Synaptotagmin I Synchronizes Transmitter Release in Mouse Hippocampal Neurons
We have asked whether loss of the Ca2+ sensor protein synaptotagmin I influences the total amount of neurotransmitter released after a presynaptic action potential. Hippocampal neurons from synaptotagmin I knock-out mice had a greatly reduced fast synchronous component of glutamate release, as repor...
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| Veröffentlicht in: | The Journal of neuroscience 2004-07, Vol.24 (27), p.6127-6132 |
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| creator | Nishiki, Tei-ichi Augustine, George J |
| description | We have asked whether loss of the Ca2+ sensor protein synaptotagmin I influences the total amount of neurotransmitter released after a presynaptic action potential. Hippocampal neurons from synaptotagmin I knock-out mice had a greatly reduced fast synchronous component of glutamate release, as reported previously. However, the amount of glutamate released during the slow asynchronous component increased in these knock-out neurons. As a result of these changes in the kinetics of release, there was no significant difference between wild-type and knock-out neurons in the total amount of transmitter released within 400 msec after a presynaptic stimulus. Fluorescence imaging experiments demonstrated that wild-type and knock-out neurons take up and release similar amounts of FM dye after depolarization, indicating normal amounts of synaptic vesicle trafficking in the knock-out neurons. These results indicate that synaptotagmin I knock-out neurons are fully capable of releasing neurotransmitter, with the increased slow component of release serving to compensate for loss of the fast component. Thus, synaptotagmin I synchronizes the rapid release of neurotransmitters after Ca2+ entry into presynaptic terminals and also appears to suppress the slower, asynchronous form of transmitter release. |
| doi_str_mv | 10.1523/JNEUROSCI.1563-04.2004 |
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Hippocampal neurons from synaptotagmin I knock-out mice had a greatly reduced fast synchronous component of glutamate release, as reported previously. However, the amount of glutamate released during the slow asynchronous component increased in these knock-out neurons. As a result of these changes in the kinetics of release, there was no significant difference between wild-type and knock-out neurons in the total amount of transmitter released within 400 msec after a presynaptic stimulus. Fluorescence imaging experiments demonstrated that wild-type and knock-out neurons take up and release similar amounts of FM dye after depolarization, indicating normal amounts of synaptic vesicle trafficking in the knock-out neurons. These results indicate that synaptotagmin I knock-out neurons are fully capable of releasing neurotransmitter, with the increased slow component of release serving to compensate for loss of the fast component. Thus, synaptotagmin I synchronizes the rapid release of neurotransmitters after Ca2+ entry into presynaptic terminals and also appears to suppress the slower, asynchronous form of transmitter release.</description><identifier>ISSN: 0270-6474</identifier><identifier>EISSN: 1529-2401</identifier><identifier>DOI: 10.1523/JNEUROSCI.1563-04.2004</identifier><identifier>PMID: 15240804</identifier><language>eng</language><publisher>United States: Soc Neuroscience</publisher><subject>Animals ; Brief Communications ; Calcium-Binding Proteins - genetics ; Calcium-Binding Proteins - metabolism ; Calcium-Binding Proteins - physiology ; Cells, Cultured ; Endocytosis - physiology ; Excitatory Postsynaptic Potentials - physiology ; Exocytosis - physiology ; Fluorescent Dyes - pharmacokinetics ; Hippocampus - cytology ; Hippocampus - metabolism ; Hippocampus - physiology ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - metabolism ; Membrane Glycoproteins - physiology ; Mice ; Mice, Knockout ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Nerve