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The Journal of Neurophysiology Vol. 84 No. 1 July 2000, pp. 289-300
Copyright ©2000 by the American Physiological Society
1Department of Neurobiology, 2Department of Cell Biology, and 3Department of Neurophysiology, Tokyo Metropolitan Institute for Neuroscience, Tokyo Metropolitan Organization for Medical Research, Fuchu, Tokyo 183-8526, Japan; and 4Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee, Memphis, Tennessee 38163
Nambu, Atsushi,
Hironobu Tokuno,
Ikuma Hamada,
Hitoshi Kita,
Michiko Imanishi,
Toshikazu Akazawa,
Yoko Ikeuchi, and
Naomi Hasegawa.
Excitatory Cortical Inputs to Pallidal Neurons Via the
Subthalamic Nucleus in the Monkey. J. Neurophysiol. 84: 289-300, 2000. How the motor-related cortical areas
modulate the activity of the output nuclei of the basal ganglia is an
important issue for understanding the mechanisms of motor control by
the basal ganglia. In the present study, by using awake monkeys, the
polysynaptic effects of electrical stimulation in the forelimb regions
of the primary motor and primary somatosensory cortices on the activity of globus pallidus (GP) neurons, especially mediated by the subthalamic nucleus (STN), have been characterized. Cortical stimulation induced an
early, short-latency excitation followed by an inhibition and a late
excitation in neurons of both the external and internal segments of the
GP. It also induced an early, short-latency excitation followed by a
late excitation and an inhibition in STN neurons. The early excitation
in STN neurons preceded that in GP neurons. Blockade of STN neuronal
activity by muscimol (GABAA receptor agonist) injection
resulted in abolishment of both the early and late excitations evoked
in GP neurons by cortical stimulation. At the same time, the
spontaneous discharge rate of GP neurons decreased, pauses between the
groups of spikes of GP neurons became prominent, and the firing pattern
became regular. Injection of (±)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) [N-methyl-D-aspartate (NMDA)
receptor antagonist], but not
1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulfonamide disodium [NBQX (non-NMDA receptor antagonist)], into the STN
attenuated the early and late excitations in GP neurons, suggesting
that cortico-subthalamic transmission is mediated mainly by NMDA
receptors. Interference with the pallido-subthalamic transmission by
bicuculline (GABAA receptor antagonist) injection into the
STN made the inhibition distinct without affecting the early
excitation. The present results indicate that the
cortico-subthalamo-pallidal pathway conveys powerful excitatory effects
from the motor-related cortical areas to the GP with shorter conduction
time than the effects conveyed through the striatum.
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