Memory Extinction, Learning Anew, and Learning the New: Dissociations in the Molecular Machinery of Learning in Cortex

TLDR

The rat insular cortex mediates conditioned taste aversion memory, with long‑term formation requiring muscarinic, β‑adrenergic receptors, MAPK, and protein synthesis. Extinction of conditioned taste aversion in the IC depends on protein synthesis and β‑adrenergic receptors but not on muscarinic receptors or MAPK, mirroring the molecular profile of learning a familiar taste and showing that extinction shares mechanisms with learning, whereas learning anew engages different pathways.

Abstract

The rat insular cortex (IC) subserves the memory of conditioned taste aversion (CTA), in which a taste is associated with malaise. When the conditioned taste is unfamiliar, formation of long-term CTA memory depends on muscarinic and β-adrenergic receptors, mitogen-activated protein kinase (MAPK), and protein synthesis. We show that extinction of CTA memory is also dependent on protein synthesis and β-adrenergic receptors in the IC, but independent of muscarinic receptors and MAPK. This resembles the molecular signature of the formation of long-term memory of CTA to a familiar taste. Thus, memory extinction shares molecular mechanisms with learning, but the mechanisms of learning anew differ from those of learning the new.