Abstract

The sensory cortex participates in emotional memory but its role is poorly understood. Here we show that inactivation of the higher order auditory cortex Te2 in rats during early memory consolidation impairs remote first- and second-order fear memories but not the association between two neutral cues. Furthermore, Te2 inactivation prevents changes in the valence of such information. Following the presentation of two auditory cues previously paired with either pleasant or painful stimuli, a large percentage of cells responds to both experiences but also a small fraction of neurons responds exclusively to one of them. The latter type of neurons signals the valence rather than the salience or the motor responses associated with the stimuli, and reflects selective associative processes. Pharmacogenetic silencing of memory-activated neurons causes amnesia. Thus, Te2 represents a crucial node for the assignment of the affective value to sensory stimuli and for the storage of such information.

Highlights

  • The sensory cortex participates in emotional memory but its role is poorly understood

  • The initial view that the auditory cortex is mostly a stimuli’s analyser that transmits sensory information to the amygdala[1], especially for more complex auditory stimuli, is changing in favour of more complex roles[9,10,11]. In support of this notion, we recently identified higher order components of the sensory cortices, in particular the temporal auditory cortex Te2, that are essential for the storage of remote, but not recent, fear memories[12]

  • During the recall of remote fear memories, a small fraction of neurons in Te2 is activated by the particular valence, but not by the salience previously associated with the sounds

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Summary

Introduction

The sensory cortex participates in emotional memory but its role is poorly understood. In support of this notion, we recently identified higher order components of the sensory cortices, in particular the temporal auditory cortex Te2, that are essential for the storage of remote, but not recent, fear memories[12] These cortices are anatomically and functionally connected to the primary cortices and to subcortical nuclei[13,14,15], such as the amygdala and the nucleus accumbens. Pharmacogenetic silencing of Te2 neurons activated by fear memories results in amnesia only for fear, but not for appetitive, information We interpret these data to mean that higher components of the auditory cortex are necessary for the encoding and storage of the affective meaning that has been associated with sensory stimuli during an experience

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