Grasping behavior is integral to basic functions in both human and non-human primates, such as eating. Previous studies have revealed a classic grasping circuit that involves several brain regions, such as the motor, pre-frontal, and parietal cortices. However, the contribution of the basal ganglia to grasping control is often overlooked. This is surprising because many basal ganglia disorders, such as Parkinson's disease (PD), have been experimentally associated with deficits in grasping control. This thesis reviews three experiments that use functional magnetic resonance imaging at 3 Tesla to examine the role of the basal ganglia-thalamo-cortical loop in precision grip force. The first experiment measured BOLD activation within individual nuclei of the basal ganglia and thalamus as healthy individuals produced grip force contractions with increasing force amplitude. A novel finding of this study was that BOLD activation within GPi and STN scales with the amplitude of grip force produced, while BOLD activation within other nuclei does not. The second experiment examined BOLD activation within the basal ganglia and cortex in healthy individuals to compare the generation of force with the relaxation of force. This study found that the caudate nucleus had greater activation while subjects generated grip force than while subjects relaxed grip force. These results demonstrate that individual basal ganglia nuclei have a unique functional role in regulating specific aspects of grip force. The third experiment examines changes in the basal ganglia, thalamus, cortex and cerebellum of patients with early stage drug naïve PD. The findings suggest that vigorous motor tasks accentuate abnormal hypoactivity in all basal ganglia nuclei of drug naïve PD and that hypoactivity becomes more pronounced with repeated task performance. In summary, the synthesis of these studies indicates that grip force control is regulated by specific nuclei in the basal ganglia and that cortical models of grasping should include the basal ganglia.