ArticleJournal of cell science2007
Phosphorylation of synapsin domain A is required for post-tetanic potentiation.
Article in Journal of cell science, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
- Munc13-1 couples DAG and CaScience advances · 2026Article
- Increased presynaptic excitability in a migraine with aura mutation.Brain : a journal of neurology · 2024Article
- Invertebrate neurons as a simple model to study the hyperexcitable state of epileptic disorders in single cells, monosynaptic connections, and polysynaptic circuits.Biophysical reviews · 2022Review
- Presynaptic Short-Term Plasticity Persists in the Absence of PKC Phosphorylation of Munc18-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Molecular Mechanisms of Short-Term Plasticity: Role of Synapsin Phosphorylation in Augmentation and Potentiation of Spontaneous Glutamate Release.Frontiers in synaptic neuroscience · 2018Article
- Calcium-Dependent Protein Kinase C Is Not Required for Post-Tetanic Potentiation at the Hippocampal CA3 to CA1 Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- The effect of α7 nicotinic receptor activation on glutamatergic transmission in the hippocampus.Biochemical pharmacology · 2015Review
- Activation of α7 nicotinic acetylcholine receptors increases intracellular cAMP levels via activation of AC1 in hippocampal neurons.Neuropharmacology · 2015Article
- Central vagal afferent endings mediate reduction of food intake by melanocortin-3/4 receptor agonist.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Myotonic dystrophy CTG expansion affects synaptic vesicle proteins, neurotransmission and mouse behaviour.Brain : a journal of neurology · 2013Article
- Selective modulation of chemical and electrical synapses of Helix neuronal networks during in vitro development.BMC neuroscience · 2013Article
- Article
- Theoretical models of synaptic short term plasticity.Frontiers in computational neuroscience · 2013Article
- Adaptive regulation maintains posttetanic potentiation at cerebellar granule cell synapses in the absence of calcium-dependent PKC.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Short-term presynaptic plasticity.Cold Spring Harbor perspectives in biology · 2012Review
- Site-specific synapsin I phosphorylation participates in the expression of post-tetanic potentiation and its enhancement by BDNF.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Synaptic functions of invertebrate varicosities: what molecular mechanisms lie beneath.Neural plasticity · 2012Review
- Calcium-dependent isoforms of protein kinase C mediate posttetanic potentiation at the calyx of Held.Neuron · 2011Article
- Short-term forms of presynaptic plasticity.Current opinion in neurobiology · 2011Review
- A novel form of presynaptic plasticity based on the fast reactivation of release sites switched off during low-frequency depression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Post-tetanic potentiation (PTP) is a form of homosynaptic plasticity important for information processing and short-term memory in the nervous system. The synapsins, a family of synaptic vesicle (SV)-associated phosphoproteins, have been implicated in PTP. Although several synapsin functions are known to be regulated by phosphorylation by multiple protein kinases, the role of individual phosphorylation sites in synaptic plasticity is poorly understood. All the synapsins share a phosphorylation site in the N-terminal domain A (site 1) that regulates neurite elongation and SV mobilization. Here, we have examined the role of phosphorylation of synapsin domain A in PTP and other forms of short-term synaptic enhancement (STE) at synapses between cultured Helix pomatia neurons. To this aim, we cloned H. pomatia synapsin (helSyn) and overexpressed GFP-tagged wild-type helSyn or site-1-mutant helSyn mutated in the presynaptic compartment of C1-B2 synapses. We found that PTP at these synapses depends both on Ca2+/calmodulin-dependent and cAMP-dependent protein kinases, and that overexpression of the non-phosphorylatable helSyn mutant, but not wild-type helSyn, specifically impairs PTP, while not altering facilitation and augmentation. Our findings show that phosphorylation of site 1 has a prominent role in the expression of PTP, thus defining a novel role for phosphorylation of synapsin domain A in short-term homosynaptic plasticity.
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