AMPA receptor trafficking in recent vs. remote memory

Ghazal, Pasha

doi:10.1016/j.brainres.2016.09.010

Cited by 3 publications

(5 citation statements)

References 26 publications

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“…de Oliveira Alvares et al, 2012;Einarsson et al, 2015;Frankland et al, 2004;Gafford et al, 2013;Ghazal, Davis & Squire, 1984;Frey, 1997;Rossato et al, 2007 4 PSI infusion during maintenance does not cause memory impairment.…”

Section: Resultsmentioning

confidence: 92%

“…de Oliveira Alvares et al, 2012;Einarsson et al, 2015;Frankland et al, 2004;Gafford et al, 2013;Ghazal, 2016 3 PSI during conditioning impairs LTM but not STM.…”

Section: Simulation Targetsmentioning

confidence: 98%

“…An interesting clue to a connection between synaptic and systems reconsolidation is provided by Ghazal (2016): reactivation of a 1-day-old fear memory triggered a strong reduction of CI-AMPARs in hippocampus but not in ACC, whereas at 30 days the opposite was true. This result is consistent with a transition from hippocampus to ACC engagement over a systemsconsolidation timeframe and with synaptic reconsolidation taking place in whichever of the two systems is engaged in the retrieval.…”

Section: Systems Consolidation and Reconsolidationmentioning

confidence: 99%

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A computational model of systems memory consolidation and reconsolidation

Helfer

Shultz

2019

Hippocampus

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In the mammalian brain, newly acquired memories depend on the hippocampus for maintenance and recall, but over time these functions are taken over by the neocortex through a process called systems memory consolidation. However, reactivation of a well-consolidated memory can return it to a hippocampus-dependent state. This is normally followed by a restoration of hippocampusindependence, a phenomenon known as systems memory reconsolidation. The neural mechanisms underlying systems memory consolidation and reconsolidation are poorly understood. Here, we propose a neural model based on well-documented mechanisms of synaptic plasticity and stability and describe a computational implementation that demonstrates the model's ability to account for a number of findings from the systems consolidation and reconsolidation literature.

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Section: Resultsmentioning

confidence: 92%

“…de Oliveira Alvares et al, 2012;Einarsson et al, 2015;Frankland et al, 2004;Gafford et al, 2013;Ghazal, 2016 3 PSI during conditioning impairs LTM but not STM.…”

Section: Simulation Targetsmentioning

confidence: 98%

Section: Systems Consolidation and Reconsolidationmentioning

confidence: 99%

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A computational model of systems memory consolidation and reconsolidation

Helfer

Shultz

2019

Hippocampus

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“…Several studies have shown that extinction of fear conditioning is regulated by glutamate receptor signaling (Mahan & Ressler, 2012), which is essential in synaptic plasticity, and antagonizing these receptors can impair extinction in rodents (Dalton, Wang, Floresco, & Phillips, 2008). Specially, the GluA1‐containing alpha‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor (AMPAR) is involved in synaptic transmission and contextual fear memory (Ghazal, 2016). Therefore, the phosphorylated and total levels of GluA1 in the hippocampus were examined on Day 15 (Figure 3e).…”

Section: Resultsmentioning

confidence: 99%

“…Specially, the GluA1-containing alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) is involved in synaptic transmission and contextual fear memory (Ghazal, 2016). Therefore, the phosphorylated and total levels of GluA1 in the hippocampus were examined on Day 15 (Figure 3e).…”

Section: Taniia Regulated the Synaptic Plasticityrelated Proteins In ...mentioning

confidence: 99%

Tanshinone IIA improves contextual fear‐ and anxiety‐like behaviors in mice via the CREB/BDNF/TrkB signaling pathway

Jiang

Wang

et al. 2022

Phytotherapy Research

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Posttraumatic stress disorder (PTSD) is one of the most common psychiatric diseases, which is characterized by the typical symptoms such as re‐experience, avoidance, and hyperarousal. However, there are few drugs for PTSD treatment. In this study, conditioned fear and single‐prolonged stress were employed to establish PTSD mouse model, and we investigated the effects of Tanshinone IIA (TanIIA), a natural product isolated from traditional Chinese herbal Salvia miltiorrhiza, as well as the underlying mechanisms in mice. The results showed that the double stress exposure induced obvious PTSD‐like symptoms, and TanIIA administration significantly decreased freezing time in contextual fear test and relieved anxiety‐like behavior in open field and elevated plus maze tests. Moreover, TanIIA increased the spine density and upregulated synaptic plasticity‐related proteins as well as activated CREB/BDNF/TrkB signaling pathway in the hippocampus. Blockage of CREB remarkably abolished the effects of TanIIA in PTSD model mice and reversed the upregulations of p‐CREB, BDNF, TrkB, and synaptic plasticity‐related protein induced by TanIIA. The molecular docking simulation indicated that TanIIA could interact with the CREB‐binding protein. These findings indicate that TanIIA ameliorates PTSD‐like behaviors in mice by activating the CREB/BDNF/TrkB pathway, which provides a basis for PTSD treatment.

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Prevention of long-term memory loss after retrieval by an endogenous CaMKII inhibitor

Vigil

Mizuno

Lucchesi

et al. 2017

Sci Rep

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CaMK2N1 and CaMK2N2 are endogenous inhibitors of calcium/calmodulin-dependent protein kinase II (CaMKII), a key synaptic signaling molecule for learning and memory. Here, we investigated the learning and memory function of CaMK2N1 by knocking-down its expression in dorsal hippocampus of mice. We found that reduced CaMK2N1 expression does not affect contextual fear long-term memory (LTM) formation. However, we show that it impairs maintenance of established LTM, but only if retrieval occurs. CaMK2N1 knockdown prevents a decrease of threonine-286 (T286) autophosphorylation of αCaMKII and increases GluA1 levels in hippocampal synapses after retrieval of contextual fear LTM. CaMK2N1 knockdown can also increase CaMK2N2 expression, but we show that such increased expression does not affect LTM after retrieval. We also found that substantial overexpression of CaMK2N2 in dorsal hippocampus impairs LTM formation, but not LTM maintenance, suggesting that CaMKII activity is not required for LTM storage. Taken together, we propose a specific function for CaMK2N1; enabling LTM maintenance after retrieval by inhibiting T286 autophosphorylation of αCaMKII.

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AMPA receptor trafficking in recent vs. remote memory

Cited by 3 publications

References 26 publications

A computational model of systems memory consolidation and reconsolidation

A computational model of systems memory consolidation and reconsolidation

Tanshinone IIA improves contextual fear‐ and anxiety‐like behaviors in mice via the CREB/BDNF/TrkB signaling pathway

Prevention of long-term memory loss after retrieval by an endogenous CaMKII inhibitor

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