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Presynaptic GABA_B Receptors Modulate Thalamic Excitation of Inhibitory and Excitatory Neurons in the Mouse Barrel Cortex

Department of Pharmacology and Toxicology, Ponce School of Medicine, Ponce, Puerto Rico, 00732

Submitted 3 January 2004; accepted in final form 8 July 2004

Cortical inhibition plays an important role in the processing of sensory information, and the enlargement of receptive fields by the in vivo application of GABA_B receptor antagonists indicates that GABA_B receptors mediate some of this cortical inhibition. Although there is evidence of postsynaptic GABA_B receptors on cortical neurons, there is no evidence of GABA_B receptors on thalamocortical terminals. Therefore to determine if presynaptic GABA_B receptors modulate the thalamic excitation of layer IV inhibitory neurons and excitatory neurons in layers II–III and IV of the somatosensory "barrel" cortex of mice, we used a thalamocortical slice preparation and patch-clamp electrophysiology. Stimulation of the ventrobasal thalamus elicited excitatory postsynaptic currents (EPSCs) in cortical neurons. Bath application of baclofen, a selective GABA_B receptor agonist, reversibly decreased AMPA receptor-mediated and N-methyl-D-aspartate (NMDA) receptor-mediated EPSCs in inhibitory and excitatory neurons. The GABA_B receptor antagonist, CGP 35348, reversed the inhibition produced by baclofen. Blocking the postsynaptic GABA_B receptor-mediated effects with a Cs⁺-based recording solution did not affect the inhibition, suggesting a presynaptic effect of baclofen. Baclofen reversibly increased the paired-pulse ratio and the coefficient of variation, consistent with the presynaptic inhibition of glutamate release. Our results indicate that the presynaptic activation of GABA_B receptors modulates thalamocortical excitation of inhibitory and excitatory neurons and provide another mechanism by which cortical inhibition can modulate the processing of sensory information.

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