ArticleMolecular and cellular neurosciences2010
Cooperative regulation of neurotransmitter release by Rab3a and synapsin II.
Article in Molecular and cellular neurosciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 29 citations in OpenAlex.
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- Article
- An interaction between synapsin and C9orf72 regulates excitatory synapses and is impaired in ALS/FTD.Acta neuropathologica · 2022Article
- Synapsin II Directly Suppresses Epileptic Seizures In Vivo.Brain sciences · 2022Article
- Proteome Analysis of Potential Synaptic Vesicle Cycle Biomarkers in the Cerebrospinal Fluid of Patients with Sporadic Creutzfeldt-Jakob Disease.Molecular neurobiology · 2017Article
- Functional role of ATP binding to synapsin I in synaptic vesicle trafficking and release dynamics.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Synapsin II and Rab3a cooperate in the regulation of epileptic and synaptic activity in the CA1 region of the hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Synapsin II desynchronizes neurotransmitter release at inhibitory synapses by interacting with presynaptic calcium channels.Nature communications · 2013Article
- Anxiety-like behavior of prenatally stressed rats is associated with a selective reduction of glutamate release in the ventral hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
To understand how the presynaptic proteins synapsin and Rab3a may interact in the regulation of the synaptic vesicle cycle and the release process, we derived a double knockout (DKO) mouse lacking both synapsin II and Rab3a. We found that Rab3a deletion rescued epileptic-like seizures typical for synapsin II gene deleted animals (Syn II(-)). Furthermore, action potential evoked release was drastically reduced in DKO synapses, although spontaneous release remained normal. At low Ca2+ conditions, quantal content was equally reduced in Rab3a(-) and DKO synapses, but as Ca2+ concentration increased, the increase in quantal content was more prominent in Rab3a(-). Electron microscopy analysis revealed that DKO synapses have a combined phenotype, with docked vesicles being reduced similar to Rab3a(-), and intraterminal vesicles being depleted similar to Syn II(-). Consistently, both Syn II(-) and DKO terminals had increased synaptic depression and incomplete recovery. Taken together, our results suggest that synapsin II and Rab3a have separate roles in maintaining the total store of synaptic vesicles and cooperate in promoting the latest steps of neuronal secretion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.