ArticleProceedings of the National Academy of Sciences of the United States of America2011
Rapid increase in clusters of synaptophysin at onset of homosynaptic potentiation in Aplysia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Prion acute synaptotoxicity is largely driven by protease-resistant PrPSc species.PLoS pathogens · 2018Article
- Late prenatal immune activation causes hippocampal deficits in the absence of persistent inflammation across aging.Journal of neuroinflammation · 2015Article
- Cyclophilin D deficiency rescues Aβ-impaired PKA/CREB signaling and alleviates synaptic degeneration.Biochimica et biophysica acta · 2014Article
- Genetic deficiency of neuronal RAGE protects against AGE-induced synaptic injury.Cell death & disease · 2014Article
- Active transport of vesicles in neurons is modulated by mechanical tension.Scientific reports · 2014Article
- Making long-term memories in minutes: a spaced learning pattern from memory research in education.Frontiers in human neuroscience · 2013Article
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Authors and funding
3 authors.
Funding
Abstract
Imaging studies have shown that even the earliest phases of long-term plasticity are accompanied by the rapid recruitment of synaptic components, which generally requires actin polymerization and may be one of the first steps in a program that can lead to the formation of new stable synapses during late-phase plasticity. However, most of those results come from studies of long-term potentiation in rodent hippocampus and might not generalize to other forms of synaptic plasticity or plasticity in other brain areas and species. For example, recruitment of presynaptic proteins during long-term facilitation by 5HT in Aplysia is delayed for several hours, suggesting that whereas activity-dependent forms of plasticity, such as long-term potentiation, involve rapid recruitment of presynaptic proteins, neuromodulatory forms of plasticity, such as facilitation by 5HT, involve more delayed recruitment. To begin to explore this hypothesis, we examined an activity-dependent form of plasticity, homosynaptic potentiation produced by tetanic stimulation of the presynaptic neuron in Aplysia. We found that homosynaptic potentiation involves presynaptic but not postsynaptic actin and a rapid (under 10 min) increase in the number of clusters of the presynaptic vesicle-associated protein synaptophysin. These results indicate that rapid recruitment of synaptic components is not limited to hippocampal potentiation and support the hypothesis that activity-dependent types of plasticity involve rapid recruitment of presynaptic proteins, whereas neuromodulatory types of plasticity involve more delayed recruitment.
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