Basolateral amygdala noradrenergic activity is required for enhancement of object recognition memory by histone deacetylase inhibition in the anterior insular cortex.

Extensive evidence indicates that noradrenergic activation of the basolateral amygdala (BLA) is essential for mediating emotional arousal effects on memory consolidation in different target regions. However, the mechanism by which BLA activation regulates such information storage processes remains largely elusive. Here we demonstrate, in male Sprague-Dawley rats, that noradrenergic activation of the BLA is critically involved in enabling facilitation of memory consolidation induced by histone acetylation, a form of chromatin modification, within the insular cortex (IC) on object recognition memory. The histone deacetylase (HDAC) inhibitor sodium butyrate (NaB) administered either systemically or directly into the anterior, but not posterior, IC immediately after object recognition training enhanced long-term memory for the identity of the object. Systemic NaB administration also enhanced memory for the location of the object. This NaB-induced enhancement of both object recognition and object location memory was selectively associated with an increased ability to assess the familiarity of the training stimulus, without affecting interaction with a novel stimulus. The β-adrenoceptor antagonist propranolol infused into the BLA concurrently abolished the NaB-induced enhancement of familiarity detection underlying both object recognition and object location memory. These findings indicate that noradrenergic activity within the BLA induced by emotional arousal interacts with chromatin modification mechanisms in its target regions to affect post-learning consolidation processes underlying long-term recognition memory and discrimination of a familiar stimulus.