Phasic, nonsynaptic GABA-A receptor-mediated inhibition entrains thalamocortical oscillations.
- Rovó Z Laboratory of Thalamus Research, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary, Department of Fundamental Neurosciences, University of Lausanne, Lausanne CH-1005, Switzerland.
- Mátyás F Laboratory of Thalamus Research, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary.
- Barthó P Laboratory of Thalamus Research, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary.
- Slézia A Laboratory of Thalamus Research, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary.
- Lecci S Department of Fundamental Neurosciences, University of Lausanne, Lausanne CH-1005, Switzerland.
- Pellegrini C Department of Fundamental Neurosciences, University of Lausanne, Lausanne CH-1005, Switzerland.
- Astori S Department of Fundamental Neurosciences, University of Lausanne, Lausanne CH-1005, Switzerland.
- Dávid C Laboratory of Thalamus Research, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary.
- Hangya B Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, and Laboratory of Cerebral Cortex Research, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary.
- Lüthi A Department of Fundamental Neurosciences, University of Lausanne, Lausanne CH-1005, Switzerland, acsady@koki.hu anita.luthi@unil.ch.
- Acsády L Laboratory of Thalamus Research, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary, acsady@koki.hu anita.luthi@unil.ch.
- 2014-05-23
Published in:
- The Journal of neuroscience : the official journal of the Society for Neuroscience. - 2014
Animals
Cerebral Cortex
Dependovirus
Excitatory Amino Acid Antagonists
GABA Antagonists
Inhibitory Postsynaptic Potentials
Mice
Mice, Inbred C57BL
Mice, Transgenic
Neural Inhibition
Neurons
Pyridazines
Receptors, GABA-A
Synapses
Thalamus
Vesicular Glutamate Transport Protein 2
gamma-Aminobutyric Acid
English
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.
- Language
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- English
- Open access status
- hybrid
- Identifiers
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- DOI 10.1523/JNEUROSCI.4386-13.2014
- PMID 24849349
- Persistent URL
- https://sonar.ch/global/documents/122984
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