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 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 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 Vagus Nerve Stimulation Enhances Extinction of Conditioned Fear in Rats and Modulates Arc Protein, CaMKII, and GluN2B-Containing NMDA Receptors in the Basolateral Amygdala

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Amanda C. Alvarez-Dieppa ◽  
Kimberly Griffin ◽  
Sheridan Cavalier ◽  
Christa K. McIntyre
Keyword(s):  
Synaptic Plasticity ◽  
Vagus Nerve ◽  
Nmda Receptors ◽  
Fear Conditioning ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Basolateral Amygdala ◽  
Conditioned Fear ◽  
Associated Proteins

Vagus nerve stimulation (VNS) enhances the consolidation of extinction of conditioned fear. High frequency stimulation of the infralimbic cortex (IL) produces long-term potentiation in the basolateral amygdala (BLA) in rats given VNS-paired extinction training, whereas the same stimulation produces long-term depression in sham-treated rats. The present study investigated the state of synaptic plasticity-associated proteins in the BLA that could be responsible for this shift. Male Sprague-Dawley rats were separated into 4 groups: auditory fear conditioning only (fear-conditioned); fear conditioning + 20 extinction trials (extended-extinction); fear conditioning + 4 extinction trials paired with sham stimulation (sham-extinction); fear conditioning + 4 extinction trials paired with VNS (VNS-extinction). Freezing was significantly reduced in extended-extinction and VNS-extinction rats. Western blots were used to quantify expression and phosphorylation state of synaptic plasticity-associated proteins such as Arc, CaMKII, ERK, PKA, and AMPA and NMDA receptors. Results show significant increases in GluN2B expression and phosphorylated CaMKII in BLA samples from VNS- and extended-extinction rats. Arc expression was significantly reduced in VNS-extinction rats compared to all groups. Administration of the GluN2B antagonist ifenprodil immediately after fear extinction training blocked consolidation of extinction learning. Results indicate a role for BLA CaMKII-induced GluN2B expression and reduced Arc protein in VNS-enhanced extinction.

scholarly journals Regulation of Presynaptic Ca2+, Synaptic Plasticity and Contextual Fear Conditioning by a N-terminal  -Amyloid Fragment

2014 ◽  
Vol 34 (43) ◽  
pp. 14210-14218 ◽  
Author(s):  
J. L. M. Lawrence ◽  
M. Tong ◽  
N. Alfulaij ◽  
T. Sherrin ◽  
M. Contarino ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Fear Conditioning ◽  
Contextual Fear Conditioning ◽  
Contextual Fear
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