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Functional mapping of GABA(B)-receptor subtypes in the thalamus

Ulrich, Daniel and Besseyrias, Valérie and Bettler, Bernhard. (2007) Functional mapping of GABA(B)-receptor subtypes in the thalamus. Journal of Neurophysiology, Vol. 98, H. 6. pp. 3791-3795.

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Official URL: http://edoc.unibas.ch/dok/A5262216

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Abstract

The thalamus plays an important role in attention mechanisms and the generation of brain rhythms. gamma-Aminobutyric acid type B (GABA(B)) receptors are known to regulate the main output neurons of the thalamus, the thalamocortical relay (TCR) cells. However, the contributions of the two predominant GABA(B)-receptor subtypes, GABA(B(1a,2)) and GABA(B(1b,2)), to the control of TCR cell activity are unknown. Here, we used genetic and electrophysiological methods to investigate subtype-specific GABA(B) effects at the inputs to TCR cells. We found that mainly GABA(B(1a,2)) receptors inhibit the release of glutamate from corticothalamic fibers impinging onto TCR cells. In contrast, both GABA(B(1a,2)) and GABA(B(1b,2)) receptors efficiently inhibit the release of GABA from thalamic reticular nucleus (TRN) neurons onto TCR neurons. Likewise, both GABA(B(1a,2)) and GABA(B(1b,2)) receptors efficiently activate somatodendritic K(+) currents in TCR cells. In summary, our data show that GABA(B(1b,2)) receptors cannot compensate for the absence of GABA(B(1a,2)) receptors at glutamatergic inputs to TCR cells. This shows that the predominant association of GABA(B(1a,2)) receptors with glutamatergic terminals is a feature that is preserved at several brain synapses. Furthermore, our data indicate that the cognitive deficits observed with mice lacking GABA(B(1a,2)) receptors could to some extent relate to attention deficits caused by disinhibited release of glutamate onto TCR neurons.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Division of Physiology > Molecular Neurobiology Synaptic Plasticity (Bettler)
UniBasel Contributors:Bettler, Bernhard
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Publisher:American Physiological Society
ISSN:0022-3077
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:22 Mar 2012 14:24
Deposited On:22 Mar 2012 13:37

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