Reduced GIRK expression in midbrain dopamine neurons during prolonged abstinence from fentanyl self-administration.

Rationale: Despite decades of research and medical development, relapse to drug seeking continues to be a significant challenge in the treatment of substance use disorders. GABA receptor (GABA-R) agonists have been shown preclinically to inhibit relapse by acting on midbrain dopamine (DA) neurons and are sometimes used off-label for the treatment of alcohol use disorder. Studies in rodent models show reduced GABA-R signaling in DA neurons after exposure to stimulants.