Abstract
Sensory stimuli are perceived and processed according to their physicochemical and affective signatures. For example, taste perception depends on the chemical identity of a tastant, as well as on its pleasantness or aversiveness. The affective value of a palatable gustatory stimulus changes if it becomes associated with gastric malaise, a phenomenon known as conditioned taste aversion (CTA)1. CTA depends on activity in the gustatory portion of the insular cortex (GC) and in the basolateral nucleus of the amygdala (BLA)2,3. Indeed, inactivation of GC or BLA impairs CTA4–8. Signaling mechanisms typically associated with induction of long term synaptic plasticity are engaged in this form of learning9,10, suggesting that the shift in perception from pleasant to aversive depends on changes in synaptic efficacy. Here we report that CTA modulates synaptic drive onto GC pyramidal neurons, and that long term synaptic depression (LTD) at BLA - GC inputs is sufficient to change the hedonic value of a taste stimulus. Our results demonstrate a direct role for amygdalocortical LTD in taste aversion learning.
Footnotes
Contributions. All authors were involved in writing and commenting the manuscript. M.S. Haley designed and performed the experiments, analyzed the data and wrote the manuscript. S. Bruno performed immediate early genes immunohistochemistry and cell counting. A. Fontanini obtained funding, designed the study and wrote the manuscript. A. Maffei obtained funding, designed the study, supervised experiments and analysis, and wrote the manuscript.
Authors’ disclosure: Alfredo Fontanini is a member of the scientific advisory board of Sage Therapeutics, Boston, MA