ArticleThe Journal of physiology2007
The role of synaptotagmin I C2A calcium-binding domain in synaptic vesicle clustering during synapse formation.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
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- Inverse Relationship between Basal Pacemaker Neuron Activity and Aversive Long-Term Memory Formation inFrontiers in cellular neuroscience · 2016Article
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- Marine compound xyloketal B reduces neonatal hypoxic-ischemic brain injury.Marine drugs · 2014Article
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- Electroporation of the hindbrain to trace axonal trajectories and synaptic targets in the chick embryo.Journal of visualized experiments : JoVE · 2013Article
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- Axonal patterns and targets of dA1 interneurons in the chick hindbrain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Caltubin, a novel molluscan tubulin-interacting protein, promotes axonal growth and attenuates axonal degeneration of rodent neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- DHA diet reduces AD pathology in young APPswe/PS1 Delta E9 transgenic mice: possible gender effects.Journal of neuroscience research · 2010Article
- Transcriptome analysis of the central nervous system of the mollusc Lymnaea stagnalis.BMC genomics · 2009Article
- Differential effects of treadmill running and wheel running on spatial or aversive learning and memory: roles of amygdalar brain-derived neurotrophic factor and synaptotagmin I.The Journal of physiology · 2009Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic vesicles aggregate at the presynaptic terminal during synapse formation via mechanisms that are poorly understood. Here we have investigated the role of the putative calcium sensor synaptotagmin I in vesicle aggregation during the formation of soma-soma synapses between identified partner cells using a simple in vitro synapse model in the mollusc Lymnaea stagnalis. Immunocytochemistry, optical imaging and electrophysiological recording techniques were used to monitor synapse formation and vesicle localization. Within 6 h, contact between appropriate synaptic partner cells up-regulated global synaptotagmin I expression, and induced a localized aggregation of synaptotagmin I at the contact site. Cell contacts between non-synaptic partner cells did not affect synaptotagmin I expression. Application of an human immunodeficiency virus type-1 transactivator (HIV-1 TAT)-tagged peptide corresponding to loop 3 of the synaptotagmin I C2A domain prevented synaptic vesicle aggregation and synapse formation. By contrast, a TAT-tagged peptide containing the calcium-binding motif of the C2B domain did not affect synaptic vesicle aggregation or synapse formation. Calcium imaging with Fura-2 demonstrated that TAT-C2 peptides did not alter either basal or evoked intracellular calcium levels. These results demonstrate that contact with an appropriate target cell is necessary to initiate synaptic vesicle aggregation during nascent synapse formation and that the initial aggregation of synaptic vesicles is dependent on loop 3 of the C2A domain of synaptotagmin I.
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