scholarly journals Synaptic Plasticity in the Lateral Amygdala: A Cellular Hypothesis of Fear Conditioning

2001 ◽  
Vol 8 (5) ◽  
pp. 229-242 ◽  
Author(s):  
H. T. Blair
Keyword(s):  
Synaptic Plasticity ◽  
Fear Conditioning ◽  
Lateral Amygdala

scholarly journals Dysbindin-1 loss compromises NMDAR-dependent synaptic plasticity and contextual fear conditioning

Hippocampus ◽  
2013 ◽  
Vol 24 (2) ◽  
pp. 204-213 ◽  
Author(s):  
W. Bailey Glen ◽  
Bryant Horowitz ◽  
Gregory C. Carlson ◽  
Tyrone D. Cannon ◽  
Konrad Talbot ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Fear Conditioning ◽  
Contextual Fear Conditioning ◽  
Contextual Fear

scholarly journals Overexpression of Homer1a in the basal and lateral amygdala impairs fear conditioning and induces an autism-like social impairment

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Anwesha Banerjee ◽  
Jonathan A. Luong ◽  
Anthony Ho ◽  
Aeshah O. Saib ◽  
Jonathan E. Ploski
Keyword(s):  
Fear Conditioning ◽  
Social Impairment ◽  
Lateral Amygdala

scholarly journals Synaptic plasticity-dependent competition rule influences memory formation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yire Jeong ◽  
Hye-Yeon Cho ◽  
Mujun Kim ◽  
Jung-Pyo Oh ◽  
Min Soo Kang ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Fear Conditioning ◽  
Long Term Potentiation ◽  
Memory Formation ◽  
Specific Pattern ◽  
Memory Encoding ◽  
Competition Rule ◽  
Term Potentiation ◽  
Input Activity

AbstractMemory is supported by a specific collection of neurons distributed in broad brain areas, an engram. Despite recent advances in identifying an engram, how the engram is created during memory formation remains elusive. To explore the relation between a specific pattern of input activity and memory allocation, here we target a sparse subset of neurons in the auditory cortex and thalamus. The synaptic inputs from these neurons to the lateral amygdala (LA) are not potentiated by fear conditioning. Using an optogenetic priming stimulus, we manipulate these synapses to be potentiated by the learning. In this condition, fear memory is preferentially encoded in the manipulated cell ensembles. This change, however, is abolished with optical long-term depression (LTD) delivered shortly after training. Conversely, delivering optical long-term potentiation (LTP) alone shortly after fear conditioning is sufficient to induce the preferential memory encoding. These results suggest a synaptic plasticity-dependent competition rule underlying memory formation.

scholarly journals Spatiotemporal Asymmetry of Associative Synaptic Plasticity in Fear Conditioning Pathways

Neuron ◽  
2006 ◽  
Vol 52 (5) ◽  
pp. 883-896 ◽  
Author(s):  
Ryong-Moon Shin ◽  
Evgeny Tsvetkov ◽  
Vadim Y. Bolshakov
Keyword(s):  
Synaptic Plasticity ◽  
Fear Conditioning

scholarly journals Fear signaling in the prelimbic-amygdala circuit: a computational modeling and recording study

2013 ◽  
Vol 110 (4) ◽  
pp. 844-861 ◽  
Author(s):  
Sandeep Pendyam ◽  
Christian Bravo-Rivera ◽  
Anthony Burgos-Robles ◽  
Francisco Sotres-Bayon ◽  
Gregory J. Quirk ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Fear Conditioning ◽  
Large Scale ◽  
Conditioned Fear ◽  
Individual Variability ◽  
Biophysical Model ◽  
Human Homolog ◽  
Lateral Amygdala ◽  
Internal Inhibition ◽  
Β Blocker

The acquisition and expression of conditioned fear depends on prefrontal-amygdala circuits. Auditory fear conditioning increases the tone responses of lateral amygdala neurons, but the increase is transient, lasting only a few hundred milliseconds after tone onset. It was recently reported that that the prelimbic (PL) prefrontal cortex transforms transient lateral amygdala input into a sustained PL output, which could drive fear responses via projections to the lateral division of basal amygdala (BL). To explore the possible mechanisms involved in this transformation, we developed a large-scale biophysical model of the BL-PL network, consisting of 850 conductance-based Hodgkin-Huxley-type cells, calcium-based learning, and neuromodulator effects. The model predicts that sustained firing in PL can be derived from BL-induced release of dopamine and norepinephrine that is maintained by PL-BL interconnections. These predictions were confirmed with physiological recordings from PL neurons during fear conditioning with the selective β-blocker propranolol and by inactivation of BL with muscimol. Our model suggests that PL has a higher bandwidth than BL, due to PL's decreased internal inhibition and lower spiking thresholds. It also suggests that variations in specific microcircuits in the PL-BL interconnection can have a significant impact on the expression of fear, possibly explaining individual variability in fear responses. The human homolog of PL could thus be an effective target for anxiety disorders.

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