Indiana University Bloomington

Neuroscience
Neuroscience
George V. Rebec

George V. Rebec

A.B., Villanova University, 1971
M.A., University of Colorado, 1974
Ph.D., University of Colorado, 1975
Postdoctoral Fellow, University of California at San Diego

Email address: rebec(at)indiana.edu

Research Interests

Research in my laboratory focuses on the neurochemical correlates of behavior. We are especially interested in the neurochemistry of the basal ganglia and related cortico-limbic areas, which have been implicated in basic behavioral processes such as movement and motivation. To assess how these brain systems operate under naturally occurring conditions, we use electrophysiological (single-unit recording and local field potentials) and electrochemical (slow- and fast-scan cyclic voltammetry) techniques to monitor neuronal function during behavior. We also use proteomic techniques to measure the expression of specific brain proteins and their post-translational modification. Our research includes two primary areas of interest: the mechanisms by which drugs of abuse such as cocaine and the amphetamines enhance drug craving and drug seeking, and the neural network dysfunctions underlying Huntington's disease, a fatally inherited neurodegenerative condition. In both lines of research, we are focusing on glutamate, an excitatory amino acid transmitter, as a major driver of the underlying neural changes and as a potential target for the development of improved therapeutics.

Further information on our research programs is available at: www.indiana.edu/~basalgan/.

Representative Publications

Hong, S.L., Barton, S.J., & Rebec, G.V. (2012). Altered neural and behavioral dynamics in Huntington's disease: An entropy conservation approach. PLoS ONE, 7 (1), e30879.

Murphy-Nakhnikian, J.M., Dorner, J.L., Fischer, B.I., Bower-Bir, N.D., & Rebec, G. V. (2012). Abnormal burst patterns of single neurons recorded in the substantia nigra reticulata of behaving 140 CAG Huntington’s disease mice. Neuroscience Letters, 512, 1-5.

Miller, B.R., Dorner, J.L., Bunner, K.D., Gaither, T.W., Klein, E.L., Barton, S. J.,& Rebec, G. V. (2012). Upregulation of GLT1 reverses the deficit in cortically evoked striatal ascorbate efflux in the R6/2 mouse model of Huntington’s disease. Journal of Neurochemistry, 121, 629-638.

Fischer-Smith, K. D., Houston, A.C.W., & Rebec, G. V. (2012). Differential effects of cocaine access and withdrawal on GLT1 expression in rat nucleus accumbens core and shell. Neuroscience, 210, 333-339.

Walker, A.G., Ummel, J.R., & Rebec, G.V. (2011). Reduced expression of conditioned fear in the R6/2 mouse model of Huntington's disease is related to abnormal activity in prelimbic cortex. Neurobiology of Disease, 43 (2), 379-387.

Wood, D.A., Walker, T.L., & Rebec G.V. (2011). Experience-dependent changes in neuronal processing in the nucleus accumbens shell in a discriminative learning task in differentially housed rats. Brain Research, 1390, 90-98.

Miller, B.R., Dorner, J.L., Gaither, T.W., Klein, E.L., Barton, S.J., & Rebec, G.V. (2011). Dysregulated neuronal activity patterns implicate corticostriatal circuit dysfunction in multiple rodent models of Huntington's disease. Frontiers in Systems Neuroscience, 5:26, 1-10.

Sari, Y., Sakai, M., Weedman J.M., Rebec G.V., & Bell R.L. (2011). Ceftriaxone, a beta-lactam antibiotic, reduces ethanol consumption in alcohol-preferring rats. Alcohol and Alcoholism, 43 (3), 239-246.

Ball, K.T., Wellman, C.L., Miller, B.R., & Rebec, G.V. (2010). Electrophysiological and structural alterations in striatum associated with behavioral sensitization to (±)3,4-Methylenedioxymethamphetamine (Ecstasy) in rats: Role of drug context. Neuroscience, 171, 794-811.

Sari, Y., Prieto, A.L., Barton, S.J., Miller, B.R., & Rebec, G.V. (2010). Ceftriaxone-induced up-regulation of cortical and striatal GLT1 in the R6/2 model of Huntington's disease. Journal of Biomedical Science, 17, 62 (1-5).

Rebec, G.V. (2010). A central role for the periphery in the rapid action of cocaine on brain neurons: focus on "Rapid EEG desynchronization and EMG activation induced by intravenous cocaine in freely moving rats: a peripheral, nondopamine neural triggering." Am J Physiol - Regulatory, Integrative and Comparative Physiology, 298 (2,) R283-284.

Miller, B.R., Walker, A.G., Fowler, S.C., von Hörsten, S., Riess, O., Johnson, M.A., & Rebec, G.V. (2010). Dysregulation of coordinated neuronal firing patterns in striatum of freely behaving transgenic rats that model Huntington's disease. Neurobiology of Disease, 37(1), 106-113.

Dorner, J.L, Miller, B.R., Klein, E.L., Murphy-Nakhnikian, A., Andrews, R.L., Barton, S.J., & Rebec, G.V. (2009). Corticostriatal dysfunction underlies diminished striatal ascorbate release in the R6/2 mouse models of Huntington's disease. Brain Research, 1290, 111-120.

Sari, Y, Smith, K.D., Ali, P.K., & Rebec, G.V. (2009). Up-regulation of GLT1 attenuates cue-induced reinstatement of cocaine seeking in rats. Journal of Neuroscience, 29(29), 9239-9243.

Fowler, S.C., Miller, B.R., Gaither, T.W., Johnson, M.A., & Rebec, G.V. (2009). Force-plate quantification of progressive behavioral deficits in the R6/2 mouse model of Huntington's disease. Behavioural Brain Research, 202, 130-137.

Ball, K.T., Wellman, C.L., Fortenberry, E., & Rebec, G.V. (2009). Sensitizing regimens of MDMA (Ecstasy) elicit enduring and differential structural alterations in the brain motive circuit. Neuroscience, 60(2), 264-274.

Wood, D.A., & Rebec, G.V. (2009). Environmental enrichment alters neuronal processing in the nucleus accumbens core during appetitive conditioning. Brain Research, 1259, 59-67.

Ball, K.T., & Rebec, G.V. (2008). Electrophysiological and morphological adaptations in cortico-striato-limbic circuitry induced by 3,4-methylenedioxymethamphetamine (MDMA; Ecstasy). In: H. David (Ed.), Nucleus Accumbens: Neurotransmitters and Related Behaviours, (pp. 297-318). Kerala, India: Research Signpost.

Walker, A.G., Miller, B.R., Fritsch, J.N., Barton, S.J., & Rebec, G.V. (2008). Altered information processing in the prefrontal cortex of Huntington's disease mouse models. Journal of Neuroscience, 28(36), 8973-8982.

Miller, B.R., Walker, A.G., Shah, A.S., Barton, S.J., & Rebec, G.V. (2008). Dysregulated information processing by medium-spiny neurons in striatum of freely behaving mouse models of Huntington's disease. Journal of Neurophysiology, 100(4), 2205-2216.