Chapter 10 Chapter 10 Sensory and Motor Systems in Primates

Author(s):  
Jon H. Kaas
Keyword(s):  
1971 ◽  
Vol 84 (1) ◽  
pp. 35 ◽  
Author(s):  
Donald G. MacKay
Keyword(s):  

1986 ◽  
Vol 24 (6-7) ◽  
pp. 539-544 ◽  
Author(s):  
P.S. Spencer ◽  
S.M. Crain ◽  
M.B. Bornstein ◽  
E.R. Peterson ◽  
T. Van De Water

1979 ◽  
Vol 237 (5) ◽  
pp. R278-R284 ◽  
Author(s):  
Y. Sakuma ◽  
D. W. Pfaff

Electrical stimulation in the mesencephalic central gray (CG) and adjacent subtectum through chronically implanted electrodes in free-moving estrogen-primed ovariectomized female rats elicited a rapid and large facilitation of the lordosis reflex in response to either male mounts or manula cutaneous stimuli. Unilateral stimulation was sufficient for this effect. The facilitation increased in a graded manner to increased stimulus intensity, and was optimally evoked by stimuli delivered at 50--150 Hz. Facilitation disappeared rapidly following the end ot electrical stimulation, and within 15 min, reflex performance returned to the prestimulation level. Lordosis facilitation appeared when no aversive responses occurred; stimulation with comparable parameters at the lateral edge of CG or in the mesencephalic reticular formation often resulted in postural changes or aversive responses but was not able to facilitate lordosis. Lordosis refelx facilitation was probably mediated by projections descending from neurons in and around the CG, and represents stimulation of a functional link between ascending somatosensory and descending motor systems for the control of lordosis behavior.


1976 ◽  
Vol 39 (6) ◽  
pp. 1246-1256 ◽  
Author(s):  
L. Ritchie

1. Areas of cerebellar cortex related to saccadic eye movements were ablated in three Macaca mulatta monkeys trained to fixate visual targets. There followed a postoperative dysmetria of saccadic eye movements which appeared to be the result of an impairment specifically within the saccadic system. 2. Convergent evidence from two experimental paradigms indicated that the saccadic deficit was a function of the position of the eye in the orbit and did not involve retinal error processing. 3. The pattern of this position-dependent dysmetria suggests that the eye was no longer fully compensating for the elastic restoring forces imposed by the orbital medium and antagonist muscle(s). 4. The similarity of these data to saccadic eye movements of human cerebellar patients and arm movements of rhesus monkeys with cerebellar lesions indicates that the inability to compensate for the differential loads placed on motor systems by the mechanics of those systems may explain several cerebellar symptoms.


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