Faculty & Research

Donita Robinson , Ph.D.

Assistant Professor
Department of Psychiatry and Bowles Center for Alcohol Studies

Office | 5007A Thurston-Bowles Bldg, CB#7178

Email | dlr@unc.edu

Lab Website | Robinson Lab

Research Interests

The nucleus accumbens is a pivotal component of the brain circuit underlying reward and motivated behavior, including the positive reinforcement that contributes to alcohol use.  My experiments examine nucleus accumbens core and shell function during ethanol reinforcement in rats, with particular focus on how dopamine input modulates accumbal activity on the millisecond timescale.   I use two approaches:   electrophysiological firing patterns of neurons in the nucleus accumbens are evaluated using multi-electrode arrays, and phasic (subsecond) dopamine activity is evaluated using fast-scan cyclic voltammetry.  

 Electrophysiological firing patterns of neurons in the nucleus accumbens.  Many aspects of goal-directed behaviors and conditioned stimuli associated with ethanol drinking in rats are reflected in vivo in the electrophysiological firing patterns of medium spiny neurons in the nucleus accumbens as transient excitations or inhibitions that are time-locked to operant events.  My data reveal that while nucleus accumbens neurons show the same types of firing patterns for ethanol and water reinforcement, the majority of these phasic cells are selective for one or the other reinforcer, a phenomenon previously reported for cocaine versus water (Carelli et al., J. Neurosci., 2000).  I am currently investigating how plastic these reinforcer-specific neurons may be to changes in motivational state or pharmacological challenge.  The clinical implication of functionally separate circuits encoding ethanol versus other reinforcers is that circuits underlying ethanol self-administration might be therapeutically targeted.   

Subsecond dopamine fluctuations in the nucleus accumbens.  The mesolimbic dopamine input to the nucleus accumbens is well known to be involved in reinforcement and addiction.  By using fast-scan cyclic voltammetry, I can measure endogenous dopamine fluctuations in awake and behaving rats.  My data have demonstrated that transient dopamine signals occur throughout the dorsal and ventral striatum under basal conditions and increase when salient stimuli (another rat, food treat) are introduced into the experimental chamber.  I am currently measuring dopamine transients in rats self-administering alcohol and water in an operant setting, and find that dopamine signals can be time-locked to cues predicting reinforcer availability and to the lever presses.

Center Line Articles

 

Recent Publications

D.L. Robinson and R.M. Wightman (2006).  Rapid dopamine release in freely moving rats.  In A.C. Michael and L.M. Borland (Eds.) Electrochemical Methods for Neuroscience, in series Frontiers in Neuroengineering Series, Vol. 1, CRC Press:  Boca Raton.

D.L. Robinson, T. Voltz, J.O. Schenk and R.M. Wightman (2005).  Acute ethanol decreases dopamine transporter velocity in rat striatum:  in vivo and in vitro electrochemical measurements.  Alcoholism: Clinical and Experimental Research, 29: 746-755.

D.L. Robinson and R.M. Wightman (2004).  Nomifensine amplifies subsecond dopamine signals in the ventral striatum of freely moving rats.  Journal of Neurochemistry, 90: 894-903.

D.L. Robinson, B.J. Trafton, M.L. Heien and R.M. Wightman (2003).  Detecting sub-second dopamine release with fast-scan cyclic voltammetry in freely-moving rats.  Clinical Chemistry, 49: 1763-1773.

D.L. Robinson, M.L. Heien and R.M. Wightman (2002).  Frequency of dopamine concentration transients increases in dorsal and ventral striatum of male rats during introduction of conspecifics.  Journal of Neuroscience, 22: 10477-10486.

R.M. Wightman and D.L. Robinson (2002).  Transient changes in brain dopamine and their association with “reward.” Journal of Neurochemistry, 82: 721-735.