Ask about this productRelated genes to: SYT3 antibody
- Gene:
- SYT3 NIH gene
- Name:
- synaptotagmin 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1995-09-27
- Date modifiied:
- 2015-11-20
Related products to: SYT3 antibody
Related articles to: SYT3 antibody
- - Source: PubMed
- Neurotransmitter co-transmission contributes to diverse physiological processes throughout the mammalian brain, including sensory integration, motivational control, and social behaviors. Projections from the globus pallidus internus (GPi; the entopeduncular nucleus, EPN, in rodents) to the lateral habenula (LHb) are well-characterized by the co-transmission of both GABA and glutamate. These dual-release inputs modulate behavioral states in chronically learned helpless (cLH) rats, influencing both the onset and recovery of pathological phenotypes. Here, we employed confocal 3D reconstructions that confirmed the presence of both vesicular transporters VGAT and VGLUT2 in EPN axon terminals within the LHb. Further investigation revealed that GABA and glutamate are packaged in distinct vesicle populations within individual presynaptic terminals. Notably, the calcium (Ca) sensors Synaptotagmin-2 (Syt2) and Synaptotagmin-3 (Syt3) are highly expressed in the EPN whereas expression of the canonical Ca sensor, Synaptotagmin 1 (Syt1), is downregulated. Additionally, using confocal microscopy, we observed selective spatial correlations of Syt2 and VGLUT2 and between Syt3 and VGAT in LHb axon terminals. These observations strongly suggested that Syt2 serves as the predominant Ca sensor for glutamatergic vesicle fusion, and Syt3 serves as the predominant Ca sensor for GABAergic vesicle fusion in the LHb. To test this hypothesis, we employed targeted antisense oligonucleotide (ASO) knockdown of Syt2 and Syt3 in EPN neurons and measured LHb glutamatergic and GABAergic currents. Syt2 knockdown resulted in an increase in mEPSC frequency, amplitude, half-width and decay, suggesting increased glutamate vesicle release probability and increased glutamate vesicle packing. However, Syt2 knockdown had no influence on mIPSCs amplitude or frequency. On the other hand, Syt3 knockdown had no apparent effect on glutamate release but caused an increase in mIPSC frequency suggesting increased quantal release probability of GABA. Together, these findings identify a molecular mechanism by which synaptotagmin isoforms govern differential glutamate and GABA release at EPN dual-transmitter terminals in the LHb. These results provide evidence for presynaptic mechanisms regulating excitatory-inhibitory balance within this brain structure and importantly provide molecular targets for pharmacological intervention. - Source: PubMed
Publication date: 2026/04/04
White Dustin NKushner J KeenanWinther Kelly EMcGovern Dillon JBasta TamaraDonaldson Zoe RHoeffer Charles ARoot David HStowell Michael H B - Endoplasmic reticulum-plasma membrane contact sites (ER-PM CS) are central hubs that coordinate lipid metabolism, membrane remodelling, calcium signalling and stress responses in plant cells. This review summarizes current knowledge on the molecular architecture and functions of ER-PM CS, with emphasis on the three tether families (synaptotagmins/SYTs, multiple-C2-domain and transmembrane region proteins/MCTPs, and VAMP-associated protein 27/VAP27 proteins) and the lipid-transfer proteins (SMP-domain proteins and oxysterol-binding protein-related/ORPs) described to date. SYTs and MCTPs use C2 domains to read PM phosphoinositides and Ca2+ signals to dynamically modulate tethering, while VAP27s scaffold multimeric complexes via MSP-FFAT interactions and link the ER to the cytoskeleton. Lipid transfer at ER-PM CS sustain the phosphatidylinositol (PI) cycle and prevents accumulation of cone-shaped lipids such as diacylglycerol (DAG) at the PM. In plants, SYT1/SYT3 form a module with diacylglycerol kinases (DGKs) to clear DAG from the PM and to channel DAG into metabolism. ORP family members function as PI/PS (and sterol) exchangers and integrate contact-site lipid exchange with signalling and autophagy. ER-PM CS also intersect with endocytosis, autophagosome biogenesis, plasmodesmata function and unfolded protein response signalling, underlining their multi-functional roles in cellular homeostasis and stress adaptation. - Source: PubMed
Publication date: 2026/03/09
Morello-López JorgePagano-Marquez RaquelJaillais YvonBotella Miguel A - Ischemic stroke is a major global cause of disability and death. Synaptotagmin-3 (Syt3), a synaptic calcium sensor, exacerbates ischemic injury by promoting pathological glutamate release. This study investigated the potential neuroprotective effect of restriction of Syt3 internalization on neuronal apoptosis and microglial reprogramming following ischemia/reperfusion (I/R). - Source: PubMed
Xu HuaMi HongboCheng RongGui TiantianHu FangzhouYang YiCheng JianXue Qun - We sought to characterize the sixth most common finding in our neuroimmunological laboratory practice (tissue assay-observed unclassified neural antibodies [UNAs]), combining protein microarray and phage immunoprecipitation sequencing (PhIP-Seq). - Source: PubMed
Publication date: 2025/11/06
Gilligan MichaelMills John RVargas PaulinaParamasivan Naveen KLesnick Connie EBasal EatiDasari SurendraFryer James PHinson Shannon RLaporta JosephEspinal AmyFitzgerald DennisGarcia CarolinaMorenkova Anna EPergami PaolaShah AnnaKnight AndrewLaFrance Corey ReghannLennon Vanda AZekeridou AnastasiaPittock Sean JDubey DivyanshuMcKeon Andrew