Conditioned odor aversion (COA) is the avoidance of an odorized-tasteless solution (the conditioned stimulus, CS), the ingestion of which precedes toxicosis. Previous works have shown that the basolateral nucleus of the amygdala (BLA) is involved in the acquisition, and more precisely, the control of the CS memory trace, of COA. Since catecholamine depletion of the amygdala induced a deficit in the potentiated version of COA, this study investigated the role of the adrenergic system in the BLA during COA. Male Wistar rats bilaterally implanted with cannulae aimed at the BLA were microinjected with the beta-adrenergic antagonist propranolol (1 microg/0.2 microl) during the acquisition (5 min before the CS presentation, pre-CS, or immediately after, post-CS) or during the retrieval test (5 min before test, pre-test). Results showed that pre-CS, but neither post-CS nor pre-test, infusions of propranolol impaired COA, suggesting that beta-adrenergic system activity in the BLA is involved in the acquisition but not the expression of COA. Moreover, the fact that pre-CS, but not post-CS, treatment disrupted COA suggests that beta-adrenergic system in the BLA is involved in the initiation but not the maintenance of the CS memory trace during COA acquisition.