scholarly journals Effects of post-training novelty exposure on contextual fear memory: An attempt to translate behavioral tagging to humans

2018 ◽  
Author(s):  
Mason McClay ◽  
Joseph E. Dunsmoor
Keyword(s):  
Virtual Reality ◽  
Time Window ◽  
Critical Time ◽  
Fear Memory ◽  
Contextual Fear Conditioning ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Null Result ◽  
Adult Humans

AbstractIn rodents, poorly formed hippocampal memories can be improved by novelty exploration within a critical time window, in line with the “behavioral tagging” hypothesis. Here, we sought to establish an analogue protocol to investigate if novelty exploration similarly operates to rescue weak hippocampal-dependent memories in humans. Adult humans underwent suboptimal contextual fear conditioning, followed 10 minutes later by open field novelty exploration in immersive 3D virtual reality. Novelty exploration did not improve long-term contextual fear memory, contrary to a behavioral tagging hypothesis. Despite this null result, we suggest further attempts to translate behavioral tagging from rodents to humans is warranted.

scholarly journals Overexpression of SIRT6 in the hippocampal CA1 impairs the formation of long-term contextual fear memory

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Xi Yin ◽  
Yuan Gao ◽  
Hai-Shui Shi ◽  
Li Song ◽  
Jie-Chao Wang ◽  
...  
Keyword(s):  
Fear Memory ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Hippocampal Ca1

scholarly journals Early β adrenoceptor dependent time window for fear memory persistence in APPswe/PS1dE9 mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Smitha Karunakaran
Keyword(s):  
Fear Conditioning ◽  
Time Window ◽  
Fear Memory ◽  
Long Term Memory ◽  
Term Memory ◽  
Contextual Fear ◽  
Adrenoceptor Agonist ◽  
Hippocampal Ca1 ◽  
Memory Persistence

AbstractIn this study we demonstrate that 2 month old APPswe/PS1dE9 mice, a transgenic model of Alzheimer’s disease, exhibited intact short-term memory in Pavlovian hippocampal—dependent contextual fear learning task. However, their long-term memory was impaired. Intra-CA1 infusion of isoproterenol hydrochloride, the β-adrenoceptor agonist, to the ventral hippocampus of APPswe/PS1dE9 mice immediately before fear conditioning restored long-term contextual fear memory. Infusion of the β-adrenoceptor agonist + 2.5 h after fear conditioning only partially rescued the fear memory, whereas infusion at + 12 h post conditioning did not interfere with long-term memory persistence in this mouse model. Furthermore, Intra-CA1 infusion of propranolol, the β-adrenoceptor antagonist, administered immediately before conditioning to their wildtype counterpart impaired long-term fear memory, while it was ineffective when administered + 4 h and + 12 h post conditioning. Our results indicate that, long-term fear memory persistence is determined by a unique β-adrenoceptor sensitive time window between 0 and + 2.5 h upon learning acquisition, in the ventral hippocampal CA1 of APPswe/PS1dE9 mice. On the contrary, β-adrenoceptor agonist delivery to ventral hippocampal CA1 per se did not enhance innate anxiety behaviour in open field test. Thus we conclude that, activation of learning dependent early β-adrenoceptor modulation underlies and is necessary to promote long-term fear memory persistence in APPswe/PS1dE9.

scholarly journals Reversal of Impaired Hippocampal Long-Term Potentiation and Contextual Fear Memory Deficits in Angelman Syndrome Model Mice by ErbB Inhibitors

2012 ◽  
Vol 72 (3) ◽  
pp. 182-190 ◽  
Author(s):  
Hanoch Kaphzan ◽  
Pepe Hernandez ◽  
Joo In Jung ◽  
Kiriana K. Cowansage ◽  
Katrin Deinhardt ◽  
...  
Keyword(s):  
Angelman Syndrome ◽  
Memory Deficits ◽  
Long Term Potentiation ◽  
Fear Memory ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Term Potentiation

scholarly journals Parvalbumin-positive interneurons mediate neocortical-hippocampal interactions that are necessary for memory consolidation

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Frances Xia ◽  
Blake A Richards ◽  
Matthew M Tran ◽  
Sheena A Josselyn ◽  
Kaori Takehara-Nishiuchi ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Fear Conditioning ◽  
Medial Prefrontal Cortex ◽  
Memory Consolidation ◽  
Fear Memory ◽  
Contextual Fear Conditioning ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Spiking Activity

Following learning, increased coupling between spindle oscillations in the medial prefrontal cortex (mPFC) and ripple oscillations in the hippocampus is thought to underlie memory consolidation. However, whether learning-induced increases in ripple-spindle coupling are necessary for successful memory consolidation has not been tested directly. In order to decouple ripple-spindle oscillations, here we chemogenetically inhibited parvalbumin-positive (PV+) interneurons, since their activity is important for regulating the timing of spiking activity during oscillations. We found that contextual fear conditioning increased ripple-spindle coupling in mice. However, inhibition of PV+ cells in either CA1 or mPFC eliminated this learning-induced increase in ripple-spindle coupling without affecting ripple or spindle incidence. Consistent with the hypothesized importance of ripple-spindle coupling in memory consolidation, post-training inhibition of PV+ cells disrupted contextual fear memory consolidation. These results indicate that successful memory consolidation requires coherent hippocampal-neocortical communication mediated by PV+ cells.

