The amygdala and conditioned taste aversion

Reconsolidation is a temporary plasticity that memories undergo when recalled, and these memories can be disrupted, usually through pharmacological intervention. Recently, a purely behavioral treatment was devised that was shown to disrupt reconsolidation of fear memories (Monfils, Cowansage, Klann & LeDoux, 2009). We applied a modified form of this treatment to the classically conditioned taste aversion paradigm, wherein rats received intraoral infusion of sucrose followed by injection of lithium chloride. During extinction each day, treatment rats received reconsolidationextinction (REX), consisting of a brief reminder infusion of sucrose one hour before a one minute extinction infusion. Control rats received standard extinction (SEX), wherein they received only the one minute infusion. Aversive orofacial behaviors were tallied and compared by percentile bootstrap tests. Each rat was extinguished until it had recovered, and then 5 days later sucrose was given again to test spontaneous recovery, measured by comparing aversive behaviors on the last extinction day to behaviors displayed on the spontaneous recovery test. The REX group recovered faster, showing significantly fewer aversive behaviors by extinction day 4. Both groups showed spontaneous recovery, but the SEX group exhibited significantly more aversive behaviors during the spontaneous recovery test. These results indicate that the REX treatment disrupted the taste aversion memory. A second experiment, conducted similarly to the first but with an additional unconditioned sucrose-only group, examined expression of the immediate early gene c-Fos in the subnuclei of the lateral, central, and basal nuclei of the amygdala. Neural tissue was collected one hour after the first extinction test, allowing assessment of amygdala participation in reconsolidation. The REX group contained more c-Fos-positive neurons than the other two groups in the dorsal lateral subnucleus of the lateral nucleus and the parvocellular subnucleus of the basal nucleus. This activity in the REX rats may reflect reconsolidation of the CTA memory and activation of an amygdalocortical pathway that suppresses extinction memory formation, respectively.