CNUP Training Faculty

Robert S. Turner, Ph.D.

Associate Professor, Neurobiology, Center for the Neural Basis of Cognition

Ph.D. University of Washington (1991)

Office: 4074 Biomedical Science Tower 3

Neurophysiology of basal ganglia-cortical networks in health and disease.

Research Summary:

Research in my lab focuses on three principal questions: 1) What functions do the basal ganglia subserve in the healthy brain? 2) What pathophysiologic processes underlie the signs of basal ganglia-related disorders? 3) How does deep brain stimulation (DBS) work to alleviate symptoms in disorders such as Parkinson's disease and dystonia?

For most of us reaching to grasp an object seems an almost effortless task, despite the profound difficulty of the underlying control problems. The central network that solves this problem includes regions of cortex, the basal ganglia, cerebellum, and thalamus. One goal of my research is to tease apart the relative roles of the basal ganglia and motor cortices in learning and controlling skillful arm movements. In recent results we found, contrary to expectation, that the basal ganglia circuit is not necessary for the execution of well-learned motor sequences. We plan to extend this work to test basal ganglia roles in several forms of motor learning (i.e., sequence learning and adaptation).

Pathology within the basal ganglia, such as the degeneration of dopamine cells in Parkinson’s disease, leads to distinct disorders of movement. Another central theme in my research is to understand the physiologic mechanisms that lead from local pathology to specific behavioral impairments (i.e., parkinsonian akinesia, bradykinesia and rigidity). We are currently testing hypotheses concerning roles of the motor cortices in these parkinsonian signs.

High frequency electrical stimulation through electrodes implanted deep in the brain (i.e., Deep Brain Stimulation, DBS) is a highly effective therapy for several medically intractable disorders. Despite the growing popularity of DBS, we are only beginning to understand the physiologic mechanisms that mediate its therapeutic effect. An ongoing project investigates the local and network-wide mechanisms of action of DBS with the goal of improving its efficacy.

Projects in my lab typically use a combination of multi-electrode neuronal recording and pharmacologic manipulations of local neuronal activity in awake behaving animals. Most experiments are conducted in non-human primates trained to perform motor tasks. A new effort in the lab will combine functional imaging with single unit recording in behaving non-human primates.

Selected Publications:

Chan, V., Starr, P.S. and Turner, R.S. Bursts and oscillations as independent properties of neural activity in the parkinsonian globus pallidus internus. Neurobiol Dis. 41: 2-10, 2011.

Pasquereau, B. and Turner, R.S. Primary motor cortex of the parkinsonian monkey: Differential effects on the spontaneous activity of pyramidal tract-type neurons. Cerebral Cortex 2010; In press. PMID: 21045003

Turner, R.S. and Desmurget, M. Basal ganglia contributions to motor control: a vigorous tutor. Curr Opin Neurobiol. 2010; In press. PMID: 20850966

Desmurget, M. and Turner, R.S. Motor sequences and the basal ganglia: kinematics, not habits. J Neurosci. 2010; 30:7685-7690. (Highlighted in Faculty of 1000 Neuroscience)

McCairn, K. and Turner, R.S. Deep brain stimulation of the globus pallidus internus in the parkinsonian primate: Local entrainment and suppression of low frequency oscillations. J Neurophysiol. 2009; 101:1941-1960.

Starr, P.A., Kang, G.A., Heath, S., Shimamoto, S. and Turner, R.S. Pallidal neuronal discharge in Huntington’s disease: support for selective loss of striatal cells originating the indirect pathway. Exp Neurol. 211:227-33, 2008.

Desmurget, M. and Turner, R.S. Testing basal ganglia motor functions through reversible inactivations in the posterior internal globus pallidus. J Neurophysiol. 99:1057, 2008.

Wu, A.K., McCairn, K., Zada, G., Wu, T. and Turner, R.S. Motor cortex stimulation: Transient benefit in a primate model of Parkinson’s Disease. J Neurosurg. 106:695-700, 2007.