Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

External Ca2+ dependency of synaptic transmission in drosophila synaptotagmin I mutants.

Journal of neurophysiology - 1 Aug 2005

Okamoto Tomonori, Tamura Takuya, Suzuki Kazuhiro, Kidokoro Yoshiaki

Abstract excerpt

To resolve some of differences in reports on the function of Synaptotagmin I (Syt I), we re-examined synaptic transmission at the neuromuscular junction of Drosophila embryos that have mutations in the Syt I gene (syt I). Two major questions addressed were which Ca2+ binding domain, C2A or C2B, sense Ca2+ and is Syt I a negative regulator of spontaneous vesicle fusion. Synaptic currents were induced by nerve...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Calcimycin
Share to Electric Stimulation
Share to Evoked Potentials

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Ionomycin

Share to Ionophores

Share to Potassium Chloride

Share to Synaptotagmin I

Share to Synaptotagmins

Source

Identifiers

PMID: 16061495
DOI: 10.1152/jn.00205.2005

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

External Ca2+ dependency of synaptic transmission in drosophila synaptotagmin I mutants.PMID 16061495Read ↗

Mutational analysis of Drosophila synaptotagmin demonstrates its essential role in Ca(2+)-activated neurotransmitter release.Semantic proximity Read ↗

Synaptotagmin I functions as a calcium sensor to synchronize neurotransmitter release.Semantic proximity Read ↗

Genetic analysis of synaptotagmin C2 domain specificity in regulating spontaneous and evoked neurotransmitter release.Semantic proximity Read ↗

The C(2)B Ca(2+)-binding motif of synaptotagmin is required for synaptic transmission in vivo.Semantic proximity Read ↗

Differential regulation of synchronous versus asynchronous neurotransmitter release by the C2 domains of synaptotagmin 1.Semantic proximity Read ↗

Transmembrane tethering of synaptotagmin to synaptic vesicles controls multiple modes of neurotransmitter release.Semantic proximity Read ↗

Drosophila synaptotagmin I null mutants show severe alterations in vesicle populations but calcium-binding motif mutants do not.Semantic proximity Read ↗

A de novo missense mutation in synaptotagmin-1 associated with neurodevelopmental disorder desynchronizes neurotransmitter releaseSemantic proximity Read ↗

A de novo missense mutation in synaptotagmin-1 associated with neurodevelopmental disorder desynchronizes neurotransmitter releaseSemantic proximity Read ↗

Disease-causing mutations in Synaptotagmin can act via dominant-negative, gain-of-function or haploinsufficient mechanismsSemantic proximity Read ↗

Synaptotagmin increases the dynamic range of synapses by driving Ca²+-evoked release and by clamping a near-linear remaining Ca²+ sensor.Semantic proximity Read ↗

Cysteine-string protein increases the calcium sensitivity of neurotransmitter exocytosis in Drosophila.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.