scholarly journals Long-Term Memory for Pavlovian Fear Conditioning Requires Dopamine in the Nucleus Accumbens and Basolateral Amygdala

PLoS ONE ◽  
2010 ◽  
Vol 5 (9) ◽  
pp. e12751 ◽  
Author(s):  
Jonathan P. Fadok ◽  
Martin Darvas ◽  
Tavis M. K. Dickerson ◽  
Richard D. Palmiter
Keyword(s):  
Nucleus Accumbens ◽  
Fear Conditioning ◽  
Basolateral Amygdala ◽  
Long Term Memory ◽  
Pavlovian Fear Conditioning ◽  
Term Memory

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.

scholarly journals An NMDA-R mediated short-term memory resistant to anesthesia in adult Danio rerio

2019 ◽  
Author(s):  
Gokul Rajan ◽  
Joby Joseph
Keyword(s):  
Fear Conditioning ◽  
Danio Rerio ◽  
Early Phase ◽  
Short Term Memory ◽  
Green Light ◽  
Long Term Memory ◽  
Adult Zebrafish ◽  
Term Memory ◽  
Vertebrate Model

ABSTRACTMemory in animals is labile in the early phase post-training. Memory in the early phase has been shown to be disrupted by treatments such as electroconvulsive shock or cold-shock (Quinn and Dudai, 1976). Using hypothermic shock and other pharmacological interventions, the various underlying memory pathways in Drosophila can be identified as an immediate short-lasting anesthesia sensitive memory and a delayed anesthesia resistant memory which is followed by a more stable protein synthesis dependent long-term memory (Margulies et al., 2005). In another ectothermic animal, Danio rerio, a popular vertebrate model, we ask if such a memory component exists which is sensitive to hypothermic disruption. To test this, we developed a fear conditioning assay with a green light at the bottom of the tank as the conditioned stimulus (CS) and electric shock as the unconditioned stimulus (US). We also standardized a cold anesthesia protocol in adult zebrafish to induce stage V anesthesia. The learning/memory was found to be NMDA-R mediated. Cold anesthesia as well as tricaine mediated anesthesia did not significantly affect the early-acting memory trace induced by a fear-conditioning protocol in adult zebrafish. We suggest future directions to tease out the underlying memory components in the early phase of memory in zebrafish.

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 Identification and Characterization of the V(D)J Recombination Activating Gene 1 in Long-Term Memory of Context Fear Conditioning

2016 ◽  
Vol 2016 ◽  
pp. 1-19 ◽  
Author(s):  
Edgardo Castro-Pérez ◽  
Emilio Soto-Soto ◽  
Marizabeth Pérez-Carambot ◽  
Dawling Dionisio-Santos ◽  
Kristian Saied-Santiago ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Dna Recombination ◽  
Cell Receptor ◽  
Long Term Memory ◽  
Dna Double Strand Breaks ◽  
Term Memory ◽  
Functional Studies ◽  
Recombination Activating Gene ◽  
Context Fear Conditioning

An increasing body of evidence suggests that mechanisms related to the introduction and repair of DNA double strand breaks (DSBs) may be associated with long-term memory (LTM) processes. Previous studies from our group suggested that factors known to function in DNA recombination/repair machineries, such as DNA ligases, polymerases, and DNA endonucleases, play a role in LTM. Here we report data using C57BL/6 mice showing that theV(D)J recombination-activating gene 1(RAG1), which encodes a factor that introduces DSBs in immunoglobulin and T-cell receptor genes, is induced in the amygdala, but not in the hippocampus, after context fear conditioning. Amygdalar induction ofRAG1mRNA, measured by real-time PCR, was not observed in context-only or shock-only controls, suggesting that the context fear conditioning response is related to associative learning processes. Furthermore, double immunofluorescence studies demonstrated the neuronal localization of RAG1 protein in amygdalar sections prepared after perfusion and fixation. In functional studies, intra-amygdalar injections ofRAG1gapmer antisense oligonucleotides, given 1 h prior to conditioning, resulted in amygdalar knockdown ofRAG1mRNA and a significant impairment in LTM, tested 24 h after training. Overall, these findings suggest that theV(D)J recombination-activating gene 1,RAG1, may play a role in LTM consolidation.

scholarly journals Perineuronal Net Receptor PTPσ Regulates Retention of Memories

2021 ◽  
Vol 13 ◽  
Author(s):  
Angelina Lesnikova ◽  
Plinio Casarotto ◽  
Rafael Moliner ◽  
Senem Merve Fred ◽  
Caroline Biojone ◽  
...  
Keyword(s):  
Object Recognition ◽  
Fear Conditioning ◽  
Cognitive Flexibility ◽  
Long Term Memory ◽  
Novel Object Recognition ◽  
Short Term ◽  
Perineuronal Net ◽  
Term Memory ◽  
Novel Object

Perineuronal nets (PNNs) have an important physiological role in the retention of learning by restricting cognitive flexibility. Their deposition peaks after developmental periods of intensive learning, usually in late childhood, and they help in long-term preservation of newly acquired skills and information. Modulation of PNN function by various techniques enhances plasticity and regulates the retention of memories, which may be beneficial when memory persistence entails negative symptoms such as post-traumatic stress disorder (PTSD). In this study, we investigated the role of PTPσ [receptor-type tyrosine-protein phosphatase S, a phosphatase that is activated by binding of chondroitin sulfate proteoglycans (CSPGs) from PNNs] in retention of memories using Novel Object Recognition and Fear Conditioning models. We observed that mice haploinsufficient for PTPRS gene (PTPσ+/–), although having improved short-term object recognition memory, display impaired long-term memory in both Novel Object Recognition and Fear Conditioning paradigm, as compared to WT littermates. However, PTPσ+/– mice did not show any differences in behavioral tests that do not heavily rely on cognitive flexibility, such as Elevated Plus Maze, Open Field, Marble Burying, and Forced Swimming Test. Since PTPσ has been shown to interact with and dephosphorylate TRKB, we investigated activation of this receptor and its downstream pathways in limbic areas known to be associated with memory. We found that phosphorylation of TRKB and PLCγ are increased in the hippocampus, prefrontal cortex, and amygdaloid complex of PTPσ+/– mice, but other TRKB-mediated signaling pathways are not affected. Our data suggest that PTPσ downregulation promotes TRKB phosphorylation in different brain areas, improves short-term memory performance but disrupts long-term memory retention in the tested animal models. Inhibition of PTPσ or disruption of PNN-PTPσ-TRKB complex might be a potential target for disorders where negative modulation of the acquired memories can be beneficial.

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