ArticleThe Journal of biological chemistry2011
Somatodendritic dopamine release requires synaptotagmin 4 and 7 and the participation of voltage-gated calcium channels.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- The landscape of multiscale transcriptomic networks and key regulators in Parkinson's disease.Nature communications · 2019Pooled it
- The Synaptic Vesicle Priming Protein Munc13 Mediates Evoked Somatodendritic Dopamine Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Age-Related Characteristics of SYT1-Associated Neurodevelopmental Disorder.Annals of clinical and translational neurology · 2026Article
- α-Synuclein oligomers slow down action potential firing and enhance dopamine release by increasing Cav2.2 currents in midbrain dopaminergic neurons.The Journal of physiology · 2026Article
- Impact of distinct neurotransmitter release modes on neuronal signaling.Molecular psychiatry · 2026Review
- The synaptic vesicle priming protein Munc13 mediates evoked somatodendritic dopamine release.bioRxiv : the preprint server for biology · 2025Article
- Mechanisms of neuromodulatory volume transmission.Molecular psychiatry · 2024Review
- Synaptotagmin-4 induces anhedonic responses to chronic stress via BDNF signaling in the medial prefrontal cortex.Experimental & molecular medicine · 2024Article
- Synaptotagmin-1-dependent phasic axonal dopamine release is dispensable for basic motor behaviors in mice.Nature communications · 2023Article
- Article
- Dopamine Transmission Imbalance in Neuroinflammation: Perspectives on Long-Term COVID-19.International journal of molecular sciences · 2023Review
- Inter-Individual Variation in DNA Methylation Patterns across Two Tissues and Leukocytes in Mature Brahman Cattle.Biology · 2023Article
- Synaptotagmin-1 is a CaCell reports · 2023Article
- Somatodendritic Release of Cholecystokinin Potentiates GABAergic Synapses Onto Ventral Tegmental Area Dopamine Cells.Biological psychiatry · 2023Article
- Differential Subcellular Distribution and Release Dynamics of Cotransmitted Cholinergic and GABAergic Synaptic Inputs Modify Dopaminergic Neuronal Excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Biological effects of inhaled crude oil vapor V. Altered biogenic amine neurotransmitters and neural protein expression.Toxicology and applied pharmacology · 2022Article
- Synaptotagmins 1 and 7 Play Complementary Roles in Somatodendritic Dopamine Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Implication of synaptotagmins 4 and 7 in activity-dependent somatodendritic dopamine release in the ventral midbrain.Open biology · 2022Article
- Article
- The Thermodynamically Expensive Contribution of Three Calcium Sources to Somatic Release of Serotonin.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatodendritic (STD) dopamine (DA) release is a key mechanism for the autoregulatory control of DA release in the brain. However, its molecular mechanism remains undetermined. We tested the hypothesis that differential expression of synaptotagmin (Syt) isoforms explains some of the differential properties of terminal and STD DA release. Down-regulation of the dendritically expressed Syt4 and Syt7 severely reduced STD DA release, whereas terminal release required Syt1. Moreover, we found that although mobilization of intracellular Ca(2+) stores is inefficient, Ca(2+) influx through N- and P/Q-type voltage-gated channels is critical to trigger STD DA release. Our findings provide an explanation for the differential Ca(2+) requirement of terminal and STD DA release. In addition, we propose that not all sources of intracellular Ca(2+) are equally efficient to trigger this release mechanism. Our findings have implications for a better understanding of a fundamental cell biological process mediating transcellular signaling in a system critical for diseases such as Parkinson disease.
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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.