Defense Date


Document Type


Degree Name

Doctor of Philosophy


Physiology and Biophysics

First Advisor

Donald D. Price


Since the early 1800's, the basal ganglia have been recognized as an extrapyramidal subcortical motor area. Much of the knowledge of basal ganglia involvement in movement has been obtained through clinical symptomology. Consideration of the basal ganglia as a pure inhibitory influence upon motor regulation was a concept generated by early researchers (24,57,58). In spite of the fact that the basal ganglia was considered an inhibitory center, it was known that the basal ganglia produced fore limb flexion or contraversive head ‘turning. At the present, both facilitatory and inhibitory influences upon motor activity have been demonstrated (50). Physiological mechanisms underlying basal ganglia involvement in movement have been difficult to assess due to the fact that: (1) electrical stimulation and discrete surgical lesions within this subcortical area fail to produce as significant a change in locomotor activity as that observed in dysfunction; and (2) the basal ganglia are many synapses removed from sensory input and from lower motoneurons. Various approaches have been utilized to elucidate motor influences of the basal ganglia. These include: (1) ablation of one or more basal ganglia structures; (2) electrical stimulation of basal ganglia structures; (3) modulation of pre-existing motor activity by electrical stimulation of regions within the basal ganglia; (4) more recently, unit recording in basal ganglia structures in chronic preparations during a task related movement.

Early investigators postulated that the basal ganglia exerted a steadying influence upon the pyramidal tract (86). Modulation of the gamma motoneuronal system by subcortical structures pertained to the alteration of background activity on a spinal level. Since some basal ganglia dysfunctions result in the alteration of tone as well as hyperactivity, one would suspect that they modulate the gamma motoneuronal system. Granit and Kaada (26) investigated basal ganglia influences upon gamma activity but did not determine the ‘pathway by which these influences were mediated. They did not investigate basal ganglia modulation of cortically induced increase in gamma discharge. Thus, the question was raised as to whether or not the basal ganglia actually modulated cortically induced increases in gamma activity.

Two general mechanisms based on anatomical studies are possible for the modulation of motor activity by the basal ganglia. These mechanisms are: (l) modulation of the output of cortical neurons that exert motor influences and (2) modulation of subcortical neurons that exert motor influences. The former mechanism would occur via a well defined pathway from basal ganglia structures via the thalamus to the cortex (See Literature Review). Modulation could also occur via basal ganglia projections to subcortical areas which in turn project to the spinal level. Differentiation between these two mechanisms was accomplished in the present study by two experimental approaches. The first was an investigation of basal ganglia modulation of flexor responses of the anterior tibialis muscle elicited by electrical stimulation of the sensorimotor cortex and pyramidal tract. These investigations were carried out in intact and in decorticate cats. The anterior tibialis muscle is activated during the first phase, the flexion phase of movement (17). Therefore, this muscle was chosen for this study since a characteristic of some basal ganglia dysfunctions involves a slow onset or initiation of movement.

The second approach was an analysis of modulation of cortically induced pyramidal tract responses by conditioning shock trains delivered to various loci within the basal ganglia. Both approaches were designed to determine whether inhibitory and facilitatory motor influences of the basal ganglia occurred at a cortical or subcortical level. A major hypothesis to be tested was whether facilitatory and inhibitory regions existed within the caudate nucleus and more specifically, whether the rostral region of the caudate nucleus was inhibitory and the caudal region facilitatory as proposed by Liles and Davis (50).


Scanned, with permission from the author, from the original print version, which resides in University Archives.


© The Author

Is Part Of

VCU University Archives

Is Part Of

VCU Theses and Dissertations

Date of Submission


Included in

Physiology Commons