN
2158-3188 (Electronic)
ISSN-L
2158-3188
Publication state
Published
Issued date
10/01/2018
Peer-reviewed
Oui
Volume
8
Number
1
Pages
16
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Abstract
Autism spectrum disorder (ASD) and temporal lobe epilepsy exhibit remarkable comorbidity, but for reasons not clearly understood. To reveal a common pathophysiological mechanism, we here describe and characterize an in vitro epileptiform activity in the rat hippocampus that exhibits common features with in vivo activity in rodent ASD models. We discovered the development of this activity in the CA1 region of horizontal slices after prolonged interictal-like epileptiform activity in the CA3 region that was provoked by incubation in high potassium artificial cerebrospinal fluid. The CA1 epileptiform bursts were insensitive to blockers of glutamatergic transmission, and were carried by synaptic as well as extrasynaptic, tonically activated gamma-aminobutyric acid type A (GABA(A)) receptors. The bursts bear resemblance to in vivo gamma-oscillatory activity found in rat ASD models with respect to their gamma frequency spectrum, their origin (in the CA1), and their sensitivity to blockers of cation-chloride pumps (NKCC1 and KCC2), as well as to oxytocin. Considering this bursting activity as an in vitro model for studying comorbidity between epilepsy and ASD may help to disentangle the intricate interactions that underlie the comorbidity between both diseases and suggests that extrasynaptic tonic GABAergic transmission could represent a potential target for ASD.
Keywords
Animals, Autism Spectrum Disorder/physiopathology, Comorbidity, Electric Stimulation, Electroencephalography, Epilepsy, Temporal Lobe/physiopathology, Hippocampus/pathology, Hippocampus/physiopathology, Rats, Rats, Wistar, Receptors, GABA-A/physiology, Synaptic Transmission, gamma-Aminobutyric Acid/metabolism
Pubmed
Web of science
Open Access
Yes
Create date
16/01/2018 11:55
Last modification date
21/11/2022 8:25
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