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.

(+)-(S)-trujillon, (+)-(S)-4-(2,2-diphenyl-1,3,2-oxazabolidin-5-oxo)propionic acid, a novel glutamatergic analog, modifies the activity of globus pallidus neurons by selective NMDA receptor activation.

Decreased levels of glutamate and changes in several markers of glutamatergic function occur in movement disorders and chronic psychiatric illnesses. Ionotropic glutamate receptors have been implicated in neuronal cell death, and have, therefore, been related to the process of neurodegenerative diseases. Drugs that interact with the glutamatergic system are important tools for the development of better therapies.