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      Mechanisms of Shared Vulnerability to Post-traumatic Stress Disorder and Substance Use Disorders


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          Psychoactive substance use is a nearly universal human behavior, but a significant minority of people who use addictive substances will go on to develop an addictive disorder. Similarly, though ~90% of people experience traumatic events in their lifetime, only ~10% ever develop post-traumatic stress disorder (PTSD). Substance use disorders (SUD) and PTSD are highly comorbid, occurring in the same individual far more often than would be predicted by chance given the respective prevalence of each disorder. Some possible reasons that have been proposed for the relationship between PTSD and SUD are self-medication of anxiety with drugs or alcohol, increased exposure to traumatic events due to activities involved in acquiring illegal substances, or addictive substances altering the brain’s stress response systems to make users more vulnerable to PTSD. Yet another possibility is that some people have an intrinsic vulnerability that predisposes them to both PTSD and SUD. In this review, we integrate clinical and animal data to explore these possible etiological links between SUD and PTSD, with an emphasis on interactions between dopaminergic, adrenocorticotropic, GABAergic, and glutamatergic neurobehavioral mechanisms that underlie different emotional learning styles.

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          Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implications.

          The loss of control over drug intake that occurs in addiction was initially believed to result from disruption of subcortical reward circuits. However, imaging studies in addictive behaviours have identified a key involvement of the prefrontal cortex (PFC) both through its regulation of limbic reward regions and its involvement in higher-order executive function (for example, self-control, salience attribution and awareness). This Review focuses on functional neuroimaging studies conducted in the past decade that have expanded our understanding of the involvement of the PFC in drug addiction. Disruption of the PFC in addiction underlies not only compulsive drug taking but also accounts for the disadvantageous behaviours that are associated with addiction and the erosion of free will.
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            The neural basis of drug craving: an incentive-sensitization theory of addiction.

            This paper presents a biopsychological theory of drug addiction, the 'Incentive-Sensitization Theory'. The theory addresses three fundamental questions. The first is: why do addicts crave drugs? That is, what is the psychological and neurobiological basis of drug craving? The second is: why does drug craving persist even after long periods of abstinence? The third is whether 'wanting' drugs (drug craving) is attributable to 'liking' drugs (to the subjective pleasurable effects of drugs)? The theory posits the following. (1) Addictive drugs share the ability to enhance mesotelencephalic dopamine neurotransmission. (2) One psychological function of this neural system is to attribute 'incentive salience' to the perception and mental representation of events associated with activation of the system. Incentive salience is a psychological process that transforms the perception of stimuli, imbuing them with salience, making them attractive, 'wanted', incentive stimuli. (3) In some individuals the repeated use of addictive drugs produces incremental neuroadaptations in this neural system, rendering it increasingly and perhaps permanently, hypersensitive ('sensitized') to drugs and drug-associated stimuli. The sensitization of dopamine systems is gated by associative learning, which causes excessive incentive salience to be attributed to the act of drug taking and to stimuli associated with drug taking. It is specifically the sensitization of incentive salience, therefore, that transforms ordinary 'wanting' into excessive drug craving. (4) It is further proposed that sensitization of the neural systems responsible for incentive salience ('for wanting') can occur independently of changes in neural systems that mediate the subjective pleasurable effects of drugs (drug 'liking') and of neural systems that mediate withdrawal. Thus, sensitization of incentive salience can produce addictive behavior (compulsive drug seeking and drug taking) even if the expectation of drug pleasure or the aversive properties of withdrawal are diminished and even in the face of strong disincentives, including the loss of reputation, job, home and family. We review evidence for this view of addiction and discuss its implications for understanding the psychology and neurobiology of addiction.
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              Getting formal with dopamine and reward.

              Recent neurophysiological studies reveal that neurons in certain brain structures carry specific signals about past and future rewards. Dopamine neurons display a short-latency, phasic reward signal indicating the difference between actual and predicted rewards. The signal is useful for enhancing neuronal processing and learning behavioral reactions. It is distinctly different from dopamine's tonic enabling of numerous behavioral processes. Neurons in the striatum, frontal cortex, and amygdala also process reward information but provide more differentiated information for identifying and anticipating rewards and organizing goal-directed behavior. The different reward signals have complementary functions, and the optimal use of rewards in voluntary behavior would benefit from interactions between the signals. Addictive psychostimulant drugs may exert their action by amplifying the dopamine reward signal.

                Author and article information

                Front Behav Neurosci
                Front Behav Neurosci
                Front. Behav. Neurosci.
                Frontiers in Behavioral Neuroscience
                Frontiers Media S.A.
                31 January 2020
                : 14
                [1] 1Neuroscience Graduate Program, University of Michigan , Ann Arbor, MI, United States
                [2] 2Department of Psychiatry, University of Michigan , Ann Arbor, MI, United States
                Author notes

                Edited by: Maria Asuncion Aguilar, University of Valencia, Spain

                Reviewed by: Robert Sears, Nathan Kline Institute for Psychiatric Research, United States; Lauren Evelyn Chaby, Cohen Veterans Bioscience, United States

                *Correspondence: Jonathan D. Morrow jonmorro@ 123456umich.edu

                Specialty section: This article was submitted to Emotion Regulation and Processing, a section of the journal Frontiers in Behavioral Neuroscience

                Copyright © 2020 María-Ríos and Morrow.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 378, Pages: 21, Words: 21724
                Funded by: National Institute on Drug Abuse 10.13039/100000026
                Award ID: R01 DA044960
                Funded by: National Science Foundation 10.13039/100000001
                Award ID: Graduate Research Fellowship Program
                Behavioral Neuroscience

                comorbidity,self-medication,sensitization,individual differences,dual-diagnosis
                comorbidity, self-medication, sensitization, individual differences, dual-diagnosis


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