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Department of Neuroscience Research

Department of Neuroscience

David Carr, Ph.D.

Assistant Professor
Director, Neuroscience Graduate Program

Contact Information
carrd@musc.edu
843-792-4993

Education

BS, University of Richmond 1993
Ph.D., University of Pittsburgh 2000

Research Interests

Electrophysiological changes in the PFC following cocaine self-administration:

It has been postulated that the preservative nature of addiction is the result of long-lasting drug-induced changes in the neural circuits responsible for processing the reward value of stimuli and mediating behavioral flexibility in the response to those stimuli if their reward value changes. The prefrontal cortex (PFC) is a key structure involved in processing the changing reward value of stimuli and converging lines of evidence have implicated PFC dysfunction in addiction. For example, during prolonged withdrawal, human cocaine users display decreased resting activity within the PFC, but significantly higher activity during periods of drug craving. These subjects also show deficits in behavioral tasks that have been shown to be sensitive to the integrity of the PFC.

Research in the Carr lab is currently using electrophysiological methods to better understand the long-term changes that occur in the circuitry of the PFC following cocaine use. In conjunction with the MUSC Addiction Research Center, Dr. Carr’s lab is also testing novel pharmaceutical strategies to try to reverse these long-term changes in PFC circuitry.

Role of serotonin in regulating PFC circuitry:

Recent work has demonstrated that the proper functioning of the PFC is critically dependent on an intact serotonin innervation. However, despite its importance, there is little known as to how serotonin influences PFC neural activity. To address this question, Dr. Carr’s laboratory utilizes single cell mRNA profiling techniques along with in vitro patch clamp electrophysiology to study the coordinated expression of serotonin receptors within identified populations of PFC neurons as well how stimulating these receptors changes the properties of the ion channels that are responsible for the input-output properties of PFC cells.

Publications

Carr, D.B., Andrews, G.D., Glen, W.B. & Lavin, A. (2007) Alpha-2 noradrenergic receptors activation enhances neuronal excitability and synaptic integration in prefrontal cortical pyramidal neurons via inactivation of HCN currents. J. Physiol.,584: 437-450.

Carr, D.B. & Surmeier, D.J. (2007) M1 Muscarinic receptors inhibit Kir2 channels and enhance synaptic integration in prefrontal cortex pyramidal neurons. J. Neurophys. 97: 3432-3438.

Day, M., Carr, D. B., Ulrich, S., Ilijic, E, Tkatch, T. & Surmeier, D.J. (2005) Dendritic excitability of mouse frontal cortex pyramidal neurons is shaped by the interaction between HCN, Kir2, and Kleak channels. J. Neurosci., 25: 8776-8787.

Carr, D.B., Day, M., Cantrell, A.R., Held, J., Scheuer, T, Catterall, W.A. & Surmeier, D.J. (2003) Transmitter modulation of slow, activity-dependent alterations in sodium channel availability endows neurons with a novel form of cellular plasticity. Neuron, 39: 793-806.

Carr, D.B., Cooper, D.C., Ulrich, S.L., Spruston, N. & Surmeier, D.J. (2002) Serotonin receptor activation inhibits sodium current and dendritic excitability in prefrontal cortex via a protein kinase C-dependent mechanism. J. Neurosci., 22: 6846-6855.

Carr, D.B., Cooper, D.C., Ulrich, S.L., Spruston, N. & Surmeier, D.J. (2002) Serotonin receptor activation inhibits sodium current and dendritic excitability in prefrontal cortex via a protein kinase C-dependent mechanism. J. Neurosci., 22: 6846-6855.

Carr, D.B. & Sesack, S.R. (2000) Projections from the rat prefrontal cortex to the ventral tegmental area: target specificity in the synaptic associations with mesoaccumbens and mesocortical neurons. J. Neurosci., 20:3864-3873.

Carr, D.B. & Sesack, S.R. (2000) GABA-containing neurons in the rat ventral tegmental area project to the prefrontal cortex. Synapse, 38:114-123.

Carr, D.B. & Sesack, S.R. (2000) Dopamine terminals synapse on callosal projection neurons in the rat prefrontal cortex. J. Comp Neurol., 425: 275-283.

Carr, D.B., O’Donnell, P., Card, J.P. & Sesack, S.R. (1999) Dopamine terminals in the rat prefrontal cortex synapse on pyramidal cells that project to the nucleus accumbens. J. Neurosci., 19:11049-11060.

Carr, D.B. & Sesack, S.R. (1999) Terminals from the rat prefrontal cortex synapse on mesoaccumbens VTA neurons that contain either TH or GABA. Ann. NY. Acad. Sci. 877: 676 678.

Carr, D.B. & Sesack, S.R. (1998) Callosal terminals in the rat prefrontal cortex: synaptic targets and association with GABA-immunoreactive structures. Synapse. 29:193-205.

Wellman, J.C., Carr, D.B., Graham, A., Jones, H., Humm J.L., Ruscio M., Billack, B., & Kinsley, C.H. (1997) Preoptic area infusions of morphine disrupt -- and naloxone restores – parental-like behavior in juvenile rats. Brain Res. Bull., 44:183-191.

Carr, D.B. & Sesack, S.R. (1996) Hippocampal afferents to the rat prefrontal cortex: synaptic targets and relation to dopamine terminals. J.Comp. Neurol., 369:1-15.

Kinsley, C.H., Wellman, J.C., Carr, D.B., & Graham, A. (1993). Opiate regulation of parental behavior in juvenile rats. Pharmacol. Biochem. Behav., 44: 763-768.

Reviews and book chapters

Sesack S.R., Carr D.B., Omelchenko N., Pinto A. (2003) Anatomical substrates for glutamate-dopamine interactions: evidence for specificity of connections and extrasynaptic actions. In: Glutamate and Disorders of Cognition and Motivation, Vol. 1003, B. Moghaddam, M.E. Wolf, eds. New York Academy of Sciences, New York, 36-52.

Sesack, S.R. & Carr, D.B. (2002) Selective prefrontal cortex inputs to dopamine cells: implications for schizophrenia. Physiology and Behavior,77: 513-517.