Matthew M. Ford

Visiting Associate Professor of Psychology

Behavioral neuroscience, psychopharmacology, animal models of alcohol and nicotine use disorders, polysubstance use, neuroactive steroids

Curriculum Vitae

Social Media

Education and Professional Positions

1992-1996, B.S., Biology, Bucknell University

1996-2002, Ph.D., Pharmacology, Wake Forest University School of Medicine

2002-2007, Postdoctoral Fellow, Behavioral Neuroscience, Oregon Health & Science University; F32 award recipient (AA015234)

2007-2012, Research Assistant Professor, Behavioral Neuroscience, Oregon Health & Science University; K01 award recipient (AA016849)

2012-2016, Staff Scientist II, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University

2013-2020, Assistant Professor, Behavioral Neuroscience, Oregon Health & Science University

2016-2020, Research Assistant Professor, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University

2020-2021, Adjunct Professor, Psychology, Lewis & Clark College

2021-2023, Visiting Assistant Professor, Psychology, Lewis & Clark College

2023-present, Visiting Associate Professor, Psychology, Reed College

Grant Funding

Principal Investigator, Animal and Resource Core (P60, PI: Tamara J. Richards), “Behavioral genomics of alcohol neuroadaptation”, AA010760, National Institute of Alcohol Abuse & Alcoholism, National Institutes of Health, 2021.

Co-Investigator, “Distinguishing preexistent and induced epigenetic risk for alcohol use disorders” (R01, PI: Rita P. Cervera Juanes), AA026278, National Institute of Alcohol Abuse & Alcoholism, National Institutes of Health, 2019-2023.

Principal Investigator, “GDNF gene therapy to block relapse of heavy alcohol use in monkeys” (R01), AA024757, National Institute of Alcohol Abuse & Alcoholism, National Institutes of Health, 2016-2020.

Co-Investigator, “The addictive and carcinogenic potential of Juuls - the new face of e-cigarette usage in middle and high school students” (Pilot Project PI: Eliot Spindel), Knight Cancer Institute, OHSU, 2019-2020.

Co-Investigator, “Translational measures of risk for excessive alcohol consumption” (P60, project 02 PI: Kathleen A. Grant), AA010760, National Institute of Alcohol Abuse & Alcoholism, National Institutes of Health, 2016-2020.

Principal Investigator, “Evaluating the efficacy of the PDE4 inhibitor, apremilast, in reducing binge-like alcohol drinking in non-human primates” (R01, administrative supplement), AA024757, National Institute of Alcohol Abuse & Alcoholism, National Institutes of Health, 2017-2018.

Sub-contract Principal Investigator, “Nezavist a novel molecule for treatment of alcohol use disorder” (U44, PI: Boris Tabakoff), AA024905, National Institute of Alcohol Abuse & Alcoholism, National Institutes of Health, 2016-2018.

Principal Investigator, “Development of new nicotine addiction therapies” (ONPRC pilot project, P51, PI: Joseph E. Robertson), OD011092, Office of the Director, National Institutes of Health, 2015-2016.

Co-Investigator, “Development of a model to study the co-morbidity of nicotine and alcohol addiction and role of clinically relevant genetic polymorphisms” (ONPRC pilot project PI: Eliot Spindel), OD011092, Office of the Director, National Institutes of Health, 2012-2013.

Principal Investigator, “Muscarinic influence on methamphetamine discrimination and intake in mice” (MARC pilot project, P50, PI: Aaron J. Janowsky), DA018165, National Institute of Drug Abuse, National Institutes of Health, 2010-2011, 2012-2013.

Principal Investigator, “Nicotine modulation of ethanol consumption and discrimination” (K01), AA016849, National Institute of Alcohol Abuse & Alcoholism, National Institutes of Health, 2007-2012.

Principal Investigator, “Schedule-induced polydipsia, stress, and ethanol drinking in mice” (INIA-Stress pilot project, U01, PI: Kathleen A. Grant), AA013641, National Institute of Alcohol Abuse & Alcoholism, National Institutes of Health, 2010-2012.

