<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pan PY</submitter><funding>Intramural NIH HHS</funding><pagination>412-24</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2656773</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>61(3)</volume><pubmed_abstract>Synaptic vesicle (SV) fusion is a fine-tuned process requiring a concert of fusion machineries. Using cortical neurons from snapin-deficient mice, we reveal a role for Snapin in facilitating synchronous release. In addition to reduced frequency of miniature excitatory postsynaptic currents (mini-EPSCs) and smaller release-ready vesicle pool (RRP) size, snapin deficiency results in EPSCs with multiple peaks and increased rise and decay times, reflecting "desynchronized" SV fusion. These defects impair both synaptic precision and efficacy during sustained neurotransmission. Transient expression of Snapin not only rescues the slowed kinetics of EPSCs, but also further accelerates the rate found in wild-type neurons. Furthermore, expression of Snapin-C66A, a dimerization-defective mutant with </pubmed_abstract><journal>Neuron</journal><pubmed_title>Snapin facilitates the synchronization of synaptic vesicle fusion.</pubmed_title><pmcid>PMC2656773</pmcid><funding_grant_id>Z01 NS002946-11</funding_grant_id><pubmed_authors>Pan PY</pubmed_authors><pubmed_authors>Sheng ZH</pubmed_authors><pubmed_authors>Tian JH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Snapin facilitates the synchronization of synaptic vesicle fusion.</name><description>Synaptic vesicle (SV) fusion is a fine-tuned process requiring a concert of fusion machineries. Using cortical neurons from snapin-deficient mice, we reveal a role for Snapin in facilitating synchronous release. In addition to reduced frequency of miniature excitatory postsynaptic currents (mini-EPSCs) and smaller release-ready vesicle pool (RRP) size, snapin deficiency results in EPSCs with multiple peaks and increased rise and decay times, reflecting "desynchronized" SV fusion. These defects impair both synaptic precision and efficacy during sustained neurotransmission. Transient expression of Snapin not only rescues the slowed kinetics of EPSCs, but also further accelerates the rate found in wild-type neurons. Furthermore, expression of Snapin-C66A, a dimerization-defective mutant with </description><dates><release>2009-01-01T00:00:00Z</release><publication>2009 Feb</publication><modification>2025-04-04T19:12:51.649Z</modification><creation>2019-03-27T00:21:17Z</creation></dates><accession>S-EPMC2656773</accession><cross_references><pubmed>19217378</pubmed><doi>10.1016/j.neuron.2008.12.029</doi></cross_references></HashMap>