Marina Wolf | |
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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.
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.
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.
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.
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
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.
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.
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.
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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.
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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.
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Antonello Bonci is an Italian-American neurologist and a neuropsychopharmacologist specialized in the long-term effects of drug exposure on the brain. In August 2019, he became president of Global Institutes on Addictions Miami. Bonci was previously the scientific director of the National Institute on Drug Abuse and a professor at the University of California, San Francisco.
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Lisa Monteggia is an American neuroscientist who is a Professor in the Department of Pharmacology, Psychiatry & Psychology as well as the Barlow Family Director of the Vanderbilt Brain Institute at Vanderbilt University in Nashville, Tennessee. Monteggia probes the molecular mechanisms underlying psychiatric disorders and has made critical discoveries about the role of the neurotrophins in antidepressant efficacy, the antidepressant mechanisms of Ketamine, as well as the epigenetic regulation of synaptic transmission by MeCP2.
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