Principal Investigator, “Neurosteroid Modulation of Ethanol Intake and Reward” (F32), AA015234, National Institute of Alcohol Abuse & Alcoholism, National Institutes of Health, 2004-2005.

Teaching

My teaching approach is influenced by my 20+ years of biomedical research experience and prior training of graduate students in hands-on applications for behavioral pharmacology. My undergraduate course coverage in the past has included courses in introductory psychology, psychological statistics, psychology methodology, introductory and advanced cognition, and biopsychology. While at Reed College my teaching focus will be on seminal conceptual frameworks and laboratory-based experiences in the fields of Behavioral Neuroscience and Psychopharmacology. For specific details on the course offerings below please refer to descriptions here.

PSY 201 Methods in Behavioral Pharmacology and Neuroscience

PSY 253 Psychedelics and Mental Health: From Taboo to Therapeutic

PSY 333 Behavioral Neuroscience

PSY 338 Psychopharmacology: Drugs and Behavior

Research

As a behavioral pharmacologist my research places particular emphasis on implementing centrally-acting therapeutics to modulate the behavioral influence of abused substances (alcohol, nicotine methamphetamine). Consistent with this overarching theme, my research interests fall under the following four concentrations:

Binge drinking and excessive intake models of alcohol use disorder (AUD). One of the biggest challenges facing the implementation of animal self-administration models to study AUD and other substance use disorders is the difficulty in establishing intake patterns that repeatedly produce intoxication, as is observed in drug-dependent subjects. First, we discovered that providing limited access to alcohol (or other drugs) approximately 2-3 hours into a rodent’s dark phase culminates in blood ethanol concentrations that exceed 0.8 mg/ml (i.e., legal intoxication limit). A second approach involves schedule-induced polydipsia (SIP) to establish dependence-level consumption of oral drug solutions. The following works are a subset of publications for this research interest:
1. Rhodes JS, Ford MM, Yu CH, Brown LL, Finn DA, Garland T Jr, Crabbe JC (2007) Mouse inbred strain differences in ethanol drinking to intoxication. Genes Brain Behav 6:1-18. PMID: 17233637.
2. Ford MM, Steele AM, McCracken AD, Finn DA, Grant KA (2013) The relationship between adjunctive drinking, blood ethanol concentration and plasma corticosterone across fixed-time intervals of food delivery in two inbred mouse strains. Psychoneuroendocrinology 38:2598-2610. PMCID: PMC3812349.
3. Crabbe JC, Metten P, Belknap JK, Spence SE, Cameron AJ, Schlumbohm JP, Huang LC, Barkley-Levenson AM, Ford MM, Phillips TJ (2014) Progress in a replicated selection for elevated blood ethanol concentrations in HDID mice. Genes Brain Behav 13:236-246. PMCID: PMC3923418.
4. Ford MM (2014) Applications of schedule-induced polydipsia in rodents for the study of an excessive ethanol intake phenotype. Alcohol 48:265-276. PMCID: PMC4016177.
Genetic contributions to drug self-administration. My interests in the genetic underpinnings of drug abuse began with my involvement in a study characterizing alcohol intake levels and preference across a large panel of inbred mouse strains. The ability to identify genetically-related behavioral phenotypes using inbred mouse strains or selected lines intrigues me to this day. Subsequent endeavors led to investigations of mouse lines selected for high/low oral methamphetamine intake and high blood ethanol concentration. Further, the impact of a single nucleotide polymorphism (D398N) in the α5 nicotinic acetylcholine receptor subunit reduced the behavioral sensitivity of cynomolgus macaques consuming oral nicotine. The following works are a subset of publications for this research interest:
