Phasic, nonsynaptic GABA-A receptor-mediated inhibition entrains thalamocortical oscillations.

Details

Ressource 1Download: 7137.full.pdf (2656.19 [Ko])
State: Public
Version: author
Serval ID
serval:BIB_32020D0588AB
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Phasic, nonsynaptic GABA-A receptor-mediated inhibition entrains thalamocortical oscillations.
Journal
Journal of Neuroscience
Author(s)
Rovó Z., Mátyás F., Barthó P., Slézia A., Lecci S., Pellegrini C., Astori S., Dávid C., Hangya B., Lüthi A., Acsády L.
ISSN
1529-2401 (Electronic)
ISSN-L
0270-6474
Publication state
Published
Issued date
2014
Peer-reviewed
Oui
Volume
34
Number
21
Pages
7137-7147
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
Abstract
GABA-A receptors (GABA-ARs) are typically expressed at synaptic or nonsynaptic sites mediating phasic and tonic inhibition, respectively. These two forms of inhibition conjointly control various network oscillations. To disentangle their roles in thalamocortical rhythms, we focally deleted synaptic, γ2 subunit-containing GABA-ARs in the thalamus using viral intervention in mice. After successful removal of γ2 subunit clusters, spontaneous and evoked GABAergic synaptic currents disappeared in thalamocortical cells when the presynaptic, reticular thalamic (nRT) neurons fired in tonic mode. However, when nRT cells fired in burst mode, slow phasic GABA-AR-mediated events persisted, indicating a dynamic, burst-specific recruitment of nonsynaptic GABA-ARs. In vivo, removal of synaptic GABA-ARs reduced the firing of individual thalamocortical cells but did not abolish slow oscillations or sleep spindles. We conclude that nonsynaptic GABA-ARs are recruited in a phasic manner specifically during burst firing of nRT cells and provide sufficient GABA-AR activation to control major thalamocortical oscillations.
Keywords
Animals, Cerebral Cortex/physiology, Dependovirus/genetics, Excitatory Amino Acid Antagonists/pharmacology, GABA Antagonists/pharmacology, Inhibitory Postsynaptic Potentials/drug effects, Inhibitory Postsynaptic Potentials/genetics, Mice, Mice, Inbred C57BL, Mice, Transgenic, Neural Inhibition/physiology, Neurons/physiology, Pyridazines/pharmacology, Receptors, GABA-A/genetics, Receptors, GABA-A/metabolism, Synapses/drug effects, Synapses/genetics, Thalamus/physiology, Vesicular Glutamate Transport Protein 2/metabolism, gamma-Aminobutyric Acid/metabolism
Pubmed
Web of science
Open Access
Yes
Create date
08/09/2014 12:42
Last modification date
20/08/2019 13:17
Usage data