Fear learning induces persistent facilitation of amygdala synaptic transmission

Authors

  • Bradley W. Schroeder,

    1. Department of Pharmacology and Toxicology, Neuroscience Graduate Program, The University of Texas Medical Branch, 301 University Blvd, Galveston, TX 77555–1031, USA
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  • Patricia Shinnick-Gallagher

    1. Department of Pharmacology and Toxicology, Neuroscience Graduate Program, The University of Texas Medical Branch, 301 University Blvd, Galveston, TX 77555–1031, USA
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Professor Patricia Shinnick-Gallagher, as above.
Email: psgallag@utmb.edu

Abstract

In the maintenance phase of fear memory, synaptic transmission is potentiated and the stimulus requirements and signalling mechanisms are altered for long-term potentiation (LTP) in the cortico-lateral amygdala (LA) pathway. These findings link amygdala synaptic plasticity to the coding of fear memories. Behavioural experiments suggest that the amygdala serves to store long-term fear memories. Here we provide electrophysiological evidence showing that synaptic alterations in rats induced by fear conditioning are evident in vitro 10 days after fear conditioning. We show that synaptic transmission was facilitated and that high-frequency stimulation dependent LTP (HFS–LTP) of the cortico-lateral amygdala pathway remained attenuated 10 days following fear conditioning. Additionally, we found that the low-frequency stimulation dependent LTP (LFS–LTP) measured 24 h after fear conditioning was absent 10 days post-training. The persistent facilitation of synaptic transmission and occlusion of HFS–LTP suggests that, unlike hippocampal coding of contextual fear memory, the cortico-lateral amygdala synapse is involved in the storage of long-term fear memories. However, the absence of LFS–LTP 10 days following fear conditioning suggests that amygdala physiology 1 day following fear learning may reflect a dynamic state during memory stabilization that is inactive during the long-term storage of fear memory. Results from these experiments have significant implications regarding the locus of storage for maladaptive fear memories and the synaptic alterations induced by these memories.

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