1. Yoneyama N, Crabbe JC, Ford MM, Murillo A, Finn DA (2008) Voluntary Ethanol Consumption in 22 Inbred Mouse Strains. Alcohol 42:149-160. PMCID: PMC2396347.
2. Shabani S, Dobbs LK, Ford MM, Mark GP, Finn DA, Phillips TJ (2012) A genetic animal model of differential sensitivity to methamphetamine reinforcement. Neuropharmacology 62:2169-2177. PMCID: PMC3320769.
3. Shorey-Kendrick LE, Ford MM, Allen DC, Kuryatov A, Lindstrom J, Wilhelm L, Grant KA, Spindel ER (2015) Nicotinic receptors in non-human primates: analysis of genetic and functional conservation with humans. Neuropharmacology 96(Pt B):263-273. PMID: 25661700.
4. Giardino WJ, Rodriguez ED, Smith ML, Ford MM, Galili D, Mitchell SH, Chen A, Ryabinin AE (2017) Control of chronic excessive alcohol drinking by genetic manipulation of the Edinger-Westphal nucleus urocortin-1 neuropeptide system. Translational Psychiatry 7:e1021. PMCID: PMC5299395.
Steroid hormone and genetic sex influences on alcohol self-administration. My earliest work evaluated the contribution of ovarian steroids (i.e., estradiol and progesterone) to the maintenance of ethanol drinking in female rats, and further characterized estrous cycle-dependent shifts in drinking patterns. I later continued my study of steroid-ethanol interactions by examining the sex-dependent effects of progesterone-derived neuroactive steroids on ethanol drinking in a mouse model. The following works are a subset of publications for this research interest:
1. Ford MM, Eldridge JC, Samson HH (2002) Microanalysis of ethanol self-administration: estrous cycle phase-related changes in consumption patterns. Alcohol Clin Exp Res 26:635-43. PMID: 12045471.
2. Ford MM, Eldridge JC, Samson HH (2004) Determination of an estradiol dose-response relationship in the modulation of ethanol intake. Alcohol Clin Exp Res 28:20-28. PMID: 14745299.
3. Finn DA, Beckley EH, Kaufman KR, Ford MM (2009) Manipulation of GABAergic steroids: Sex differences in the effects on alcohol drinking- and withdrawal-related behaviors. Horm Behav 57:12-22. PMCID: PMC2813380.
4. Ford MM, Nickel JD, Strong MN, Finn DA (2014) Null mutation of 5α-reductase type I gene alters ethanol consumption patterns in a sex-dependent manner. Behav Genet 45:341-353. PMCID: PMC4425631.
Discriminative stimulus properties of abused drugs. I have a long-standing interest in studying the receptor basis of ethanol, nicotine, methamphetamine and drug combinations. Specifically, understanding how ethanol and nicotine interact to alter the perception of combined stimulus effects is likely to inform treatment strategies for the highly prevalent co-abuse of alcohol and nicotine. A novel approach of training mice to discriminate different dose ratios of the drug combination was pursued. The following works are a subset of publications for this research interest:
1. Stolerman IP, Childs E, Ford MM, Grant KA (2011) Role of training dose in drug discrimination: a review. Behav Pharmacol 22:415-429. PMCID: PMC3155633.
2. Ford MM, McCracken AD, Davis NL, Ryabinin AE, Grant KA (2012) Discrimination of ethanol-nicotine drug mixtures in mice: dual interactive mechanisms of overshadowing and potentiation. Psychopharmacology 224:537-548. PMCID: PMC3496813.
3. Ford MM, Davis NL, McCracken AD, Grant KA (2013) Contribution of NMDA glutamate and nicotinic acetylcholine receptor mechanisms in the discrimination of ethanol-nicotine mixtures. Behav Pharmacol 24:617-622. PMCID: PMC3925192.
4. Allen DC, Ford MM, Grant KA (2017) Cross-species translational findings in the discriminative stimulus effects of ethanol. Curr Top Behav Neurosci 39:95-111. PMCID: PMC5612861.

Publications

A complete list of peer-reviewed articles & reviews can be found at the following public site:
‘My NCBI Bibliography’