Pallidal GABA B receptors: involvement in cortex beta dynamics and thalamic reticular nucleus activity

The external globus pallidus (GP) firing rate synchronizes the basal ganglia-thalamus-cortex network controlling GABAergic output to different nuclei. In this context, two findings are significant: the activity and GABAergic transmission of the GP modulated by GABA B receptors and the presence of the GP-thalamic reticular nucleus (RTn) pathway, the functionality of which is unknown. The functional participation of GABA B receptors through this network in cortical dynamics is feasible because the RTn controls transmission between the thalamus and cortex. To analyze this hypothesis, we used single-unit recordings of RTn neurons and electroencephalograms of the motor cortex (MCx) before and after GP injection of the GABA B agonist baclofen and the antagonist saclofen in anesthetized rats. We found that GABA B agonists increase the spiking rate of the RTn and that this response decreases the spectral density of beta frequency bands in the MCx. Additionally, injections of GABA B antagonists decreased the firing activity of the RTn and reversed the effects in the power spectra of beta frequency bands in the MCx. Our results proved that the GP modulates cortical oscillation dynamics through the GP-RTn network via tonic modulation of RTn activity.

Automated summary

This study found that the firing rate of the external globus pallidus (GP) controls GABAergic output in the basal ganglia-thalamus-cortex network. GABA B receptors modulate the activity and transmission of the GP, and the GP-thalamic reticular nucleus (RTn) pathway plays a functional role. The experiments showed that GABA B agonists increased the firing rate of the RTn and decreased the power spectra of beta frequency bands in the motor cortex (MCx), while GABA B antagonists had the opposite effects.