Marina Wolf

Last updated
Marina Wolf
Alma mater Yale University
Scientific career
Institutions Oregon Health & Science University
Sinai-Grace Hospital
Thesis Regulation of Dopamine Synthesis and Release in Striatal and Prefrontal Cortical Brain Slices  (1986)

Marina Elizabeth Wolf is an American neuroscientist and Professor of Behavioral Neuroscience at Oregon Health & Science University. Previously she served as Professor and Chair of the Department of Neuroscience in the Chicago Medical School at Rosalind Franklin University of Medicine and Science. She has been a pioneer in studying the role of neuronal plasticity in drug addiction. Her laboratory is particularly interested in understanding why individuals recovering from substance use disorder remain vulnerable to drug craving and relapse even after long periods of abstinence.

Contents

Education and career

Wolf was born in Milwaukee, Wisconsin. She received her B.A. in biochemistry (with highest distinction) from Northwestern University. [1] Here she received her introduction to neuroscience research working in the laboratory of Dr. Aryeh Routtenberg and later in the laboratory of Dr. David U'Prichard. Wolf earned her doctoral degree in Pharmacology in 1986 at Yale University under the mentorship of Dr. Robert Henry Roth. [1] She was a postdoctoral fellow in the laboratory of Dr. Gregory Kapatos at the Center for Cell Biology at Sinai Hospital of Detroit, now Sinai-Grace Hospital, affiliated with Wayne State University. She was Assistant Professor of Psychiatry at Wayne State University before moving to the Chicago Medical School at Rosalind Franklin University of Medicine & Science in 1992 where she rose through the ranks, serving as Chair of Neuroscience from 2003 to 2018. She moved to OHSU in 2018.

Research

As a Ph.D. student, postdoctoral fellow, and in the early years of her laboratory at Wayne State University, Dr. Wolf's work focused on fundamental properties of dopamine neurons and their relationship to antipsychotic drug action. At Wayne State, many of her colleagues studied the neurobiological basis of drug addiction. She therefore learned about prominent theories of addiction, all of which focused on events intrinsic to dopamine neurons. Excited by the groundbreaking work on glutamate receptors and LTP that was coming out at the time, she hypothesized in the late 1980s that the cascade leading to addiction might depend upon glutamate and synaptic plasticity. Her laboratory went on to use behavioral, biochemical, cell biological and electrophysiological approaches to demonstrate that glutamate synapses in the reward circuitry, especially the nucleus accumbens, undergo complex plasticity after exposure to drugs of abuse and that this plasticity in some cases plays a causal role in behavioral changes that model drug addiction. Her lab continues to characterize synaptic plasticity during abstinence from stimulants and opioids, and to test strategies to harness the understanding of drug-induced synaptic plasticity to develop therapeutic approaches to aid in recovery from substance use disorder.

Awards and honors

Dr. Wolf's laboratory has been continuously supported by NIDA since 1992. She has previously been the recipient of a Merit Award from NIDA (R37) as well as a Senior Scientist Research and Mentorship Award (K05). She has served as a member of the NIDA Advisory Council, the NIH Council of Councils, and the NIDA Board of Scientific Counselors, the Council of the American College of Neuropsychopharmacology (ACNP), the Scientific Council of the Brain & Behavior Research Foundation, and the American Brain Coalition. She has been a member of many NIH study sections, and was Chair of MNPS from 2015 to 2017. She served as President of the ACNP in 2019. Dr. Wolf was elected a Fellow of the American Association for the Advancement of Science in 2017.

Select publications

Wolf ME (1998) The role of excitatory amino acids in behavioral sensitization to psychomotor stimulants. Progress in Neurobiology 54:679-720. PMID 9560846

Wolf ME (2010) The Bermuda triangle of cocaine-induced neuroadaptations. TINS 33:391-398. PMC2935206

Wolf ME, Tseng KY (2012) Calcium-permeable AMPA receptors in the VTA and nucleus accumbens after cocaine exposure: when, how and why? Front Molecular Neurosci 5:72. PMC3384237

Wolf ME (2016) Synaptic mechanisms underlying persistent cocaine craving. Nat Rev Neurosci 17:351-365. PMC5466704

Related Research Articles

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.

<span class="mw-page-title-main">Nucleus accumbens</span> Region of the basal forebrain

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.

<span class="mw-page-title-main">Dopamine receptor</span> Class of G protein-coupled receptors

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.

In internal medicine, relapse or recidivism is a recurrence of a past condition. For example, multiple sclerosis and malaria often exhibit peaks of activity and sometimes very long periods of dormancy, followed by relapse or recrudescence.

Neuropharmacology is the study of how drugs affect function in the nervous system, and the neural mechanisms through which they influence behavior. There are two main branches of neuropharmacology: behavioral and molecular. Behavioral neuropharmacology focuses on the study of how drugs affect human behavior (neuropsychopharmacology), including the study of how drug dependence and addiction affect the human brain. Molecular neuropharmacology involves the study of neurons and their neurochemical interactions, with the overall goal of developing drugs that have beneficial effects on neurological function. Both of these fields are closely connected, since both are concerned with the interactions of neurotransmitters, neuropeptides, neurohormones, neuromodulators, enzymes, second messengers, co-transporters, ion channels, and receptor proteins in the central and peripheral nervous systems. Studying these interactions, researchers are developing drugs to treat many different neurological disorders, including pain, neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease, psychological disorders, addiction, and many others.

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.

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<span class="mw-page-title-main">Reward system</span> Group of neural structures responsible for motivation and desire

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.

<span class="mw-page-title-main">Methamphetamine</span> Central nervous system stimulant

Methamphetamine is a potent central nervous system (CNS) stimulant that is mainly used as a recreational drug and less commonly as a second-line treatment for attention deficit hyperactivity disorder and obesity. Methamphetamine was discovered in 1893 and exists as two enantiomers: levo-methamphetamine and dextro-methamphetamine. Methamphetamine properly refers to a specific chemical substance, the racemic free base, which is an equal mixture of levomethamphetamine and dextromethamphetamine in their pure amine forms, but the hydrochloride salt, commonly called crystal meth, is widely used. Methamphetamine is rarely prescribed over concerns involving human neurotoxicity and potential for recreational use as an aphrodisiac and euphoriant, among other concerns, as well as the availability of safer substitute drugs with comparable treatment efficacy such as Adderall and Vyvanse. Dextromethamphetamine is a stronger CNS stimulant than levomethamphetamine.

<span class="mw-page-title-main">FOSB</span> Protein

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.

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References

  1. 1 2 "Marina Wolf Ph.D. | OHSU People | OHSU". www.ohsu.edu. Retrieved 2021-01-20.