The brain has a remarkable capacity for controlling movement and for thinking, using sensory information and the memory of past experience. Disorders of these processes lead to Parkinson's disease, cerebellar ataxia, spasticity, dystonia, cerebral palsey and schizophrenia. My colleagues and I are studying these processes using a variety of approaches: 1) recording the messages transmitted along neuroanatomically defined pathways in behaving animals using microelectrodes; 2) investigating structural-functional correlations using a variety of contemporary neuroanatomical methods; 3) utlizing fMRI imaging to identify the brain networks that participate in any give task, and 4) synthesizing these diverse findings using adaptive network models of neural signal processing.

There is growing evidence that both motor programs and thinking algorithms are stored in the basal ganglia and cerebellum. Special ion channels and a combination of positive and negative feedback loops between the cerebellum, red nucleus, and motor cortex provide the mechanisms for the recall and execution of motor programs. Our studies of the cellular mechanisms and glutamate receptors that support positive feedback in this network may lead to novel approaches to the control of hyperactivity in these loops as occurs in spasticity, dystonia and cerebral palsey. Loops through the basal ganglia can either enable or disable the selection of discrete motor programs, through the action of parallel search through a very large data base that has been constructed from our past experiences. We are approaching these issues from many perspectives with the goal of identifying their fundamental systems level, cellular level and molecular level mechanisms. We strive to synthesize these discoveries into a coherent theory of normal limb movement control and of thinking. We are also interested in understanding the neurological and psychiatric disorders that disrupt these functions.