Insights into the Neurobiology of Craving in Opioid Use Disorder
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OPIOID USE IN AN OPIOID EPIDEMIC (S DALAL, SECTION EDITOR)
Insights into the Neurobiology of Craving in Opioid Use Disorder Lindsay M. Lueptow 1,2,3 & Elizabeth C. Shashkova 2,4 & Margaret G. Miller 2,4 & Christopher J. Evans 1,2,3,4,5 & Catherine M. Cahill 1,2,3,4,5 Accepted: 14 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review Opioids remain the most potent form of pain relief currently available yet have a high abuse liability. Here we discuss underlying neurobiological changes in opioid use disorder (OUD) that likely contribute to drug craving, which in turn drives continued drug use and relapse. Recent Findings Craving has emerged as a strong indicator in drug-seeking and relapse. Studies have demonstrated a number of allostatic changes in circuitry that facilitate learning of drug-stimuli relationships, thereby augmenting cue-triggered drug use and relapse. Summary This review will focus on key neurobiological changes in underlying circuitry observed during the initial and continued exposure to opioids that result in an increase in neural-reactivity to drug-related intrinsic and extrinsic drug cues and to enhanced learning of drug-context correlations. This sensitized learning state may be an indication of the underlying framework that drives craving and ultimately motivates increased salience of drug cues and drives drug-seeking. Keywords Opioid use disorder . Drug craving . Incentive sensitization . Negative reinforcement . Stress . Negative affect
Introduction While opioid prescriptions in the USA declined from 2012 to 2018 [1], partially due to increased awareness of risks for both patients and physicians and measures implemented by the Center for Disease Control, opioid-related overdoses, and deaths continued to rise [2]. Also worrying is the increasing This article is part of the Topical Collection on Opioid Use in an Opioid Epidemic * Lindsay M. Lueptow [email protected] * Catherine M. Cahill [email protected] 1
Department of Psychiatry and Biobehavioral Sciences, 675 Charles E Young Drive South, Los Angeles, CA 90095, USA
2
Shirley and Stefan Hatos Center for Neuropharmacology, 675 Charles E Young Drive South, Los Angeles, CA 90095, USA
3
Department of Psychology at University of California Los Angeles, 675 Charles E Young Drive South, Los Angeles, CA 90095, USA
4
David Geffen School of Medicine, 675 Charles E Young Drive South, Los Angeles, CA 90095, USA
5
Jane & Terry Semel Institute for Neuroscience and Human Behavior, 675 Charles E Young Drive South, Los Angeles, CA 90095, USA
availability of illicit, low cost and very potent alternatives, including etorphine, fentanyl, and fentanyl derivatives such as carfentanil and sufentanil [3–5]. Despite decades of research on the underlying mechanisms leading to opioid use disorder (OUD), there has been limited progress in stemming its impact. Though it is likely that a number of genetic, biological, and environmental factors play a role in the development of OUD, ultimately, it
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