Extinction of aversive taste memory homeostatically prevents the maintenance of in vivo insular cortex LTP: Calcineurin participation

• Published in: Neurobiology of learning and memory 2018-10, Vol.154, p.54-61
• Main Authors: Rivera-Olvera, Alejandro, Nelson-Mora, Janikua, Gonsebatt, María E., Escobar, Martha L.
• Format: Article
• Language: English
• Subjects: CTA; Extinction; Insular cortex; LTP; Metaplasticity
• ISSN: 1074-7427; 1095-9564
• DOI: 10.1016/j.nlm.2018.04.005

•Extinction of CTA allows the induction but not the maintenance of IC-LTP.•CTA extinction training increases the calcineurin expression in the IC.•CTA training increases Akt phosphorylation.•Calcineurin inhibition reverts the effect of CTA-extinction on the maintenance of in vivo IC-LTP.•CTA extinction promotes a homeostatic regulation of subsequent IC synaptic plasticity maintenance. Accumulating evidence indicates that homeostatic plasticity mechanisms dynamically adjust synaptic strength to promote stability that is crucial for memory storage. Our previous studies have shown that prior training in conditioned taste aversion (CTA) prevents the subsequent induction of long-term potentiation (LTP) in the projection from the basolateral nucleus of the amygdala (Bla) to the insular cortex (IC) in vivo. We have also reported that induction of LTP in the Bla-IC pathway modifies the CTA extinction. Memoryextinction involves the formation of a new associativememorythat inhibits a previously conditioned association. The aim of the present study was to analyze the effect of CTA extinction on the ability to induce subsequent LTP in the Bla-IC projection in vivo. Thus, 48 h after CTA extinction animals received high frequency stimulation in order to induce IC-LTP. Our results show that extinction training allows the induction but not the maintenance of IC-LTP. In addition, with the purpose of exploring part of the mechanisms involved in this process and since a body of evidence suggests that protein phosphatase calcineurin (CaN) is involved in the extinction of some behavioral tasks, we analyzed the participation of this phosphatase. The present results show that extinction training increases the CaN expression in the IC, as well as that the inhibition of this phosphatase reverts the effects of the CTA-extinction on the IC-LTP. These findings reveal that CTA extinction promotes a homeostatic regulation of subsequent IC synaptic plasticity maintenance through increases in CaN levels.