Consolidation of altered associability information by amygdala central nucleus

Abstract

The surprising omission of a reinforcer can enhance the associability of the stimuli that were present when the reward prediction error was induced, so that they more readily enter into new associations in the future. Previous research from this laboratory identified brain circuit elements critical to the enhancement of stimulus associability by the omission of an expected event and to the subsequent expression of that altered associability in more rapid learning. These elements include the amygdala, the midbrain substantia nigra, the basal forebrain substantia innominata, the dorsolateral striatum, the secondary visual cortex, and the posterior parietal cortex. Here, we found that consolidation of a surprise-enhanced associability memory in a serial prediction task depends on processing in the amygdala central nucleus (CeA) after completion of sessions that included the surprising omission of an expected event. Post-surprise infusions of anisomycin, lidocaine, or muscimol prevented subsequent display of surprise-enhanced associability. Because previous studies indicated that CeA function is unnecessary for the expression of associability enhancements that were induced previously when CeA function was intact (Holland & Gallagher, 2006), we interpreted these results as indicating that post-surprise activity of CeA (“surprise replay”) is necessary for the consolidation of altered associability memories elsewhere in the brain, such as the posterior parietal cortex (Schiffino, et al., 2014a).

The Recruitment of a Neuronal Ensemble in the Central Nucleus of the Amygdala During the First Extinction Episode Has Persistent Effects on Extinction Expression

“…Eliminating such neurons would thus grant the latter association the upper hand in behavioural control. On the other hand, the deleted ensemble might be critical for restoring attention to the cue in the face of unexpected reward omission and increasing the rate of extinction learning elsewhere (10,31). Although our data are not able to dissociate between these possibilities, both accounts predict that the behavioural scales should be persistently tilted in favour of acquisition, consistent with our findings.…”

Anatomic alterations across amygdala subnuclei in medication-free patients with obsessive–compulsive disorder

“…Although associative learning happens primarily in the BLA (particularly the lateral nucleus), 40 the CeA is more involved in the generation and processing of prediction error signals. 41,42 Impairment of the CeA may thus contribute to OCD symptoms by reducing the flexibility of behavioural response preferences as a result of a reduction in signalling prediction errors when behavioural choices or preferences are not optimal. Outcome prediction error signalling is crucial for responding to the omission of expected rewards or the occurrence of unexpected punishments, and these are important for modifying learned behaviour to adjust to dynamically changing environments: the hallmark of flexible, adaptive goal-directed behaviour.…”

Mini-review: Prediction errors, attention and associative learning

“…Another set of studies (Schiffino, 2015; Schiffino & Holland, 2016a) showed that the consolidation of a surprise-enhanced associability memory in the SPT depends on CeA processing 1-4 hours after surprise sessions. Post-surprise infusions of anisomycin, lidocaine, or muscimol prevented subsequent display of surprise-enhanced associability.…”