Terry Earl Robinson | |
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Occupation(s) | Biopsychologist and neuroscientist |
Academic background | |
Education | BA., Psychology (1972) MA., Biopsychology (1974) PhD., Biopsychology (1978) |
Alma mater | University of Lethbridge University of Saskatchewan University of Western Ontario |
Thesis | Brainstem Influences On Hippocampal And Neocortical Slow Wave Activation During Waking Behavior And Sleep (1978) |
Academic work | |
Institutions | The University of Michigan (Ann Arbor) |
Terry Earl Robinson is a biopsychologist and neuroscientist,and the Elliot S. Valenstein Distinguished University Professor of Psychology &Neuroscience [1] at The University of Michigan (Ann Arbor). [2]
Robinson is most known for his research on the persistent psychological and neurobiological effects of repeated drug use,and how these may contribute to addiction and relapse. From 2010 onwards,his research has focused on how individual differences in attributing incentive salience to reward-associated cues may contribute to impulse-control disorders like addiction. He has published over 260 articles,edited two books and was listed on ISI HighlyCited.com as one of the highest cited (top 0.5%) scientists in Neuroscience. [3] His papers have been cited over 62,000 times and his h-Index is 110. [4] He is the recipient of APA's D.O Hebb Distinguished Scientific Contribution Award, [5] Distinguished Scientific Contributions Award, [6] and Neal Miller Lecturer, [7] EBPS' Distinguished Scientist Award, [8] APS' William James Fellow Award for Lifetime Achievement, [9] and Grawemeyer Award for Outstanding Ideas in Psychology. [10] He has also received The Henry Russel Lectureship,which is the U-M's highest honor for senior faculty, [11] a Honorary Doctor of Science (honoris causa) degree from the University of Lethbridge,Canada,and was listed on the Stanford University Names World's Top 2% Scientists in 2021. [12]
Robinson is a Fellow of the American Association for the Advancement of Science (AAAS),a Charter Fellow of the American Psychological Society (APS), [13] and a Fellow of Eastern Psychological Association. [14] He was President of the European Behavioral Pharmacology Society (EBPS) from 2015 to 2017. [3] In 2003,he served as chair for the Gordon Research Conference on Catecholamines at The Queen's College,Oxford. [15] He has participated in multiple NIH grant review panels,and held a NIH Research Career Development,NIDA Senior Scientist, [16] and NIDA-funded MERIT Award. In addition,he was the Editor-in-Chief of the journal, Behavioural Brain Research ,from 1996 until 2010. [17]
Robinson earned a B.A. in psychology from the University of Lethbridge in 1972,followed by an M.A. in the same field from the University of Saskatchewan in 1974. Subsequently,he obtained a Ph.D. in Biopsychology from the University of Western Ontario in 1978,and received postdoctoral training with Gary Lynch at the University of California,Irvine in the same year. [18]
Robinson completed his Ph.D. research under the mentorship of C.H. Vanderwolf at the University of Western Ontario in 1978. He joined the University of Michigan as an assistant professor of psychology in 1978. In 2001,he was appointed the Elliot S. Valenstein Collegiate Professor of Behavioral Neuroscience,and since 2011 has been the Elliot S. Valenstein Distinguished University Professor of Psychology &Neuroscience at the University of Michigan,Ann Arbor. [19] [11]
Robinson has maintained a research program focusing on the psychological and neurobiological basis of addiction,especially the persistent effects of repeated psychostimulant drug use on behavior and neurobiology,and with his colleague Kent C. Berridge he has also contributed highly cited theoretical articles on the role of incentive-sensitization in addiction. [20] [21] [22] [23]
In the early 1980s,Robinson initiated studies using the amphetamine-induced rotational behavior model to explore the mesostriatal dopamine system's function and the influence of sex and gonadal hormones with Jill Becker. These studies revealed behavioral sensitization,where a single amphetamine injection increased subsequent behavioral responses,indicating drug-induced brain changes. [24] [25] He then launched a long series of studies in the 1980s and 1990s to characterize the behavioral and neurobiological basis of sensitization,initially emphasizing it as a model of amphetamine psychosis. These studies include the first reports of sex differences and gonadal steroid modulation of sensitization,enhanced amphetamine-stimulated dopamine release in vitro (1982), [24] and in vivo (1988), [26] sensitization to cocaine after a single injection (1985), [27] cross-sensitization with stress (1985), [28] and its persistence,lasting over a year post-drug treatment (1991). [29]
