Differential effects of beta-adrenergic receptor blockade in basolateral amygdala or insular cortex on incidental and associative taste learning.

The importance of central beta-adrenergic system has been essentially investigated in aversive/emotional learning tasks. However, recent data suggest that the beta-adrenergic system is also required for incidental taste learning. In the present study we evaluated in rats whether beta-adrenergic receptor activity is required for taste habituation, an incidental taste learning, and also for conditioned taste aversion (CTA) learning, an associative learning. To address this issue, a low dose of the beta-adrenergic antagonist propranolol was infused before learning in either the basolateral amygdala (BLA) or the insular cortex (IC), two forebrain areas reported to play a key role in taste memory formation. Incidental taste learning was assessed using a single presentation of the sweet taste saccharin 0.1%, which is sufficient to increase saccharin consumption (relative to water baseline) during a second presentation. CTA was assessed by pairing the first saccharin 0.1% presentation with a delayed gastric malaise, thus causing a decrease in saccharin consumption (relative to water baseline) during a second presentation. Propranolol infusion in BLA (1microg/0.2microl) or IC (2.5microg/0.5microl) before the first taste exposure impaired incidental taste learning but did not affect CTA. These results highlight the important role played by the beta-adrenergic receptor activation in cortical and amygdaloid structures during taste learning. Moreover, they are the first to suggest that incidental learning is more sensitive to blockade of noradrenergic system than associative learning.

Basolateral amygdala noradrenergic activity is involved in the acquisition of conditioned odor aversion in the rat.

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.