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J Neurophysiol 102: 132-145, 2009. First published April 29, 2009; doi:10.1152/jn.00016.2009
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Signaling of Grasp Dimension and Grasp Force in Dorsal Premotor Cortex and Primary Motor Cortex Neurons During Reach to Grasp in the Monkey

Claudia M. Hendrix, Carolyn R. Mason and Timothy J. Ebner

Department of Neuroscience, University of Minnesota, Minneapolis, Minnesota

Submitted 6 January 2009; accepted in final form 22 April 2009

A fundamental question is how the CNS controls the hand with its many degrees of freedom. Several motor cortical areas, including the dorsal premotor cortex (PMd) and primary motor cortex (M1), are involved in reach to grasp. Although neurons in PMd are known to modulate in relation to the type of grasp and neurons in M1 in relation to grasp force and finger movements, whether specific parameters of whole hand shaping are encoded in the discharge of these cells has not been studied. In this study, two monkeys were trained to reach and grasp 16 objects varying in shape, size, and orientation. Grasp force was explicitly controlled, requiring the monkeys to exert either three or five levels of grasp force on each object. The animals were unable to see the objects or their hands. Single PMd and M1 neurons were recorded during the task, and cell firing was examined for modulation with object properties and grasp force. The firing of the vast majority of PMd and M1 neurons varied significantly as a function of the object presented as well as the object grasp dimension. Grasp dimension of the object was an important determinant of the firing of cells in both PMd and M1. A smaller percentage of PMd and M1 neurons were modulated by grasp force. Linear encoding was prominent with grasp force but less so with grasp dimension. The correlations with grasp dimension and grasp force were stronger in the firing of M1 than PMd neurons and across both regions the modulation with these parameters increased as reach to grasp proceeded. All PMd and M1 neurons that signaled grasp force also signaled grasp dimension, yet the two signals showed limited interactions, providing a neural substrate for the independent control of these two parameters at the behavioral level.


Address for reprint requests and other correspondence: T. J. Ebner, Dept. of Neuroscience, Univ. of Minnesota, Lions Research Bldg., Rm. 421, 2001 Sixth St. SE, Minneapolis, MN 55455 (E-mail: ebner001{at}umn.edu)







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