In the 1980s,dopamine was believed to mediate the pleasure derived from reward consumption. However,in 1989,Kent Berridge,along with Robinson,reported that complete dopamine depletions had no effect on rats' hedonic reactions to tastes, [30] leading to the hypothesis that dopamine mediates motivation ('wanting') rather than pleasure ('liking'). Building on this,they proposed that addiction may result from neural sensitization,causing pathological 'wanting' for drugs,even if not particularly 'liked'. This concept gave rise to incentive-sensitization theory (1993), [31] influencing subsequent research on the role of incentive motivational processes in addiction. This paper ranked 15th among the 100 most cited articles in Neuroscience [32] and was listed as the single most cited paper in addiction research in 2021. [33] Their papers,are cited widely,and earned them the Grawemeyer Award in Psychology in 2019. [10] [34] [35] [36]
Continuing studies on behavioral and neural sensitization,Robinson,with Aldo Badiani,observed that environmental factors significantly influenced both the induction and expression of sensitization. Animals tested in a novel drug context often failed to express behavioral sensitization,termed context-specific sensitization. Simultaneously,the drug's context played a crucial role in sensitization induction,leading to research from 1996 to the mid-2000s on how context modulates the behavioral and neurobiological consequences of stimulant or opiate exposure,affecting dopamine neurotransmission and gene expression. [37] [38] [39] Additionally,in 2002,it was discovered that the speed of drug delivery to the brain greatly influences sensitization induction. These findings led to the hypothesis that rapidly reaching the brain enhances addiction potential by promoting sensitization-related neuroplasticity. [40]
Collaborating with Bryan Kolb,Robinson hypothesized that long-lasting behavioral effects of drug exposure involve changes in synaptic connectivity,which would be reflected by changes in dendritic structure. In the late 1990s,they published the first paper on structural plasticity after amphetamine administration in 1997, [41] followed by studies on cocaine and morphine in 1999. [42] They also established patterns of changes in brain regions (e.g.,dorsal vs. ventral striatum,prefrontal cortical subregions,other areas of the neocortex),their similarity after experimenter- or self-administered drugs (2002), [43] and the impact of past experience (2003), [44] and context (2004), [45] along with other features. [46]
Robinson has focused on individual differences in the extent to which reward cues,including drug cues,acquire motivational value (incentive salience). Initial studies,with Shelly Flagel,showed that only some animals (sign-trackers) attribute incentive salience to reward cues,which makes them attention-grabbing and desirable in their own right. It is established that only if reward cues act as incentive stimuli do they come to attract,incite,provoke,spur,and motivate,leading to potentially maladaptive behavior. Notably,sign-tracking is dopamine-dependent whereas goal-tracking,which is observed in animals that fail to attribute motivational value to cues,is not dopamine-dependent. Furthermore,Martin Sarter and colleagues have shown that sign-trackers have deficient choline transporters leading to poor executive/attentional control over behavior,relative to goal-trackers. Robinson has speculated that the combination of enhanced "bottom-up" motivational processes and poor "top-down" inhibitory control may render sign-trackers especially prone to addiction. [47]
Finally,Robinson has initiated an investigation into the impact of pharmacokinetic factors on the emergence of addiction-like behavior,using the Intermittent Access (IntA) self-administration procedure. Their findings have demonstrated IntA cocaine self-administration is especially effective in inducing addiction-like behavior,psychomotor,incentive,and dopamine sensitization,consistent with Incentive-Sensitization Theory. [48] [49] [50]
Amphetamine is a central nervous system (CNS) stimulant that is used in the treatment of attention deficit hyperactivity disorder (ADHD),narcolepsy,and obesity. Amphetamine was discovered as a chemical in 1887 by Lazăr Edeleanu,and then as a drug in the late 1920s. It exists as two enantiomers:levoamphetamine and dextroamphetamine. Amphetamine properly refers to a specific chemical,the racemic free base,which is equal parts of the two enantiomers in their pure amine forms. The term is frequently used informally to refer to any combination of the enantiomers,or to either of them alone. Historically,it has been used to treat nasal congestion and depression. Amphetamine is also used as an athletic performance enhancer and cognitive enhancer,and recreationally as an aphrodisiac and euphoriant. It is a prescription drug in many countries,and unauthorized possession and distribution of amphetamine are often tightly controlled due to the significant health risks associated with recreational use.
