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Chronic opioid exposure suppresses endogenous endorphin/enkephalin activity and induces compensatory changes in brain stress and arousal systems. A key site is the locus coeruleus, where opioids acutely inhibit noradrenergic neurons; over time, the system adapts by increasing cyclic AMP signaling. When opioids are reduced or stopped, the “rebound” produces noradrenergic hyperactivity—manifesting as lacrimation, rhinorrhea, piloerection, mydriasis, GI upset, and anxiety—hallmarks of withdrawal. Tolerance reflects reduced responsiveness due to receptor desensitization and downstream adaptations, prompting higher doses for the same effect. Option A is incorrect because mu-opioid receptors are typically desensitized/downregulated with tolerance, not upregulated. Option C describes dopaminergic changes more associated with stimulant use. Option D references GABA modulation of the VTA, which plays a role in reward but doesn’t directly explain opioid-specific tolerance/withdrawal physiology. Understanding these mechanisms informs counseling, anticipatory guidance, and coordination with prescribers for evidence-based medications (e.g., buprenorphine, methadone) and psychosocial interventions.