Abstract
Opioid use disorder (OUD) rarely presents as a unitary psychiatric condition, and the comorbid symptoms likely depend upon the diverse risk factors and mechanisms by which OUD can arise. These factors are heterogeneous and include genetic predisposition, exposure to prescription opioids, and environmental risks. Crucially, one key environmental risk factor for OUD is early life adversity (ELA). OUD and other substance use disorders are widely considered to derive in part from abnormal reward circuit function, which is likely also implicated in comorbid mental illnesses such as depression, bipolar disorder, and schizophrenia. ELA may disrupt reward circuit development and function in a manner predisposing to these disorders. Here, we describe new findings addressing the effects of ELA on reward circuitry that lead to OUD and comorbid disorders, potentially via shared neural mechanisms. We discuss some of these OUD-related problems in both humans and animals. We also highlight the increasingly apparent, crucial contribution of biological sex in mediating the range of ELA-induced disruptions of reward circuitry which may confer risk for the development of OUD and comorbid neuropsychiatric disorders.
Highlights
Opioid use disorder (OUD) is a growing epidemic in the United States and globally
While a variety of the physical and mental health outcomes following early life adversity (ELA) may lead to enhanced risk for OUD and its many comorbidities, here we focus on the effects of ELA on reward-related behaviors and underlying circuitry and propose that disrupted reward processing is a common developmental mechanism by which OUD and its comorbidities may arise following ELA
Together with evidence from human subjects, these findings demonstrate that ELA alters important reward-related circuit nodes to provoke vulnerability to poor psychiatric outcomes
Summary
Edited by: Christopher Jonathan Evans, University of California, Los Angeles, United States. Opioid use disorder (OUD) rarely presents as a unitary psychiatric condition, and the comorbid symptoms likely depend upon the diverse risk factors and mechanisms by which OUD can arise. These factors are heterogeneous and include genetic predisposition, exposure to prescription opioids, and environmental risks. ELA may disrupt reward circuit development and function in a manner predisposing to these disorders. We highlight the increasingly apparent, crucial contribution of biological sex in mediating the range of ELA-induced disruptions of reward circuitry which may confer risk for the development of OUD and comorbid neuropsychiatric disorders
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