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The basal ganglia play a critical but enigmatic role in many aspects of brain function including movement, motivation, reward and addiction. The vast number of neurologic disorders, such as Parkinson's disease, Huntington's disease, Tourette’s syndrome, Dystonia and Schizophrenia, which involve the basal ganglia are a testament to the importance of this role. However, precisely defining the purpose of the basal ganglia in the normal control of movement or motivation is surprisingly difficult. The goal of the experiments described here is to explore the influence of basal ganglia in adaptive learning and motor control in awake-behaving primates and in human subjects undergoing surgery. Our lab is uniquely positioned to investigate basal ganglia function in nonhuman primates and in humans undergoing surgery for movement disorders.
Areas of research focus:
Most experimental paradigms in primates involve over-training the animals to perform a specific task. However, such an approach does not provide the opportunity to record while the animal is learning since the behavior is too variable. In these experiments the animal is explicitly forced to quickly learn new stimulus-response mappings. Our prediction is that successful stimulus - movement pairing will be associated with significantly different patterns of activity than unsuccessful pairings. Secondly, we predict that the dorsal (caudate nucleus) and ventral (nucleus accumbens) aspects of the anterior striatum will have dissociative roles in learning novel stimulus - response mappings.
Dopamine is believed to play a significant role in learning new and performing behaviors already learned. Furthermore, dopamine depletion or dysfunction has been implicated in the underlying pathological mechanisms of a number of movement and psychological disorders. Using the electrochemical method of fixed-potential amperometry, we intend to examine the dynamic regulation of dopamine in the striatum during the execution of learned motor behaviors and during the learning of new motor behaviors.
An intriguing manifestation of Parkinson's disease is the ability of patients to overcome their akinesia when presented with compelling visual cues. This suggests that sensory cues exert their effects by either transiently normalizing disordered basal ganglia activity or by employing different circuitry that bypasses the basal ganglia altogether. However, the basis for this observation is unknown. Comparing visually cued versus spontaneously generated movements is a potentially powerful method of exploring the functional derangements of Parkinson's disease.
Sensorimotor Integration Lab
Edwards Research Building
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