ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Mobilization of calcium from intracellular stores facilitates somatodendritic dopamine release.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 108 citations in OpenAlex.
- α-Synuclein expression is required for somatodendritic dopamine release and immediate early gene induction.Science advances · 2026Article
- Formation, Organization, and Maintenance of Synaptic Vesicle Pools: From Molecules to Structure and Dynamics.Advances in neurobiology · 2026Review
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- Insights into the mediation of CaJournal of cell communication and signaling · 2023Article
- The Effects of Carvacrol on Transient Receptor Potential (TRP) Channels in an Animal Model of Parkinson's Disease.Neurotoxicity research · 2023Article
- A CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 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
- Role of the endoplasmic reticulum in synaptic transmission.Current opinion in neurobiology · 2022Review
- The Thermodynamically Expensive Contribution of Three Calcium Sources to Somatic Release of Serotonin.International journal of molecular sciences · 2022Review
- 1,2-Dimyristoyl-RSC advances · 2021Article
- Activity-dependent somatodendritic dopamine release in the substantia nigra autoinhibits the releasing neuron.Cell reports · 2021Article
- Crosstalk among Calcium ATPases: PMCA, SERCA and SPCA in Mental Diseases.International journal of molecular sciences · 2021Review
- Extrasynaptic Communication.Frontiers in molecular neuroscience · 2021Article
- Progress in opioid reward research: From a canonical two-neuron hypothesis to two neural circuits.Pharmacology, biochemistry, and behavior · 2021Review
- Dopamine receptors in emesis: Molecular mechanisms and potential therapeutic function.Pharmacological research · 2020Review
- Article
- The SERCA2: A Gatekeeper of Neuronal Calcium Homeostasis in the Brain.Cellular and molecular neurobiology · 2018Review
- TRPC Channels and Parkinson's Disease.Advances in experimental medicine and biology · 2017Review
- Dendritic Release of Neurotransmitters.Comprehensive Physiology · 2016Review
- Striatal dopamine neurotransmission: regulation of release and uptake.Basal ganglia · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Somatodendritic dopamine (DA) release in the substantia nigra pars compacta (SNc) shows a limited dependence on extracellular calcium concentration ([Ca(2+)](o)), suggesting the involvement of intracellular Ca(2+) stores. Here, using immunocytochemistry we demonstrate the presence of the sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase 2 (SERCA2) that sequesters cytosolic Ca(2+) into the endoplasmic reticulum (ER), as well as inositol 1,4,5-triphosphate receptors (IP(3)Rs) and ryanodine receptors (RyRs) in DAergic neurons. Notably, RyRs were clustered at the plasma membrane, poised for activation by Ca(2+) entry. Using fast-scan cyclic voltammetry to monitor evoked extracellular DA concentration ([DA](o)) in midbrain slices, we found that SERCA inhibition by cyclopiazonic acid (CPA) decreased evoked [DA](o) in the SNc, indicating a functional role for ER Ca(2+) stores in somatodendritic DA release. Implicating IP(3)R-dependent stores, an IP(3)R antagonist, 2-APB, also decreased evoked [DA](o). Moreover, DHPG, an agonist of group I metabotropic glutamate receptors (mGluR1s, which couple to IP(3) production), increased somatodendritic DA release, whereas CPCCOEt, an mGluR1 antagonist, suppressed it. Release suppression by mGluR1 blockade was prevented by 2-APB or CPA, indicating facilitation of DA release by endogenous glutamate acting via mGluR1s and IP(3)R-gated Ca(2+) stores. Similarly, activation of RyRs by caffeine increased [Ca(2+)](i) and elevated evoked [DA](o). The increase in DA release was prevented by a RyR blocker, dantrolene, and by CPA. Importantly, the efficacy of dantrolene was enhanced in low [Ca(2+)](o), suggesting a mechanism for maintenance of somatodendritic DA release with limited Ca(2+) entry. Thus, both mGluR1-linked IP(3)R- and RyR-dependent ER Ca(2+) stores facilitate somatodendritic DA release in the SNc.
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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.