To test the hypothesis that unconditioned and conditioned opioid withdrawal enhance memory consolidation through shared neurobiological mechanisms, the current study focused on the central amygdala (CeA) and local corticotropin-releasing factor (CRF) neurotransmission. In the unconditioned withdrawal experiments, male Sprague-Dawley rats were implanted with subcutaneous osmotic mini-pumps releasing 3.5 mg/kg/day heroin (or sham surgery) and injected with 3 mg/kg naloxone (NLX) to precipitate withdrawal. In the conditioned withdrawal experiments, rats injected with heroin (2 mg/kg x 2 injections) received 3 mg/kg NLX immediately prior to confinement to one compartment (CS+) of a place conditioning apparatus, or vehicle prior to confinement in the alternative compartment (CS-). Using immunohistochemistry, it was established that both precipitated withdrawal and confinement to the withdrawal-paired CS + compartment elevated c-Fos expression within the CeA. More importantly, using the post-training approach to target consolidation of object memory, it was found that intra-CeA infusions of the CRF1 receptor antagonist ANT (0.2-2 μg/inf) blocked the memory-enhancing effects of both precipitated withdrawal and exposure to the withdrawal-paired CS + compartment. These findings indicate that pharmacological and conditioned opioid withdrawal influence memory consolidation through a common CRF-mediated mechanism within the CeA.