Dorsal Hippocampal Administration of Triiodothyronine Enhances Long-Term Memory for Trace Cued and Delay Contextual Fear Conditioning in Rats

2006 ◽  
Vol 18 (11) ◽  
pp. 811-819 ◽  
Author(s):  
L. Sui ◽  
F. Wang ◽  
F. Liu ◽  
J. Wang ◽  
B. M. Li
Keyword(s):  
Fear Conditioning ◽  
Contextual Fear Conditioning ◽  
Long Term Memory ◽  
Term Memory ◽  
Contextual Fear ◽  
Dorsal Hippocampal

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.

Corticosteroid-Binding Globulin Deficiency Specifically Impairs Contextual and Recognition Memory Consolidation in Male Mice

2019 ◽  
Vol 109 (4) ◽  
pp. 322-332
Author(s):  
Gabriela F. de Medeiros ◽  
Pauline Lafenêtre ◽  
Yoottana Janthakhin ◽  
Juan-Carlos Cerpa ◽  
Chun-Lei Zhang ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Memory Performance ◽  
Recognition Task ◽  
Contextual Fear Conditioning ◽  
Long Term Memory ◽  
Male Mice ◽  
Odor Aversion ◽  
Term Memory ◽  
Corticosteroid Binding Globulin

Background/Aims: Glucocorticoids are essential in modulating memory processes of emotionally arousing experiences and we have shown that corticosteroid-binding globulin (CBG) influences glucocorticoid delivery to the brain. Here, we investigated the role of CBG in contextual and recognition long-term memory according to stress intensity. Method: We used adult male mice totally deficient in CBG (Cbg KO) or brain-specific Cbg KO (CbgCamk KO) to examine their performance in contextual fear conditioning (CFC) and au­ditory fear conditioning, both at short (1 h) and long-term (24 h). Long-term memory in Cbg KO was further analyzed in conditioned odor aversion and in novel object recognition task (NORT) with different paradigms, that is, with and without prior habituation to the context, with a mild or strong stressor applied during consolidation. In the NORT experiments, total and free glucocorticoid levels were measured during consolidation. Results: Impaired memory was observed in the Cbg KO but not in the CbgCamk KO in the CFC and the NORT without habituation when tested 24 h later. However, Cbg KO displayed normal behavior in the NORT with previous habituation and in the NORT with a mild stressor. In condition of the NORT with a strong stressor, Cbg KO retained good 24 h memory performance while controls were impaired. Total and free glucocorticoids levels were always higher in controls than in Cbg KO except in NORT with mild stressor where free glucocorticoids were equivalent to controls. Conclusions: These data indicate that circulating but not brain CBG influences contextual and recognition long-term memory in relation with glucocorticoid levels.

scholarly journals Interplay between α2-chimaerin and Rac1 activity determines dynamic maintenance of long-term memory

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Li Lv ◽  
Yunlong Liu ◽  
Jianxin Xie ◽  
Yan Wu ◽  
Jianjian Zhao ◽  
...  
Keyword(s):  
Contextual Fear Conditioning ◽  
Long Term Memory ◽  
Single Trial ◽  
Term Memory ◽  
Contextual Fear ◽  
Bidirectional Regulation ◽  
Rac1 Activity ◽  
Maintenance Stage ◽  
Dynamic Maintenance

AbstractMemory consolidation theory suggests that once memory formation has been completed, memory is maintained at a stable strength and is incapable of further enhancement. However, the current study reveals that even long after formation, contextual fear memory could be further enhanced. Such unexpected enhancement is possible because memory is dynamically maintained at an intermediate level that allows for bidirectional regulation. Here we find that both Rac1 activation and expression of α2-chimaerin are stimulated by single-trial contextual fear conditioning. Such sustained Rac1 activity mediates reversible forgetting, and α2-chimaerin acts as a memory molecule that reverses forgetting to sustain memory through inhibition of Rac1 activity during the maintenance stage. Therefore, the balance between activated Rac1 and expressed α2-chimaerin defines dynamic long-term memory maintenance. Our findings demonstrate that consolidated memory maintains capacity for bidirectional regulation.

scholarly journals Long-Term Memory Deficits in Pavlovian Fear Conditioning in Ca2+/Calmodulin Kinase Kinase α-Deficient Mice

2006 ◽  
Vol 26 (23) ◽  
pp. 9105-9115 ◽  
Author(s):  
Frank Blaeser ◽  
Matthew J. Sanders ◽  
Nga Truong ◽  
Shanelle Ko ◽  
Long Jun Wu ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Long Term Potentiation ◽  
Long Term Memory ◽  
Term Memory ◽  
Calmodulin Kinase ◽  
Element Binding Protein ◽  
Long Term Follow Up ◽  
Responsive Element ◽  
Deficient Mice

ABSTRACT Signaling by the Ca2+/calmodulin kinase (CaMK) cascade has been implicated in neuronal gene transcription, synaptic plasticity, and long-term memory consolidation. The CaM kinase kinase α (CaMKKα) isoform is an upstream component of the CaMK cascade whose function in different behavioral and learning and memory paradigms was analyzed by targeted gene disruption in mice. CaMKKα mutants exhibited normal long-term spatial memory formation and cued fear conditioning but showed deficits in context fear during both conditioning and long-term follow-up testing. They also exhibited impaired activation of the downstream kinase CaMKIV/Gr and its substrate, the transcription factor cyclic AMP-responsive element binding protein (CREB) upon fear conditioning. Unlike CaMKIV/Gr-deficient mice, the CaMKKα mutants exhibited normal long-term potentiation and normal levels of anxiety-like behavior. These results demonstrate a selective role for CaMKKα in contextual fear memory and suggest that different combinations of upstream and downstream components of the CaMK cascade may serve distinct physiological functions.

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