Effects of stimulation of the centromedian nucleus of the thalamus on the activity of striatal cells in awake rhesus monkeys.
Although the existence of a massive projection from the caudal intralaminar nuclei of the thalamus [i.e. the centromedian (CM) and parafascicular nuclei] to the striatum is well documented, the effects of CM activation upon striatal cells remain poorly understood. Therefore, we studied the effects of electrical stimulation of CM on the electrophysiological activity of striatal neurons, and on striatal levels of gamma-aminobutyric acid (GABA) and acetylcholine in rhesus monkeys. Striatal cells did not respond to single-pulse stimulation (bipolar biphasic stimulation, 175-500 muA), but the large majority of recorded neurons responded to burst stimulation (100 Hz, 1 s, 150-175 muA) of CM, often with a delay of tens of milliseconds. Striatal phasically active neurons, which likely correspond to projection neurons, responded mainly with increases in firing (13/28 cells), while tonically active neurons (likely cholinergic interneurons) often showed combinations of increases and decreases in firing (24/46 cells). In microdialysis studies, CM stimulation led to a reduction of striatal acetylcholine levels. This effect was prevented by addition of the GABA-A receptor antagonist gabazine to the microdialysis fluid. We conclude that CM stimulation frequently results in striatal response patterns with excitatory and inhibitory components. Under the conditions chosen here, the specific patterns of striatal responses to CM stimulation are likely the result of striatal processing of thalamic inputs. Through these indirect effects, local CM stimulation may engage large portions of the striatum. These effects may be relevant in the interpretation of the therapeutic effects of CM stimulation for the treatment of neurological disorders.
Nanda
Bijli
B
Yerkes National Primate Research Center, Emory University, Atlanta, GA 30329, USA.
Galvan
Adriana
A
Smith
Yoland
Y
Wichmann
Thomas
T
D000109:Acetylcholine / Q000378:metabolism; D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D001931:Brain Mapping; D003342:Corpus Striatum / Q000166:cytology / Q000502:physiology*; D004558:Electric Stimulation; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology; D018756:GABA Antagonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists; D053444:Inhibitory Postsynaptic Potentials / Q000502:physiology; D007395:Interneurons / Q000502:physiology; D020646:Intralaminar Thalamic Nuclei / Q000166:cytology / Q000502:physiology*; D008253:Macaca mulatta; D009434:Neural Pathways / Q000166:cytology / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D011930:Reaction Time / Q000502:physiology; D011963:Receptors, GABA-A / Q000378:metabolism; D009435:Synaptic Transmission / Q000502:physiology; D014851:Wakefulness / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid; D000109:Acetylcholine