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Jerry B. Richards, PhD

Jerry B. Richards, PhD

Senior Research Scientist

Psychobiology

Research Assistant Professor, Pharmacology and Toxicology

Contact Information

1021 Main Street
Buffalo, NY  14203-1016
Phone: (716) 887-2211
Email: jrichard@ria.buffalo.edu

Primary Research Areas

Drug abuse, animal and human models of impulsivity, sensation seeking, behavioral neuroscience, and the experimental analysis of behavior.

Do Stimulant Drugs Prevent Habituation of Reinforcer Effectiveness in Humans

Richards

Research suggests that smokers’ daily behaviors are enhanced by nicotine, an addictive chemical in tobacco. For instance, the simple act of listening to music becomes more pleasurable during cigarette consumption. Among nonsmokers, however, pleasure derived from every-day activities tends to decrease when those activities are consistently repeated. To test the hypothesis that nicotine dependence may be partially maintained via the enhancement of rewarding behaviors associated with cigarette consumption, smokers will complete a brief computer task while brain activity is continuously recorded. Most importantly, we will examine changes in brain activity during regular smoking and while individuals temporarily abstain from smoking. Funded by RIA's Howard T. Blane Director’s Award for Development of Innovative Research in the Addictions (BDAA), 2014-2015.

Drug Abuse and Impulsivity: Tests of Animal Models

Richards | de Wit

These studies were designed to advance the understanding of impulsive behavior and its relation to drug abuse by developing valid animal models of impulsive behavior and operationalizing different concepts of impulsivity. In addition, the research examined how both acute and chronic exposure to methamphetamine (METH) affects impulsive behavior and the roles the neurotransmitter systems dopamine (DA) and serotonin (5HT) in impulsive behavior. Relationships between measures of discounting, delayed reward, risk taking, and the ability to stop drug use were assessed. This project was conducted in parallel to a separate project using humans at the University of Chicago. Together these studies will advance the understanding of the behavioral and neural processes mediating impulsive behaviors, and of the effect of drugs of abuse on these behaviors. Dr. Harriet de Wit, University of Chicago’s Department of Psychiatry, is the co-investigator. This project was transferred from UB’s Department of Pediatrics in June, 2004. Funded by a grant of $793,537 from NIDA.

Drug Abuse and Impulsivity: Tests of Animal Models

This project investigated impulsivity as a predisposing factor for drug abuse. Drug abuse researchers have extensively studied “reward-related” factors that facilitate drug-seeking behaviors, including both unconditioned and conditioned positive affective responses to drugs while ignoring “impulsivity-related” processes that normally inhibit or limit the use of drugs. Dr. Richards believes that processes related to impulsivity may be as important as reward processes in determining whether an individual will use drugs. One reason for the failure to consider “impulsivity-related” factors has been the lack of adequate laboratory models. Although there are a variety of laboratory models designed to investigate the rewarding effects of drugs, there are few models designed to investigate processes that may cause an individual not to take drugs. The primary objective of the research is to develop and use laboratory-based, behavioral measures of impulsivity to study the relationship between impulsive processes and drug abuse. Dr. Richards’ team has identified three distinct behavioral processes that may underlie the occurrence of maladaptive “impulsive behaviors” such as using drugs of abuse. First, preference for the immediate small rewards associated with drug taking over the delayed but larger rewards associated with abstaining may result in drug taking. Second, the inability to inhibit or stop a pre-potent response may result in occurrence of drug taking. And third, lapses of attention may be associated with relapse to drug abuse. This study examined the strength of the association between cocaine self-administration and the three behavioral processes identified as underlying the occurrence of impulsive behaviors by investigating acquisition of drug-taking, escalation of drug intake, extinction of drug-taking, and cue-induced reinstatement of drug-taking. This research will provide important new information concerning putative animal models of impulsivity and the ability of these models to predict cocaine self-administration in humans. Funded by a grant of $554,750 from NIDA. This project is supported through funds provided by the American Recovery and Reinvestment Act (ARRA), 2009-2012.

Effects of Negative Consequences on Drug Self Administration in Rats

The primary objective of this research was to develop a rodent model of self administration (SA) in which drug consumption has delayed negative consequences. SA procedures in which the animals make responses that are reinforced by IV drug injections are widely used and are perhaps the most convincing non-human animal models of drug abuse. Non-human animal SA models, however, may not model important aspects of human drug SA. In humans, impulsivity is considered an important component of drug abuse because individuals take drugs despite the knowledge of negative (often delayed) outcome associated with drug use. In contrast, standard laboratory animal models of SA have no explicit negative outcomes associated with the SA of the drug. Because there are currently no SA models that incorporate negative consequences, the impact of negative outcomes is not generally incorporated into current ideas about the underlying behavioral and neurobiological mechanisms mediating drug abuse. This study will advance our understanding of drug abuse by determining if punishment or delays to punishment have similar (or dissimilar) effects on drug and natural reinforcers of equivalent reinforcing efficacy. The results will help to determine if a “punished” SA model is a valuable tool with which to investigate the behavioral and cognitive regulation of drug abuse by negative consequences. Funded by a grant of $431,356 from NIDA. This project is supported through funds provided by the American Recovery and Reinvestment Act (ARRA), 2009-2011.

Inhibitory Control and Clinical Response in ADHD

Hawk | Pelham | Richards | Waxmonsky | Wilding

Dr. Larry Hawk of the UB Department of Psychology investigated the effects of both methylphenidate (MPH) and performance-based motivational incentives (i.e., monetary rewards, an analogue of behavioral treatment) on laboratory measures of inhibitory control, working memory, sustained attention, and delay-related impulsivity in children with ADHD. This research was the first to test the extent to which MPH affects basic processes assessed in the lab, and whether these processes actually mediate, or account for, individual differences in clinical response to MPH. The researchers have helped to bridge basic and clinical research in ADHD in this work and paved the way for new translational research and theory in ADHD. Dr. William Pelham of UB’s Department of Psychology was co-principal investigator. Co-investigators included Drs. Jerry Richards, RIA, James Waxmonsky, UB Department of Psychiatry, and Gregory Wilding, UB Department of Biostatistics. Funded by NIMH to Dr. Hawk, 2005-2010.

Sensory reinforcement and drug abuse. Investigating the effects of the psychomotor stimulants on the reward value of sensory stimuli. We hypothesize that psychomotor stimulants increase the rewarding value of sensory stimuli and that this increase in reward contributes to the addictive potential of psychomotor stimulants such as methamphetamine and nicotine. This research has important implications for understanding the processes through which individuals become addicted to psychomotor stimulant drugs.

Genetic and Behavioral Dissection of Inhibitory Control

Zhuang | Richards

This study investigated biochemical changes underlying impaired inhibitory control in dopamine transporter expression (DAT knockdown) mice. Researchers tested the hypothesis that impaired postsynaptic dopamine D2 receptor function underlies impaired inhibitory control using a pharmacological rescue approach. They also tested the hypothesis that impaired D2 receptor function underlies impaired inhibitory control using mice that lack or have reduced postsynaptic D2 receptors. Funded by NIMH to Dr. Xiaoxi Zhuang, University of Chicago’s Neurobiology/Pharmacology/Physiology Department; subaward to Dr. Jerry Richards, RIA, 2003-2008.