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Synaptic plasticity from amygdala to perirhinal cortex: a possible mechanism for emotional enhancement of visual recognition memory?

Authors

  • Alessandra Perugini,

    1. MRC Centre for Synaptic Plasticity, School of Physiology and Pharmacology, University of Bristol, Bristol, UK
    2. Department of Human and General Physiology, University of Bologna, Bologna, Italy
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    • Present address: Department of Pharmacology and Therapeutics, Institute of Neuroscience, Trinity College Dublin, Dublin 2, Ireland.

  • Michael Laing,

    1. MRC Centre for Synaptic Plasticity, School of Physiology and Pharmacology, University of Bristol, Bristol, UK
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  • Nicola Berretta,

    1. Experimental Neurology, Fondazione Santa Lucia IRCCS, Roma, Italy
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  • Giorgio Aicardi,

    1. Department of Human and General Physiology, University of Bologna, Bologna, Italy
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  • Zafar I. Bashir

    1. MRC Centre for Synaptic Plasticity, School of Physiology and Pharmacology, University of Bristol, Bristol, UK
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Zafar I. Bashir, as above.
E-mail: z.i.bashir@bris.ac.uk

Abstract

Emotionally salient experiences are better remembered than events that have little emotional context. Several lines of evidence indicate that the amygdala plays an important role in this emotional enhancement of memory. Visual recognition memory relies on synaptic plasticity in the perirhinal cortex, but little is known about the mechanisms involved in emotional enhancement of this form of memory. The results of the present study, performed in rat brain slices, show for the first time that the amygdala input to the perirhinal cortex undergoes synaptic plasticity. Stimulation in the amygdala resulted in long-term potentiation (LTP) in perirhinal cortex that was dependent on β-adrenoceptors and L-type voltage-dependent calcium channels (L-VDCCs) but was NMDAR-independent. In contrast, intracortical perirhinal stimulation resulted in LTP that was NMDAR-dependent but β-adrenoceptor- and L-VDCC-independent. In addition, the present results provide the first evidence that stimulation of the amygdala can reduce the threshold for LTP in the perirhinal cortex. Interestingly, this associative form of LTP requires β-adrenoceptor activation but not NMDA or L-VDCC activation. Knowing the mechanisms that control amygdala–perirhinal cortex interactions will allow better understanding of how emotionally charged visual events are remembered, and may help to understand how memories can consolidate and become intrusive in anxiety-related disorders.

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