Somatodendritic dopamine release requires synaptotagmin 4 and 7 and the participation of voltage-gated calcium channels.
Identifieur interne : 000B96 ( PubMed/Corpus ); précédent : 000B95; suivant : 000B97Somatodendritic dopamine release requires synaptotagmin 4 and 7 and the participation of voltage-gated calcium channels.
Auteurs : Jose Alfredo Mendez ; 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
Links to Exploration step
pubmed:21576241Le document en format XML
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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></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21576241</PMID><DateCreated><Year>2011</Year><Month>07</Month><Day>04</Day></DateCreated><DateCompleted><Year>2011</Year><Month>09</Month><Day>08</Day></DateCompleted><DateRevised><Year>2015</Year><Month>02</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1083-351X</ISSN><JournalIssue CitedMedium="Internet"><Volume>286</Volume><Issue>27</Issue><PubDate><Year>2011</Year><Month>Jul</Month><Day>08</Day></PubDate></JournalIssue><Title>The Journal of biological chemistry</Title><ISOAbbreviation>J. Biol. Chem.</ISOAbbreviation></Journal><ArticleTitle>Somatodendritic dopamine release requires synaptotagmin 4 and 7 and the participation of voltage-gated calcium channels.</ArticleTitle><Pagination><MedlinePgn>23928-37</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1074/jbc.M111.218032</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mendez</LastName><ForeName>Jose Alfredo</ForeName><Initials>JA</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, Groupe de Recherche sur le Système Nerveux Central, Faculty of Medicine, Université de Montréal, Montréal, Québec H3C 3J7, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bourque</LastName><ForeName>Marie-Josée</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Fasano</LastName><ForeName>Caroline</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Kortleven</LastName><ForeName>Christian</ForeName><Initials>C</Initials></Author><Author 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mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494303">Syt7 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>134193-27-4</RegistryNumber><NameOfSubstance UI="D050857">Synaptotagmins</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 1995 Jul;65(1):192-200</RefSource><PMID Version="1">7790860</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Exp Brain Res. 1994;100(3):395-406</RefSource><PMID Version="1">7813678</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurophysiol. 1995 Sep;74(3):1137-48</RefSource><PMID Version="1">7500139</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 1996 Apr 1;16(7):2411-20</RefSource><PMID Version="1">8601820</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Pharmacol Exp Ther. 1996 May;277(2):1177-87</RefSource><PMID Version="1">8627530</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Synapse. 1997 Aug;26(4):359-69</RefSource><PMID Version="1">9215595</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 1997 Aug 1;17(15):5738-46</RefSource><PMID Version="1">9221772</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 1998 Apr;70(4):1532-40</RefSource><PMID Version="1">9523570</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 1998 May 15;18(10):3548-53</RefSource><PMID Version="1">9570786</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res Brain Res Rev. 2004 Dec;47(1-3):126-44</RefSource><PMID Version="1">15572168</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2004 Dec 10;279(50):52677-84</RefSource><PMID Version="1">15456748</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroscience. 2005;135(2):545-54</RefSource><PMID Version="1">16111820</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Trends Cell Biol. 2005 Nov;15(11):626-31</RefSource><PMID Version="1">16168654</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2005 Dec 20;102(51):18664-9</RefSource><PMID Version="1">16352718</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2006 Jan 11;26(2):372-80</RefSource><PMID Version="1">16407532</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2006 Feb;96(3):645-55</RefSource><PMID Version="1">16405515</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2006 Mar;96(6):1740-9</RefSource><PMID Version="1">16539689</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur J Neurosci. 2006 Jul;24(2):617-24</RefSource><PMID Version="1">16903863</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2007 Feb 15;53(4):563-75</RefSource><PMID Version="1">17296557</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2007 May 24;54(4):567-81</RefSource><PMID Version="1">17521570</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2008 Mar 25;105(12):4904-9</RefSource><PMID Version="1">18347345</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochem Biophys Res Commun. 2008 Jul 11;371(4):781-6</RefSource><PMID Version="1">18468511</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2008 Jun 18;28(25):6309-18</RefSource><PMID Version="1">18562601</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochem Biophys Res Commun. 2008 Sep 5;373(4):665-9</RefSource><PMID Version="1">18601902</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2008 Aug 1;283(31):21799-807</RefSource><PMID Version="1">18508778</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Physiol. 2009 Mar 15;587(Pt 6):1169-78</RefSource><PMID Version="1">19171650</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuropsychopharmacology. 2009 Apr;34(5):1233-44</RefSource><PMID Version="1">18784647</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2009 May 20;29(20):6568-79</RefSource><PMID Version="1">19458227</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2009 Aug 19;29(33):10424-35</RefSource><PMID Version="1">19692618</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2009 Aug 27;63(4):482-96</RefSource><PMID Version="1">19709630</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Neurosci. 2009 Jun;12(6):767-76</RefSource><PMID Version="1">19448629</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 2009 Nov 6;465(1):31-5</RefSource><PMID Version="1">19729048</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Cell Biol. 2009 Oct 19;187(2):295-310</RefSource><PMID Version="1">19822673</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Neurosci. 2010 Jan;13(1):45-52</RefSource><PMID Version="1">20010821</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroscience. 2010 Apr 28;167(1):135-42</RefSource><PMID Version="1">20138128</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 1999 Oct 21;401(6755):800-4</RefSource><PMID Version="1">10548106</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Cell Biol. 2000 Mar 20;148(6):1141-49</RefSource><PMID Version="1">10725327</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur J Neurosci. 2000 Sep;12(9):3172-80</RefSource><PMID Version="1">10998101</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 2001 Mar 1;410(6824):41-9</RefSource><PMID Version="1">11242035</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur J Neurosci. 2001 Feb;13(4):773-80</RefSource><PMID Version="1">11207812</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2001 May 22;98(11):6423-8</RefSource><PMID Version="1">11353855</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2001 May;30(2):459-73</RefSource><PMID Version="1">11395007</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2001 Oct 1;21(19):7841-7</RefSource><PMID Version="1">11567075</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2010 May 19;30(20):6975-83</RefSource><PMID Version="1">20484639</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 2001 Sep 28;293(5539):2465-70</RefSource><PMID Version="1">11577238</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroscience. 2003;120(3):757-64</RefSource><PMID Version="1">12895515</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Cell Biol. 2003 Aug 18;162(4):543-9</RefSource><PMID Version="1">12925704</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2003 Oct 15;12(20):2587-97</RefSource><PMID Version="1">12925569</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurophysiol. 2004 Mar;91(3):1450-4</RefSource><PMID Version="1">14645383</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2004 Mar 10;24(10):2566-74</RefSource><PMID Version="1">15014132</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Cell Neurosci. 2004 Mar;25(3):394-405</RefSource><PMID Version="1">15033168</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur J Neurosci. 2004 May;19(10):2909-12</RefSource><PMID Version="1">15147325</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochem J. 2004 Jun 15;380(Pt 3):875-9</RefSource><PMID Version="1">15015935</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2004 Jun 24;42(6):939-46</RefSource><PMID Version="1">15207238</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2004 Jun 22;101(25):9441-6</RefSource><PMID Version="1">15197251</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosci Biobehav Rev. 2004 Jul;28(4):415-31</RefSource><PMID Version="1">15289006</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res. 1975 Jan 17;83(3):531-7</RefSource><PMID Version="1">1111820</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell. 1994 Nov 18;79(4):717-27</RefSource><PMID Version="1">7954835</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 1994 Dec;13(6):1303-13</RefSource><PMID Version="1">7993624</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 1995 Jun 15;375(6532):594-9</RefSource><PMID 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