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Journal of Neurophysiology, Vol 53, Issue 6 1401-1416, Copyright © 1985 by APS
ARTICLES |
G. E. Alexander and M. R. DeLong
Microstimulation was carried out at over 1,250 sites in the putamen in four unanesthetized rhesus monkeys. At numerous sites, microstimulation resulted in movements of individual body parts including leg, arm, and face. Microstimulation-evoked limb movements were invariably contralateral to the stimulating electrode. In nearly all instances, the response at threshold was restricted to or maximal about a single joint. A small percentage of stimulation-evoked axial and orofacial movements were bilateral. The same motor response was frequently evoked over distances of up to 1,200 micron along a single penetration, suggesting that a relatively homogeneous motor-response zone underlies the observed micro-stimulation effects. We have designated these presumptive functional units striatal microexcitable zones (SMZ). The boundaries of adjacent SMZ involved in different movements frequently appeared to overlap. Amplitude, velocity, and acceleration of microstimulation-evoked elbow movements were assessed quantitatively. With increasing stimulus current, each of these parameters increased monotonically until saturation occurred. The spread of intrastriatal microstimulation currents was found to be comparable to that reported for motor cortex. The effective radius of 40-microA putamen microstimulation currents was estimated to be approximately 150 micron. This effectively rules out the possibility of current spread to the internal capsule. Microstimulation effects were abolished by fiber-sparing lesions produced by microinjections of the neurotoxin ibotenic acid. Moreover, chronaxie measurements in putamen (327 +/- 47 microseconds) were significantly higher than for capsular stimulation (150 +/- 32 microseconds). These observations are consistent with the proposal that movements evoked by putamen microstimulation resulted from activation of putamen output neurons. On the other hand, a possible contribution from the antidromic activation of corticostriate afferent terminals or axons cannot be excluded.
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