David Rossi, Ph.D.

David Rossi, Ph.D.

Associate Professor
Office: Veterinary and Biomedical Research Building (VBR) room 355
Email: rossid@vetmed.wsu.edu
Telephone: (509) 335-7671

Recruiting Ph.D. students for fall 2017

David Rossi title=

Current Positions

Associate Professor, IPN, Washington State University, Pullman, WA
Adjunct Professor, Behavioral Neuroscience, Oregon Health & Science University, Portland, OR


1989 B.S. Psychology; University of Wisconsin, Madison, IL
1995 Ph.D Neuroscience; Northwestern University, Chicago, IL

Prior Academic Appointments

2002-2008 Assistant Scientist, Oregon Health and Science University, Portland, OR
2008-2014 Assistant Professor, Oregon Health and Science University, Portland, OR


Our overall research interest is in understanding how neurotransmitters interact with receptors, transporters and synaptic morphology to generate the vast diversity of signaling events that underlie cognition, emotion and action, and on how altered genetics or environmental insults alter those processes and lead to pathology. Current NIH-funded and intramurally funded research focuses on 1) how the brain adapts to chronic abuse of alcohol, and how such alterations lead to acute and long-term withdrawal symptoms, both of which contribute to the maintenance of alcohol addiction (NIAAA), 2) how transient episodes of hypoxia-ischemia affect the developing brain and consequent pathology (NINDS), and 3) how environmental toxins, including pesticides and drugs of abuse, affect the developing brain (intramural). Broadly, all three projects examine how exogenous perturbations of the native nervous system affect synaptic signaling in developing and mature brain tissue, and how such alterations mediate behavioral outcomes. In all cases, we aim to identify the cellular/molecular mechanisms that trigger and mediate damage and malfunction, with the long-term goal of identifying potential targets for pharmacological prevention or treatment of such damage, and consequent pathology. 

We also have an active program examining mechanisms that mediate genetic predilection for developing an alcohol use disorder (AUD). In particular, we identify molecular, cellular and neural processes that respond to low concentrations of alcohol, and we examine how such responses vary across rodent genotypes with divergent alcohol consumption phenotypes. These studies are of particular importance because it is thought that aspects of the initial neurological responses to socially relevant concentrations of alcohol (≤10mM), and individual differences in those responses play a key role in determining vulnerability or resilience to developing an AUD, but the underlying mechanism are not well understood. 

For all projects, we use electrophysiology and optogenetics, combined with various forms of imaging (conventional fluorescence, confocal fluorescence, patterned light illumination, and electron microscopy) to characterize fine details of the interplay among transmitters, receptors and synaptic morphology under healthy conditions and when challenged by drugs, toxins or ischemia. Ultimately, often in collaboration, we use behavioral paradigms to test the role of discovered mechanisms or malfunctions in relevant behaviors: Motor control, consumption of rewarding substances, establishment of reward or aversions, social interactions.  

Current Funding

National Institute on Alcohol Abuse & Alcoholism
National Institute of Neurological Disorders & Stroke 


1. Rossi D.J. and Slater N.T. (1993). The developmental onset of NMDA receptor-channel activity during neuronal migration. Neuropharmacol. 32:1239-1248. PMID: 7509049 

2. Rossi D.J. and Hamann, H. (1998) Spillover-mediated transmission at inhibitory synapses promoted by high affinity 6 subunit GABAA receptors and glomerular geometry. Neuron 20:783-795. PMID: 9581769.

3. Rossi D.J., Oshima, T., and Attwell, D. (2000) Reversed uptake is the major mechanism of glutamate release in severe brain ischaemia. Nature 403:316-321. PMID: 10659851.

4. Hamann M., Rossi, D.J., and Attwell D. (2002) Tonic and spillover inhibition of granule cells control information flow through cerbellar cortex. Neuron 33:1-20. PMID: 11856535.

5. Rossi D.J., Brady J.D., Mohr C (2007) Astrocyte metabolism and signaling during brain ischemia. Nature Neurosci. 10:1377-1386. PMID: 17965658.

6. Mohr C., Brady J.D. and Rossi D.J. (2010) Young age and low temperature, but not female gender delay ATP loss and glutamate release, and protect Purkinje cells during simulated ischemia in cerebellar slices. Neuropharmacol. 58:392-403. PMID: 19825379 

7. Kaplan, J.S., Mohr, C. and Rossi, D.J. (2013) Opposite actions of alcohol on tonic GABAA receptor currents mediated by nNOS and PKC activity. Nature Neurosci. 16:1783-1793. PMID: 24162656.

8. Kaplan, J.S., Mohr, C., Hostetler, C.M., Ryabinin, A.E., Finn, D.A., and Rossi, D.J. (2016) Alcohol suppresses tonic GABAA receptor currents in cerebellar granule cells in the prairie vole: a neural signature of high alcohol consuming genotypes. Alcohol: Clin. & Exp. Res. 40(8):1617. 

9. Kaplan, J.S., Nipper, M.A., Richardson, B.D., Jensen, J., Helms, M., Finn, D.A., and Rossi, D.J. (2016) Pharmacologically counteracting a phenotypic difference in cerebellar GABAA receptor responses to alcohol prevents excessive alcohol consumption in a high alcohol-consuming rodent genotype. J. Neurosci. 36(35): 9019-25. PMID: 27581446.

10. Arguello, A.A., Richardson, B.D., Hall, J.L., Wang, R., Hodges, M.A, Mitchell, M.P., Stuber, G.D., Rossi, D.J., and Fuchs, R.A. (2016) Role of a lateral orbital frontal cortex-basolateral amygdala circuit in cue-induced cocaine-seeking behavior. Neuropsychopharmacol. PMID 27534268