Faculty

Integrative Physiology and Neuroscience Faculty

Chair:  Steve Simasko
(509) 335-6624
Departmental FAX: (509) 335-4650


Faculty

Pullman

David Rossi

David Rossi

Associate Professor

david.rossi@wsu.edu

Office
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

Education

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

Research

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)
List of Publications

 

Spokane

David Rossi

David Rossi

Associate Professor

david.rossi@wsu.edu

Office
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

Education

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

Research

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)
List of Publications

 

Vancouver

David Rossi

David Rossi

Associate Professor

david.rossi@wsu.edu

Office
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

Education

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

Research

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)
List of Publications

 

Neuroscience Graduate Faculty

Pullman

David Rossi

Associate Professor

david.rossi@wsu.edu

Office
Room: VBR 355
Phone: (509)-335-7671

David Rossi

 

Current Positions

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

Education

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

Research

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)

 

Spokane

David Rossi

Associate Professor

david.rossi@wsu.edu

Office
Room: VBR 355
Phone: (509)-335-7671

David Rossi

 

Current Positions

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

Education

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

Research

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)

 

Vancouver

David Rossi

Associate Professor

david.rossi@wsu.edu

Office
Room: VBR 355
Phone: (509)-335-7671

David Rossi

 

Current Positions

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

Education

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

Research

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)

 

Research Track Faculty

Pullman

David Rossi

Associate Professor

david.rossi@wsu.edu

Office
Room: VBR 355
Phone: (509)-335-7671

David Rossi

 

Current Positions

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

Education

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

Research

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)

 

Emeritus Faculty

David Rossi

Associate Professor

david.rossi@wsu.edu

Office
Room: VBR 355
Phone: (509)-335-7671

David Rossi

 

Current Positions

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

Education

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

Research

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)

 

Montana State University Adjunct Faculty

David Rossi

Associate Professor

david.rossi@wsu.edu

Office
Room: VBR 355
Phone: (509)-335-7671

David Rossi

 

Current Positions

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

Education

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

Research

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)

 

Utah State University Adjunct Faculty

David Rossi

Associate Professor

david.rossi@wsu.edu

Office
Room: VBR 355
Phone: (509)-335-7671

David Rossi

 

Current Positions

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

Education

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

Research

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)

 

All Other Adjunct Faculty

David Rossi

Associate Professor

david.rossi@wsu.edu

Office
Room: VBR 355
Phone: (509)-335-7671

David Rossi

 

Current Positions

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

Education

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

Research

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)