SUMOylation Is Required for Glycine-Induced Increases in AMPA Receptor Surface Expression (ChemLTP) in Hippocampal Neurons

Jaafari, Nadia; Konopacki, Filip A.; Owen, Thomas F.; Kantamneni, Sriharsha; Rubin, Philip; Craig, Timothy; Wilkinson, Kevin A.; Henley, Jeremy M.

doi:10.1371/journal.pone.0052345

Cited by 56 publications

(71 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We wanted to know whether a similar phenomenon might operate for CPEB3 in the hippocampus. We found an increase in CPEB3 protein 30 min after LTP induction ( Figure 1B) and in hippocampal neurons in culture stimulated with glutamate or glycine (Figures 1A and S1) (Jaafari et al, 2013). We also detected an increase in the levels of CPEB3 when we applied dopamine, essential for L-LTP, to hippocampal slices ( Figure S1) (Smith et al, 2005).…”

Section: Cpeb3 Protein Is Increased and Becomes Aggregated Following mentioning

confidence: 60%

The Persistence of Hippocampal-Based Memory Requires Protein Synthesis Mediated by the Prion-like Protein CPEB3

Fioriti¹,

Myers²,

Huang³

et al. 2015

Neuron

181

223

View full text Add to dashboard Cite

Consolidation of long-term memories depends on de novo protein synthesis. Several translational regulators have been identified, and their contribution to the formation of memory has been assessed in the mouse hippocampus. None of them, however, has been implicated in the persistence of memory. Although persistence is a key feature of long-term memory, how this occurs, despite the rapid turnover of its molecular substrates, is poorly understood. Here we find that both memory storage and its underlying synaptic plasticity are mediated by the increase in level and in the aggregation of the prion-like translational regulator CPEB3 (cytoplasmic polyadenylation element-binding protein). Genetic ablation of CPEB3 impairs the maintenance of both hippocampal long-term potentiation and hippocampus-dependent spatial memory. We propose a model whereby persistence of long-term memory results from the assembly of CPEB3 into aggregates. These aggregates serve as functional prions and regulate local protein synthesis necessary for the maintenance of long-term memory.

show abstract

Section: Cpeb3 Protein Is Increased and Becomes Aggregated Following mentioning

confidence: 60%

The Persistence of Hippocampal-Based Memory Requires Protein Synthesis Mediated by the Prion-like Protein CPEB3

Fioriti¹,

Myers²,

Huang³

et al. 2015

Neuron

181

223

View full text Add to dashboard Cite

show abstract

“…Other post-translational modifications have also been shown to regulate synaptic plasticity. Sumoylation of the GluA1 AMPAR subunit is required for its surface expression during long-term potentiation (LTP) (127). Decreased sumoylation showed a marked reduction in surface expression of AMPAR, emphasizing the role of SUMO in synaptic plasticity.…”

Section: Importance Of Proteomics In Identifying Mechanismsmentioning

confidence: 99%

Molecular and Cellular Mechanisms of Axonal Regeneration After Spinal Cord Injury

Niekerk

Tuszynski

et al. 2016

Molecular & Cellular Proteomics

View full text Add to dashboard Cite

Following axotomy, a complex temporal and spatial coordination of molecular events enables regeneration of the peripheral nerve. In contrast, multiple intrinsic and extrinsic factors contribute to the general failure of axonal regeneration in the central nervous system. In this review, we examine the current understanding of differences in protein expression and post-translational modifications, activation of signaling networks, and environmental cues that may underlie the divergent regenerative capacity of central and peripheral axons. We also highlight key experimental strategies to enhance axonal regeneration via modulation of intraneuronal signaling networks and the extracellular milieu. Finally, we explore potential applications of proteomics to fill gaps in the current understanding of molecular mechanisms underlying regeneration, and to provide insight into the development of more effective approaches to promote axonal regeneration following injury to the nervous system. Molecular & Cellular Proteomics

show abstract

“…A role for SUMOylation in synaptic plasticity has begun to emerge in recent years (Cheng et al, 2013; Jaafari et al, 2013; Luo et al, 2013). SUMOylation occurs in hippocampal neurons, and is regulated by neuronal stimulation (Loriol et al, 2013).…”

Section: Epigenetic Regulation Of Hippocampal Memorymentioning

confidence: 99%

Epigenetic regulation of estrogen-dependent memory

Fortress

Frick

2014

Frontiers in Neuroendocrinology

View full text Add to dashboard Cite

Hippocampal memory formation is highly regulated by post-translational histone modifications and DNA methylation. Accordingly, these epigenetic processes play a major role in the effects of modulatory factors, such as sex steroid hormones, on hippocampal memory. Our laboratory recently demonstrated that the ability of the potent estrogen 17β-estradiol (E2) to enhance hippocampal-dependent novel object recognition memory in ovariectomized female mice requires ERK-dependent histone H3 acetylation and DNA methylation in the dorsal hippocampus. Although these data provide valuable insight into the chromatin modifications that mediate the memory-enhancing effects of E2, epigenetic regulation of gene expression is enormously complex. Therefore, more research is needed to fully understand how E2 and other hormones employ epigenetic alterations to shape behavior. This review discusses the epigenetic alterations shown thus far to regulate hippocampal memory, briefly reviews the effects of E2 on hippocampal function, and describes in detail our work on epigenetic regulation of estrogenic memory enhancement.

show abstract

SUMOylation Is Required for Glycine-Induced Increases in AMPA Receptor Surface Expression (ChemLTP) in Hippocampal Neurons

Cited by 56 publications

References 31 publications

The Persistence of Hippocampal-Based Memory Requires Protein Synthesis Mediated by the Prion-like Protein CPEB3

The Persistence of Hippocampal-Based Memory Requires Protein Synthesis Mediated by the Prion-like Protein CPEB3

Molecular and Cellular Mechanisms of Axonal Regeneration After Spinal Cord Injury

Epigenetic regulation of estrogen-dependent memory

Contact Info

Product

Resources

About