Prelimbic Cortical Stimulation Disrupts Fear Memory Consolidation through Ventral Hippocampal Dopamine 2 Receptors

2021 ◽  
Author(s):  
Shawn Zheng Kai Tan ◽  
Chi Him Poon ◽  
Ying‐Shing Chan ◽  
Lee Wei Lim
Keyword(s):  
Memory Consolidation ◽  
Fear Memory ◽  
Cortical Stimulation

scholarly journals Causal role for sleep-dependent reactivation of learning-activated sensory ensembles for fear memory consolidation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Brittany C. Clawson ◽  
Emily J. Pickup ◽  
Amy Ensing ◽  
Laura Geneseo ◽  
James Shaver ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Memory Consolidation ◽  
Critical Role ◽  
Visual Presentation ◽  
Fear Memory ◽  
Memory Recall ◽  
Visual Cue ◽  
V1 Neurons ◽  
Targeted Recombination

AbstractLearning-activated engram neurons play a critical role in memory recall. An untested hypothesis is that these same neurons play an instructive role in offline memory consolidation. Here we show that a visually-cued fear memory is consolidated during post-conditioning sleep in mice. We then use TRAP (targeted recombination in active populations) to genetically label or optogenetically manipulate primary visual cortex (V1) neurons responsive to the visual cue. Following fear conditioning, mice respond to activation of this visual engram population in a manner similar to visual presentation of fear cues. Cue-responsive neurons are selectively reactivated in V1 during post-conditioning sleep. Mimicking visual engram reactivation optogenetically leads to increased representation of the visual cue in V1. Optogenetic inhibition of the engram population during post-conditioning sleep disrupts consolidation of fear memory. We conclude that selective sleep-associated reactivation of learning-activated sensory populations serves as a necessary instructive mechanism for memory consolidation.

Ketamine anesthesia enhances fear memory consolidation via noradrenergic activation in the basolateral amygdala

2021 ◽  
Vol 178 ◽  
pp. 107362
Author(s):  
Maria Morena ◽  
Paola Colucci ◽  
Giulia F. Mancini ◽  
Valentina De Castro ◽  
Andrea Peloso ◽  
...  
Keyword(s):  
Memory Consolidation ◽  
Basolateral Amygdala ◽  
Fear Memory ◽  
Ketamine Anesthesia

Impairment of fear memory consolidation and expression by antihistamines

2013 ◽  
Vol 1493 ◽  
pp. 19-26 ◽  
Author(s):  
Ayako Nonaka ◽  
Fumitaka Masuda ◽  
Hiroshi Nomura ◽  
Norio Matsuki
Keyword(s):  
Memory Consolidation ◽  
Fear Memory

scholarly journals Memory Consolidation for Contextual and Auditory Fear Conditioning Is Dependent on Protein Synthesis, PKA, and MAP Kinase

1999 ◽  
Vol 6 (2) ◽  
pp. 97-110 ◽  
Author(s):  
Glenn E. Schafe ◽  
Nicole V. Nadel ◽  
Gregory M. Sullivan ◽  
Alexander Harris ◽  
Joseph E. LeDoux
Keyword(s):  
Protein Synthesis ◽  
Map Kinase ◽  
Fear Conditioning ◽  
Memory Consolidation ◽  
Molecular Mechanisms ◽  
Short Term Memory ◽  
Long Term Potentiation ◽  
Fear Memory ◽  
Term Memory

Fear conditioning has received extensive experimental attention. However, little is known about the molecular mechanisms that underlie fear memory consolidation. Previous studies have shown that long-term potentiation (LTP) exists in pathways known to be relevant to fear conditioning and that fear conditioning modifies neural processing in these pathways in a manner similar to LTP induction. The present experiments examined whether inhibition of protein synthesis, PKA, and MAP kinase activity, treatments that block LTP, also interfere with the consolidation of fear conditioning. Rats were injected intraventricularly with Anisomycin (100 or 300 μg), Rp-cAMPS (90 or 180 μg), or PD098059 (1 or 3 μg) prior to conditioning and assessed for retention of contextual and auditory fear memory both within an hour and 24 hr later. Results indicated that injection of these compounds selectively interfered with long-term memory for contextual and auditory fear, while leaving short-term memory intact. Additional control groups indicated that this effect was likely due to impaired memory consolidation rather than to nonspecific effects of the drugs on fear expression. Results suggest that fear conditioning and LTP may share common molecular mechanisms.

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