Differential inhibition of globus pallidus neurons by electrical or chemical stimulation of the striatum.

The reciprocal connections between the globus pallidus (GP) and other basal ganglia (BG) nuclei indicate that the GP plays a significant role in controlling the neuronal activity of the entire BG; in turn, the activity of GP neurons is controlled by several major inputs that involve the striatum. Here, we determined the relative contributions of the selective (chemical) or massive (electrical) activation of the striatal GABAergic transmission to the GP spiking activity. In vivo extracelullar single-unit recordings were performed in the GP of ketamine-anesthetized rats. Both chemical and electrical stimulation of the striatum caused a significant GP spike rate reduction; however, chemical stimulation of the striatum produced a complete firing arrest on most GP neurons, something not seen with electrical stimulation. In addition, chemical stimulation of the striatum with NMDA evoked a significant long-lasting post-inhibitory spike rate increase, an effect that was not seen under glutamate infusion or electrical stimulation. Furthermore, the selective intrapallidal blockade of AMPA/kainate glutamate receptors facilitates the inhibitory effect of intrastriatal electrical stimulation. Our results suggest a differential effect of electrical or chemical stimulation of the striatum on the spiking activity of GP neurons, which involves the activation of intrapallidal AMPA/kainate receptors and striatal en passant fibers.