scholarly journals Limited replicability of drug-induced amnesia after contextual fear memory retrieval in rats

2019 ◽  
Author(s):  
Natalie Schroyens ◽  
Joaquin Matias Alfei Palloni ◽  
Anna Elisabeth Schnell ◽  
Laura Luyten ◽  
Tom Beckers
Keyword(s):  
Memory Retrieval ◽  
Fear Memory ◽  
Contextual Fear Conditioning ◽  
Memory Retention ◽  
Conditioning Context ◽  
Drug Induced ◽  
Systemic Injection ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Systemic Drug

With the ultimate goal of investigating boundary conditions for post-reactivation amnesia, we set out to replicate studies in which systemic, post-reactivation administration of midazolam, propranolol, or cycloheximide resulted in amnesia for contextual fear memories. Our experiments involved conceptual as well as exact replications of previously published studies. In most of our experiments, we adopted a procedure that conformed to the standard 3-day protocol typically used in the literature, with contextual fear conditioning on day 1, unreinforced re-exposure to the conditioning context followed by systemic injection of the amnestic drug on day 2, and a memory retention test on day 3. Given the plethora of successful studies with large effects sizes and the absence of any failed replications in the literature, we were surprised to find that we were generally unable to replicate those findings. Our results suggest that post-reactivation amnesia by systemic drug administration in rats is more difficult to obtain than what would be expected based on published empirical reports. At present, it remains unclear which conditions determine the success of this procedure.

Roles of CREB Signaling Pathway in Regulation of Fear Memory

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
S. Kida
Keyword(s):  
Gene Expression ◽  
Gene Expression Regulation ◽  
Fear Memory ◽  
Brain Regions ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
New Gene ◽  
Activity Dependent

Activity-dependent gene expression through activation of Ca2+-CREB signal transduction pathways has been thought to play a central role in fear memory formation. On the other hand, retrieval of fear memory triggers two time-dependent phases of reactivated memory; reconsolidation and extinction. To understand the mechanisms for determining the fate of the reactivated fear memory, we investigated roles of CREB in reconsolidation and extinction of contextual fear memory and then analyzed the brain-regions regulating reconsolidation and extinction by identifying regions where CREB-mediated gene expression is activated and then examining the role of protein synthesis in those regions on reconsolidation and extinction. We first showed that activation of CREB-mediated transcription is required for reconsolidation and long-term extinction of contextual fear memory. Using immunocytochemical analyses, we demonstrated that CREB is activated in the hippocampus/amygdala and amygdala/medial prefrontal cortex (mPFC) in the reconsolidation and extinction phases, respectively. Similar results were observed by analyzing the expression of a CREB-dependent gene, Arc. We finally showed that reconsolidation and long-term extinction of the contextual fear memory depended on new gene expression in the hippocampus/amygdala and amygdala/mPFC, respectively. Thus reactivated contextual fear memory is reconsolidated or extinguished through distinct CREB-mediated gene expression regulation in the hippocampus, amygdala and mPFC.

scholarly journals Contextual Fear Memory Formation and Destabilization Induce Hippocampal RyR2 Calcium Channel Upregulation

2018 ◽  
Vol 2018 ◽  
pp. 1-11
Author(s):  
Jamileth More ◽  
María Mercedes Casas ◽  
Gina Sánchez ◽  
Cecilia Hidalgo ◽  
Paola Haeger
Keyword(s):  
Spatial Memory ◽  
Fear Memory ◽  
Contextual Fear Conditioning ◽  
Male Rats ◽  
Endoplasmic Reticulum Membrane ◽  
Memory Retention ◽  
Contextual Fear ◽  
Memory Processes ◽  
Contextual Fear Memory ◽  
Protein Levels

Hippocampus-dependent spatial and aversive memory processes entail Ca2+ signals generated by ryanodine receptor (RyR) Ca2+ channels residing in the endoplasmic reticulum membrane. Rodents exposed to different spatial memory tasks exhibit significant hippocampal RyR upregulation. Contextual fear conditioning generates robust hippocampal memories through an associative learning process, but the effects of contextual fear memory acquisition, consolidation, or extinction on hippocampal RyR protein levels remain unreported. Accordingly, here we investigated if exposure of male rats to contextual fear protocols, or subsequent exposure to memory destabilization protocols, modified the hippocampal content of type-2 RyR (RyR2) channels, the predominant hippocampal RyR isoforms that hold key roles in synaptic plasticity and spatial memory processes. We found that contextual memory retention caused a transient increase in hippocampal RyR2 protein levels, determined 5 h after exposure to the conditioning protocol; this increase vanished 29 h after training. Context reexposure 24 h after training, for 3, 15, or 30 min without the aversive stimulus, decreased fear memory and increased RyR2 protein levels, determined 5 h after reexposure. We propose that both fear consolidation and extinction memories induce RyR2 protein upregulation in order to generate the intracellular Ca2+ signals required for these distinct memory processes.

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