Abstract

The persistence of newly acquired memories is supported by the activity of PKMζ, an atypical isoform of protein kinase C (PKC). Whether the activity of conventional and atypical PKC isoforms contributes to reactivated memories to persist is still unknown. Similarly, whether memory reactivation is a prerequisite for interventions to be able to change memory persistence is scarcely investigated. Based on the above, we examined the role of conventional and atypical PKC isoforms in the prelimbic cortex in reconsolidation and persistence of a reactivated contextual fear memory in male Wistar rats. It is shown that (i) inhibiting the PKC activity with chelerythrine or the PKMζ activity with ZIP impaired the persistence of a reactivated memory for at least 21 days; (ii) ZIP given immediately after memory reactivation affected neither the reconsolidation nor the persistence process. In contrast, when given 1 h later, it impaired the memory persistence; (iii) chelerythrine given immediately after memory reactivation impaired the reconsolidation; (iv) omitting memory reactivation prevented the chelerythrine- and ZIP-induced effects: (v) the ZIP action is independent of the time elapsed between its administration and the initial memory test. The results indicate that prelimbic cortex PKC and PKMζ are involved in memory reconsolidation and persistence.

Highlights

  • PKMζ in fear memory reconsolidation and persistence following reactivation Thiago Rodrigues da Silva[1], Ana Maria Raymundi[1], Leandro José Bertoglio[2], Roberto Andreatini1 & Cristina A

  • It was shown that: 1) activity of both protein kinase C (PKC) and PKMζ are necessary for the persistence of a reactivated memory; 2) effects of PKC or PKMζ inhibition require prior memory reactivation; 3) effects of PKMζ inhibition are independent of the initial test 1 day after ZIP infusion; 4)

  • These findings indicate that PL cortex PKC and PKMζ have a differential involvement in the processes examined

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Summary

Introduction

PKMζ in fear memory reconsolidation and persistence following reactivation Thiago Rodrigues da Silva[1], Ana Maria Raymundi[1], Leandro José Bertoglio[2], Roberto Andreatini1 & Cristina A. The persistence of newly acquired memories is supported by the activity of PKMζ, an atypical isoform of protein kinase C (PKC). We examined the role of conventional and atypical PKC isoforms in the prelimbic cortex in reconsolidation and persistence of a reactivated contextual fear memory in male Wistar rats. PKMζ expression in this medial prefrontal cortex sub-region seems to support the maintenance of newly acquired aversive memories[22]. Based on these facts, we hypothesized that PKC and the PKMζ isoform could support the persistence of a reactivated aversive memory. The main objective of the present work was to investigate the role of PL

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