Abstract
Corticotropin releasing factor (CRF) has been shown to induce various behavioral changes related to adaptation to stress. Dysregulation of the CRF system at any point can lead to a variety of psychiatric disorders, including substance use disorders (SUDs). CRF has been associated with stress-induced drug reinforcement. Extensive literature has identified CRF to play an important role in the molecular mechanisms that lead to an increase in susceptibility that precipitates relapse to SUDs. The CRF system has a heterogeneous role in SUDs. It enhances the acute effects of drugs of abuse and is also responsible for the potentiation of drug-induced neuroplasticity evoked during the withdrawal period. We present in this review the brain regions and circuitries where CRF is expressed and may participate in stress-induced drug abuse. Finally, we attempt to evaluate the role of modulating the CRF system as a possible therapeutic strategy for treating the dysregulation of emotional behaviors that result from the acute positive reinforcement of substances of abuse as well as the negative reinforcement produced by withdrawal.
Highlights
Drug addiction is a chronic condition characterized by periods of abstinence and relapse
Later studies in ethanol-dependent rats corroborated that CRFalcohol interaction on GABAergic transmission in the central nucleus of the amygdala (CeA) is more pronounced during alcohol dependence (Roberto et al, 2004)
It is evident that the Corticotropin releasing factor (CRF) system significantly facilitates the induction and maintenance of plasticity in the ventral tegmental area (VTA) and amygdala, with resulting enhancement of glutamate-mediated excitation and reduction of GABA-mediated inhibition, contributing to the molecular basis of drug addiction
Summary
Stress and addiction: contribution of the corticotropin releasing factor (CRF) system in neuroplasticity. Corticotropin releasing factor (CRF) has been shown to induce various behavioral changes related to adaptation to stress. Dysregulation of the CRF system at any point can lead to a variety of psychiatric disorders, including substance use disorders (SUDs). We present in this review the brain regions and circuitries where CRF is expressed and may participate in stress-induced drug abuse. We attempt to evaluate the role of modulating the CRF system as a possible therapeutic strategy for treating the dysregulation of emotional behaviors that result from the acute positive reinforcement of substances of abuse as well as the negative reinforcement produced by withdrawal
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have