scholarly journals Distributed learning episodes create a context fear memory outside the hippocampus that depends on perirhinal and anterior cingulate cortices

2021 ◽  
Vol 28 (11) ◽  
pp. 405-413
Author(s):  
Elizabeth H. Shepherd ◽  
Neil M. Fournier ◽  
Robert J. Sutherland ◽  
Hugo Lehmann
Keyword(s):  
Retrograde Amnesia ◽  
Memory Retrieval ◽  
Distributed Learning ◽  
Perirhinal Cortex ◽  
Contextual Fear Conditioning ◽  
Anterior Cingulate ◽  
Contextual Fear ◽  
Combined Lesions ◽  
Cortical Regions ◽  
Context Memory

Damage to the hippocampus (HPC) typically causes retrograde amnesia for contextual fear conditioning. Repeating the conditioning over several sessions, however, can eliminate the retrograde amnesic effects. This form of reinstatement thus permits modifications to networks that can support context memory retrieval in the absence of the HPC. The present study aims to identify cortical regions that support the nonHPC context memory. Specifically, the contribution of the perirhinal cortex (PRH) and the anterior cingulate cortex (ACC) were examined because of their established importance to context memory. The findings show that context memories established through distributed reinstatement survive damage limited only to the HPC, PRH, or ACC. Combined lesions of the HPC and PRH, as well as the HPC and ACC, caused retrograde amnesia, suggesting that network modifications in the PRH and ACC enable context fear memories to become resistant to HPC damage.

Memory retrieval after contextual fear conditioning induces c-Fos and JunB expression in CA1 hippocampus

2003 ◽  
Vol 2 (1) ◽  
pp. 3-10 ◽  
Author(s):  
T. Strekalova ◽  
B. Zörner ◽  
C. Zacher ◽  
G. Sadovska ◽  
T. Herdegen ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Memory Retrieval ◽  
Contextual Fear Conditioning ◽  
Contextual Fear

scholarly journals Neurogenesis-induced forgetting is associated with reduced neuronal activity in CA1 during context fear memory retrieval

2021 ◽  
Author(s):  
Alexandria Evans ◽  
Gavin A. Scott ◽  
Jonathan R. Epp
Keyword(s):  
Memory Retrieval ◽  
Wheel Running ◽  
Fear Memory ◽  
Hippocampal Neurogenesis ◽  
Contextual Fear Conditioning ◽  
Early Gene ◽  
Population Activity ◽  
Contextual Fear ◽  
Induced Forgetting

AbstractHippocampal neurogenesis has a role in many essential learning and memory processes, including forgetting. This forgetting process is important because it prevents proactive interference between old and new memories. While several studies have now established the role of neurogenesis in forgetting, the specific mechanisms mediating neurogenesis-induced forgetting have not been elucidated. The goal of this study was to examine how increased neurogenesis affects the recall of context fear memory in addition to its effects on population activity within hippocampal subregions. We trained mice in contextual fear conditioning and then increased neurogenesis via 4 weeks of voluntary wheel running. Increased neurogenesis led to a reduction in freezing behaviour during context testing, replicating previous studies showing that increased neurogenesis causes forgetting of context fear memories. Additionally, we mapped the expression of the immediate early gene c-Fos within hippocampal subregions and found that increasing neurogenesis led to reduced CA1 c-Fos expression during context testing. The results suggest that reduced CA1 population activity may underlie the association between increased neurogenesis and forgetting.

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.

scholarly journals Prefrontal pathways provide top down control of memory for sequences of events

2018 ◽  
Author(s):  
Maanasa Jayachandran ◽  
Stephanie Linley ◽  
Maximilian Schlecht ◽  
Stephen V. Mahler ◽  
Robert P. Vertes ◽  
...  
Keyword(s):  
Memory Retrieval ◽  
Perirhinal Cortex ◽  
Prelimbic Cortex ◽  
Control Sequence ◽  
Retrieval Strategy ◽  
Top Down ◽  
Nucleus Reuniens ◽  
Retrieval Strategies ◽  
Sequence Memory ◽  
Context Memory

SummaryWe remember our lives as sequences of events, but it is unclear how these memories are controlled during retrieval. In rats, prelimbic cortex (PL) is positioned to influence sequence memory through extensive top down inputs to the nucleus reuniens of the thalamus (RE) and perirhinal cortex (PER), regions heavily interconnected with the hippocampus. Here, we tested the hypothesis that specific PL➔RE and PL➔PER projections regulate sequence memory retrieval using an hM4Di synaptic-silencing approach. First, we show that the suppression of PL activity impairs sequence memory. Second, we show that inhibiting PL➔RE and PL➔PER pathways effectively eliminated sequence memory. Last, we performed a sequential lag analysis showing that the PL➔RE pathway contributes to a working memory retrieval strategy, and the PL➔PER pathway contributes to a temporal context memory retrieval strategy. These results demonstrate that the PL➔RE and PL➔PER pathways serve as top down mechanisms that control sequence memory retrieval strategies.

Synaptic Correlates of Anterograde Amnesia and Intact Retrograde Memory in a Mouse Model of Alzheimer’s Disease

2020 ◽  
Vol 17 (3) ◽  
pp. 259-268 ◽  
Author(s):  
Emanuela Rizzello ◽  
Silvia Middei ◽  
Cristina Marchetti
Keyword(s):  
Alzheimer’S Disease ◽  
Patch Clamp ◽  
Mouse Model ◽  
Fear Conditioning ◽  
Contextual Fear Conditioning ◽  
Anterior Cingulate ◽  
Wild Type ◽  
Synaptic Currents ◽  
Contextual Fear ◽  
Tg2576 Mice

Background: Clinical evidence indicates that patients affected by Alzheimer's Disease (AD) fail to form new memories although their memories for old events are intact. This amnesic pattern depends on the selective vulnerability to AD-neurodegeneration of the hippocampus, the brain region that sustains the formation of new memories, while cortical regions that store remote memories are spared. Objective: To identify the cellular mechanisms underlying impaired recent memories and intact remote memories in a mouse model of AD. Method: Glutamatergic synaptic currents were recorded by patch-clamp in acute hippocampal and anterior Cingulate Cortical (aCC) slices of AD-like Tg2576 mice and Wild-type (Wt) littermates subjected to the Contextual Fear Conditioning (CFC) task or in naïve conditions. Results: Glutamatergic synaptic currents were recorded by patch-clamp in acute hippocampal and anterior Cingulate Cortical (aCC) slices of AD-like Tg2576 mice and Wild-type (Wt) littermates subjected to the Contextual Fear Conditioning (CFC) task or in naïve conditions. Conclusion: Our data suggest that in the early AD stages synaptic plasticity of CA1 synapses, crucial to form new memories, is lost, while plasticity of aCC synapses is intact and contributes to the persistence of long-term memories.

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