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Tiffany A. Wills, Ph.D.

Assistant Professor
Department of Cell Biology and Anatomy

1901 Perdido Street, Room 6110
New Orleans, LA  70112

Phone:  (504) 568-2012
Fax:      (504) 568-4392

twills@lsuhsc.edu

Degrees

B.S. Psychology (2003)
Indiana University Purdue University in Indianapolis (IUPUI)

Ph.D. Neurobiology (2009)
University of North Carolina at Chapel Hill

Postdoctoral Fellowship
Vanderbilt University

Research Interests

The Wills lab is focused on understanding the neuroadaptations that occur in alcohol dependence, particularly those produced by adolescent alcohol use. To do this, we utilize a wide range of techniques that include electrophysiology, proteomics, and behavioral analysis using a rodent model of alcohol dependence. Much of our work evaluates alcohol-induced changes in the bed nucleus of the stria terminalis (BNST), a region critical for relapse. Further, our studies in this region have highlighted a key role of NMDA receptor signaling in alcohol’s effects.

Below are brief summaries of our current projects:

1.  Adolescent Alcohol Use

This research will evaluate the dynamic regulation of NMDAR subunit composition and signaling during adolescence, which is a population vulnerable to      alcohol addiction. In adults, GluN2B-NMDAR signaling is highly regulated by alcohol in the BNST. Previous work in the BNST demonstrated that NMDAR transmission is uniquely altered by alcohol. Future studies will utilize a combination of electrophysiology and proteomics to explore alcohol-induced changes in NMDAR function and signaling following adolescent alcohol exposure.

2.  NMDA Receptor Trafficking

This work will examine the mechanisms by which withdrawal from chronic alcohol exposure relocalizes NMDA receptors from synaptic to extrasynaptic domains. Our pervious work finds that GluN2B-NMDA receptors dissociate from PSD scaffolding proteins during alcohol withdrawal. Future work will further evaluate these mechanisms and determine how NMDA receptor relocation may alter signaling.

Selected Publications

Wills TA, Baucum AJ, Louderback KM, Chen Y, Pasek JG, Tabb DL, Delpire E, Colbran RJ, Winder DG (2015). Chronic intermittent alcohol disrupts the GluN2B-associated proteome ans specifically regulates group 1 mGlu receptor dependent long-term depression. Addiction Biology

Wills TA, Kash TL, and Winder DG (2013). Developmental changes in the acute ethanol sensitivity of glutamatergic and GABAergic transmission in the BNST. Alcohol, 47:  531-7.  PMID: 24103431.

Wills TA, Klug JR, Silberman Y, Baucum AJ, Weitlauf C, Colbran RJ, Delpire E, Winder DG (2012).  GluN2B subunit deletion reveals key role in acute and chronic ethanol sensitivity of glutamate synapses in bed nucleus of the stria terminalis. Proc Natl Acad Sci U S A.,109:  E278-87. PMID:  22219357

 Wills TA, Knapp DJ, Overstreet DH, Breese, GR (2010).  Interactions of stress and CRF in ethanol-withdrawal induced anxiety in adolescent and adult rats.  Alcoholism: Clinical and Experimental Research, 34: 1603-12, PMCID: PMC2948468.

Wills TA, Knapp DJ, Overstreet DH, Breese, GR (2009). Sensitization, duration, and pharmacological blockade of anxiety-like behavior following repeated withdrawals in adolescent and adult rats. Alcoholism: Clinical and Experimental Research, 33: 455-63, PMCID: PMC2847263.

Wills TA, Knapp DJ, Overstreet DH, Breese, GR (2008). Differential dietary ethanol intake and blood ethanol levels in adolescent and adult rats: Effects on anxiety-like behavior and seizure thresholds. Alcoholism: Clinical and Experimental Research, 32:  1350-1360, PMCID: PMC2855489.

Additional Info

Funding
K99/R00 “Alcohol Regulation of Synaptic and Extrasynaptic GluN2B-NMDA Receptors in BNST”