Dopamine is a neuromodulatory molecule that plays several important roles in cells. It is an organic chemical of the catecholamine and phenethylamine families. Dopamine constitutes about 80% of the catecholamine content in the brain. It is an amine synthesized by removing a carboxyl group from a molecule of its precursor chemical,L-DOPA,which is synthesized in the brain and kidneys. Dopamine is also synthesized in plants and most animals. In the brain,dopamine functions as a neurotransmitter—a chemical released by neurons to send signals to other nerve cells. Neurotransmitters are synthesized in specific regions of the brain,but affect many regions systemically. The brain includes several distinct dopamine pathways,one of which plays a major role in the motivational component of reward-motivated behavior. The anticipation of most types of rewards increases the level of dopamine in the brain,and many addictive drugs increase dopamine release or block its reuptake into neurons following release. Other brain dopamine pathways are involved in motor control and in controlling the release of various hormones. These pathways and cell groups form a dopamine system which is neuromodulatory.
The mesolimbic pathway,sometimes referred to as the reward pathway,is a dopaminergic pathway in the brain. The pathway connects the ventral tegmental area in the midbrain to the ventral striatum of the basal ganglia in the forebrain. The ventral striatum includes the nucleus accumbens and the olfactory tubercle.
Dextroamphetamine is a potent central nervous system (CNS) stimulant and enantiomer of amphetamine that is prescribed for the treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy. It is also used as an athletic performance and cognitive enhancer,and recreationally as an aphrodisiac and euphoriant.
The nucleus accumbens is a region in the basal forebrain rostral to the preoptic area of the hypothalamus. The nucleus accumbens and the olfactory tubercle collectively form the ventral striatum. The ventral striatum and dorsal striatum collectively form the striatum,which is the main component of the basal ganglia. The dopaminergic neurons of the mesolimbic pathway project onto the GABAergic medium spiny neurons of the nucleus accumbens and olfactory tubercle. Each cerebral hemisphere has its own nucleus accumbens,which can be divided into two structures:the nucleus accumbens core and the nucleus accumbens shell. These substructures have different morphology and functions.
Dopaminergic pathways in the human brain are involved in both physiological and behavioral processes including movement,cognition,executive functions,reward,motivation,and neuroendocrine control. Each pathway is a set of projection neurons,consisting of individual dopaminergic neurons.
Dopamine receptors are a class of G protein-coupled receptors that are prominent in the vertebrate central nervous system (CNS). Dopamine receptors activate different effectors through not only G-protein coupling,but also signaling through different protein interactions. The neurotransmitter dopamine is the primary endogenous ligand for dopamine receptors.
Motivational salience is a cognitive process and a form of attention that motivates or propels an individual's behavior towards or away from a particular object,perceived event or outcome. Motivational salience regulates the intensity of behaviors that facilitate the attainment of a particular goal,the amount of time and energy that an individual is willing to expend to attain a particular goal,and the amount of risk that an individual is willing to accept while working to attain a particular goal.
Sensitization is a non-associative learning process in which repeated administration of a stimulus results in the progressive amplification of a response. Sensitization often is characterized by an enhancement of response to a whole class of stimuli in addition to the one that is repeated. For example,repetition of a painful stimulus may make one more responsive to a loud noise.
