David Rossi

David Rossi

Associate Professor

Accepting Graduate Students
Room: VBR 355
Phone: (509)-335-7671


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

NIH Cerebellar Contributions to Alcohol Use Disorders (PI)
NIH Context-Induced Cocaine Relapse: Influence of Memory Reconsolidation (Co-I)
ADARP Cannabinoid Impacts on the Developing Brain (PI)
ADARP Nicotine and Cannabidiol Interactions with Alcohol Withdrawal (PI)
Select Publications
  • Rossi DJ, Oshima T, Attwell D (2000) Glutamate release in severe brain ischaemia is mainly by reversed uptake Nature 403(6767), 316-21 PMID: 10659851 PMCID:
  • Rossi DJ, Hamann M (1998) Spillover-mediated transmission at inhibitory synapses promoted by high affinity alpha6 subunit GABA(A) receptors and glomerular geometry Neuron 20(4), 783-95 PMID: 9581769 PMCID:
  • Rossi DJ, Slater NT (1993) The developmental onset of NMDA receptor-channel activity during neuronal migration Neuropharmacology 32(11), 1239-48 PMID: 7509049 PMCID:
  • Arguello AA, Richardson BD, Hall JL, Wang R, Hodges MA, Mitchell MP, Stuber GD, Rossi DJ, Fuchs RA (2017) Role of a Lateral Orbital Frontal Cortex-Basolateral Amygdala Circuit in Cue-Induced Cocaine-Seeking Behavior Neuropsychopharmacology 42(3), 727-735 PMID: 27534268 PMCID: PMC5240178
  • Kaplan JS, Mohr C, Hostetler CM, Ryabinin AE, Finn DA, Rossi DJ (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), 1617-26 PMID: 27426857 PMCID: PMC4961518
  • Kaplan JS, Nipper MA, Richardson BD, Jensen J, Helms M, Finn DA, Rossi DJ (2016) Pharmacologically Counteracting a Phenotypic Difference in Cerebellar GABAA Receptor Response to Alcohol Prevents Excessive Alcohol Consumption in a High Alcohol-Consuming Rodent Genotype J Neurosci 36(35), 9019-25 PMID: 27581446 PMCID: PMC5005716
  • Kaplan JS, Mohr C, Rossi DJ (2013) Opposite actions of alcohol on tonic GABA(A) receptor currents mediated by nNOS and PKC activity Nat Neurosci 16(12), 1783-93 PMID: 24162656 PMCID: PMC4022289
  • Mohr C, Brady JD, Rossi DJ (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 Neuropharmacology 58(2), 392-403 PMID: 19825379 PMCID: PMC2813327
  • Rossi DJ, Brady JD, Mohr C (2007) Astrocyte metabolism and signaling during brain ischemia Nat Neurosci 10(11), 1377-86 PMID: 17965658 PMCID:
  • Hamann M, Rossi DJ, Attwell D (2002) Tonic and spillover inhibition of granule cells control information flow through cerebellar cortex Neuron 33(4), 625-33 PMID: 11856535 PMCID:

List of Publications