Abstract

Recent findings have shown that the auditory cortex, and specifically the higher order Te2 area, is necessary for the consolidation of long-term fearful memories and that it interacts with the amygdala during the retrieval of long-term fearful memories. Here, we tested whether the reversible blockade of Te2 during memory consolidation may affect the activity changes occurring in the amygdala during the retrieval of fearful memories. To address this issue, we blocked Te2 in a reversible manner during memory consolidation processes. After 4 weeks, we assessed the activity of Te2 and individual nuclei of the amygdala during the retrieval of long-term memories. Rats in which Te2 was inactivated upon memory encoding showed a decreased freezing and failed to show Te2-to-basolateral amygdala (BLA) synchrony during memory retrieval. In addition, the expression of the immediate early gene zif268 in the lateral, basal and central amygdala nuclei did not show memory-related enhancement. As all sites were intact upon memory retrieval, we propose that the auditory cortex represents a key node in the consolidation of fear memories and it is essential for amygdala nuclei to support memory retrieval process.

Highlights

  • Sensory stimuli that have acquired a threatening significance following an aversive experience are encoded in an intricate brain circuit composed of cortical and subcortical structures

  • As all sites were intact upon memory retrieval, we propose that the auditory cortex represents a key node in the consolidation of fear memories and it is essential for amygdala nuclei to support memory retrieval process

  • To establish the effects that Te2 blockade performed during the consolidation of auditory fear memories may have on Te2to-basolateral amygdala (BLA) crosstalk on BLA activity occurring during memory retrieval process, we reversibly blocked the Te2 at 1 day after training and we subsequently tested long-term memory retention and Te2-BLA interplay 1 month later (Figures 1, 2A)

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Summary

Introduction

Sensory stimuli that have acquired a threatening significance following an aversive experience are encoded in an intricate brain circuit composed of cortical and subcortical structures. Several cortical and subcortical areas interact with the amygdala during the encoding and retrieval of fearful memories. The amygdala exchanges information with the medial prefrontal cortex (mPF; Likhtik et al, 2014; Stujenske et al, 2014; Do-Monte et al, 2015; Karalis et al, 2016), which plays an important role in the processing of emotional stimuli (Corcoran and Quirk, 2007; Likhtik and Paz, 2015; Dejean et al, 2016; Do Monte et al, 2016). In addition to the mPF, the sensory cortex, such as the auditory cortex in the case of auditory stimuli paired to aversive events, is involved in fearful memory processes

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