Kent C. Berridge is an American academic,currently working as a professor of psychology (biopsychology) and neuroscience at the University of Michigan. Berridge was a joint winner of the 2018 Grawemeyer Award for Psychology.
DNQX (6,7-dinitroquinoxaline-2,3-dione) is a competitive antagonist at AMPA and kainate receptors,two ionotropic glutamate receptor (iGluR) subfamilies. It is used in a variety of molecular biology subfields,notably neurophysiology,to assist researchers in determining the properties of various types of ion channels and their potential applications in medicine.
The reward system is a group of neural structures responsible for incentive salience,associative learning,and positively-valenced emotions,particularly ones involving pleasure as a core component. Reward is the attractive and motivational property of a stimulus that induces appetitive behavior,also known as approach behavior,and consummatory behavior. A rewarding stimulus has been described as "any stimulus,object,event,activity,or situation that has the potential to make us approach and consume it is by definition a reward". In operant conditioning,rewarding stimuli function as positive reinforcers;however,the converse statement also holds true:positive reinforcers are rewarding.
Cocaine- and amphetamine-regulated transcript,also known as CART,is a neuropeptide protein that in humans is encoded by the CARTPT gene. CART appears to have roles in reward,feeding,and stress,and it has the functional properties of an endogenous psychostimulant.
Protein fosB,also known as FosB and G0/G1 switch regulatory protein 3 (G0S3),is a protein that in humans is encoded by the FBJ murine osteosarcoma viral oncogene homolog B (FOSB) gene.
Behavioral addiction,process addiction,or non-substance-related disorder is a form of addiction that involves a compulsion to engage in a rewarding non-substance-related behavior –sometimes called a natural reward –despite any negative consequences to the person's physical,mental,social or financial well-being. In the brain's reward system,a gene transcription factor known as ΔFosB has been identified as a necessary common factor involved in both behavioral and drug addictions,which are associated with the same set of neural adaptations.
Amphetamine dependence refers to a state of psychological dependence on a drug in the amphetamine class. Stimulants such as amphetamines and cocaine do not cause somatic symptoms upon cessation of use but rather neurological-based mental symptoms.
Addiction is a neuropsychological disorder characterized by a persistent and intense urge to use a drug or engage in a behaviour that produces natural reward,despite substantial harm and other negative consequences. Repetitive drug use often alters brain function in ways that perpetuate craving,and weakens self-control. This phenomenon –drugs reshaping brain function –has led to an understanding of addiction as a brain disorder with a complex variety of psychosocial as well as neurobiological factors that are implicated in addiction's development. Classic signs of addiction include compulsive engagement in rewarding stimuli,preoccupation with substances or behavior,and continued use despite negative consequences. Habits and patterns associated with addiction are typically characterized by immediate gratification,coupled with delayed deleterious effects.
Addiction is a state characterized by compulsive engagement in rewarding stimuli,despite adverse consequences. The process of developing an addiction occurs through instrumental learning,which is otherwise known as operant conditioning.
Addiction vulnerability is an individual's risk of developing an addiction during their lifetime. There are a range of genetic and environmental risk factors for developing an addiction that vary across the population. Genetic and environmental risk factors each account for roughly half of an individual's risk for developing an addiction;the contribution from epigenetic risk factors to the total risk is unknown. Even in individuals with a relatively low genetic risk,exposure to sufficiently high doses of an addictive drug for a long period of time can result in an addiction. In other words,anyone can become an individual with a substance use disorder under particular circumstances. Research is working toward establishing a comprehensive picture of the neurobiology of addiction vulnerability,including all factors at work in propensity for addiction.
Evolutionary models of drug use seek to explain human drug usage from the perspective of evolutionary fitness. Plants for instance,may provide fitness benefits by relieving pain. Proponents of this model of drug use suggest that the consumption of pharmacological substances for medicinal purposes evolved in the backdrop of human-plant coevolution as a means of self-medication. Humans thus learned to ignore the cues of plant toxicity because ingesting the bioactive compounds of plants in small amounts was therapeutic.