Somatodendritic dopamine release requires synaptotagmin 4 and 7 and the participation of voltage-gated calcium channels.
Identifieur interne : 000B96 ( PubMed/Curation ); précédent : 000B95; suivant : 000B97Somatodendritic dopamine release requires synaptotagmin 4 and 7 and the participation of voltage-gated calcium channels.
Auteurs : Jose Alfredo Mendez [Canada] ; Marie-Josée Bourque ; Caroline Fasano ; Christian Kortleven ; Louis-Eric TrudeauSource :
- The Journal of biological chemistry [ 1083-351X ] ; 2011.
English descriptors
- KwdEn :
- Animals, Calcium (metabolism), Calcium Channels (genetics), Calcium Channels (metabolism), Dendrites (secretion), Dopamine (secretion), Gene Expression Regulation (genetics), Humans, Mice, Mice, Transgenic, Nerve Tissue Proteins (genetics), Nerve Tissue Proteins (metabolism), Parkinson Disease (genetics), Parkinson Disease (metabolism), Synaptotagmins (genetics), Synaptotagmins (metabolism).
- MESH :
- chemical , genetics : Calcium Channels, Nerve Tissue Proteins, Synaptotagmins.
- chemical , metabolism : Calcium, Calcium Channels, Nerve Tissue Proteins, Synaptotagmins.
- genetics : Gene Expression Regulation, Parkinson Disease.
- metabolism : Parkinson Disease.
- secretion : Dendrites, Dopamine.
- Animals, Humans, Mice, Mice, Transgenic.
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.
DOI: 10.1074/jbc.M111.218032
PubMed: 21576241
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pubmed:21576241Le document en format XML
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<front><div type="abstract" xml:lang="en">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.</div>
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