Fear learning induces persistent facilitation of amygdala synaptic transmission
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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Suppression of amygdala LTP 10 days after fear conditioning.
“Schroeder and Shinnick-Gallagher [341] found a suppression of amygdala LTP 10 days after fear conditioning.”
From The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law (2007) · cites this paper as Schroeder and Shinnick-Gallagher [341]
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- Authors
- Schroeder, B. W., & Shinnick‐Gallagher, P.
- Affiliations
- The University of Texas Medical Branch at Galveston (US)
- Corresponding author
- Shinnick‐Gallagher, Patricia
- Venue
- European Journal of Neuroscience
- Publisher
- Wiley
- Published
- 2005-10
- Volume
- 22
- Issue
- 7
- Pages
- 1775-1783
- ISSN
- 0953-816X (ISSN-L)
- 1460-9568
- OpenAlex
- W2033726811
- Cited by
- 81
- References
- 54
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 4 · 2022: 1 · 2021: 4 · 2020: 4 · 2019: 2 · 2018: 4 · 2017: 3 · 2016: 1 · 2015: 8 · 2014: 5 · 2013: 6 · 2012: 3
- FWCI
- 2.15
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Journal of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5f30mh067458-02)
- National Institute of Mental Health (F 30 MH067458, MH58327, R01MH058327)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory Processes and Influences
- Keywords
- fear memory, amygdala, synaptic transmission, long-term potentiation, fear conditioning, synaptic plasticity, memory storage, memory stabilization, low-frequency stimulation, high-frequency stimulation, contextual fear
- MeSH terms
- Amygdala, Analysis of Variance, Animals, Behavior, Animal, Dose-Response Relationship, Radiation, Electric Stimulation, Fear, Learning, Male, Synaptic Transmission, Time Factors, Rats, Sprague-Dawley, Excitatory Postsynaptic Potentials, Rats, In Vitro Techniques
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