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

Détails

Ressource 1Télécharger: 29317612.pdf (2065.36 [Ko])
Etat: Serval
Version: Final published version
ID Serval
serval:BIB_C1071CD33539
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Gamma oscillatory activity in vitro: a model system to assess pathophysiological mechanisms of comorbidity between autism and epilepsy.
Périodique
Translational psychiatry
Auteur(s)
Subramanian D., Pralong E., Daniel R.T., Chacko A.G., Stoop R., Babu K.S.
ISSN
2158-3188 (Electronic)
ISSN-L
2158-3188
Statut éditorial
Publié
Date de publication
10/01/2018
Peer-reviewed
Oui
Volume
8
Numéro
1
Pages
16
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Résumé
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.
Mots-clé
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
Oui
Création de la notice
16/01/2018 12:55
Dernière modification de la notice
09/05/2019 0:44
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