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Functional Mapping of GABA_B-Receptor Subtypes in the Thalamus

Department of Biomedicine, Institute of Physiology, Pharmazentrum, University of Basel, Basel, Switzerland

Submitted 6 July 2007; accepted in final form 19 September 2007

The thalamus plays an important role in attention mechanisms and the generation of brain rhythms. -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.

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