Tissue Proteins - physiology ; Neurons - metabolism ; Neurons - physiology ; Neurotransmitter Agents - metabolism ; Patch-Clamp Techniques ; Stimulation, Chemical ; Synaptic Transmission - physiology ; Synaptotagmin I ; Synaptotagmins</subject><ispartof>The Journal of neuroscience, 2004-07, Vol.24 (27), p.6127-6132</ispartof><rights>Copyright © 2004 Society for Neuroscience 0270-6474/04/246127-06.00/0 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c539t-a19fb76b8d000f1ea2dc5c036106f556743f1fec7766d5b3a893b82be35de1fa3</citedby><cites>FETCH-LOGICAL-c539t-a19fb76b8d000f1ea2dc5c036106f556743f1fec7766d5b3a893b82be35de1fa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6729667/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6729667/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15240804$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nishiki, Tei-ichi</creatorcontrib><creatorcontrib>Augustine, George J</creatorcontrib><title>Synaptotagmin I Synchronizes Transmitter Release in Mouse Hippocampal Neurons</title><title>The Journal of neuroscience</title><addtitle>J Neurosci</addtitle><description>We have asked whether loss of the Ca2+ sensor protein synaptotagmin I influences the total amount of neurotransmitter released after a presynaptic action potential. Hippocampal neurons from synaptotagmin I knock-out mice had a greatly reduced fast synchronous component of glutamate release, as reported previously. However, the amount of glutamate released during the slow asynchronous component increased in these knock-out neurons. As a result of these changes in the kinetics of release, there was no significant difference between wild-type and knock-out neurons in the total amount of transmitter released within 400 msec after a presynaptic stimulus. Fluorescence imaging experiments demonstrated that wild-type and knock-out neurons take up and release similar amounts of FM dye after depolarization, indicating normal amounts of synaptic vesicle trafficking in the knock-out neurons. These results indicate that synaptotagmin I knock-out neurons are fully capable of releasing neurotransmitter, with the increased slow component of release serving to compensate for loss of the fast component. Thus, synaptotagmin I synchronizes the rapid release of neurotransmitters after Ca2+ entry into presynaptic terminals and also appears to suppress the slower, asynchronous form of transmitter release.</description><subject>Animals</subject><subject>Brief Communications</subject><subject>Calcium-Binding Proteins - genetics</subject><subject>Calcium-Binding Proteins - metabolism</subject><subject>Calcium-Binding Proteins - physiology</subject><subject>Cells, Cultured</subject><subject>Endocytosis - physiology</subject><subject>Excitatory Postsynaptic Potentials - physiology</subject><subject>Exocytosis - physiology</subject><subject>Fluorescent Dyes - pharmacokinetics</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - physiology</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Membrane Glycoproteins - physiology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Nerve Tissue Proteins - physiology</subject><subject>Neurons - metabolism</subject><subject>Neurons - physiology</subject><subject>Neurotransmitter Agents - metabolism</subject><subject>Patch-Clamp Techniques</subject><subject>Stimulation, Chemical</subject><subject>Synaptic Transmission - physiology</subject><subject>Synaptotagmin I</subject><subject>Synaptotagmins</subject><issn>0270-6474</issn><issn>1529-2401</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUlrG0EQhZsQEytO_oKZU3Iau3qfuQSMsGMZL-Dl3PT01EgdZnP3yML59Wkh4cSnnKqK-t6jikfIMYUTKhk_vbo9f7q_e5gv0qh4DuKEAYgPZJa2Zc4E0I9kBkxDroQWh-RzjL8AQAPVn8hhggQUIGbk5uG1t-M0THbZ-T5bZGl2qzD0_jfG7DHYPnZ-mjBk99iijZgl6mZYp-bSj-PgbDfaNrvFddLEL-SgsW3Er_t6RJ4uzh_nl_n13c_F_Ow6d5KXU25p2VRaVUWdTmooWlY76YArCqqRUmnBG9qg01qpWlbcFiWvClYhlzXSxvIj8mPnO66rDmuH_RRsa8bgOxtezWC9eb_p_coshxejNCuV0sng294gDM9rjJPpfHTYtrbH9JxRShVSlvS_IC1AlsBUAtUOdGGIMWDzdg0Fs43MvEVmtpEZEGYbWRIe__vLX9k-owR83wErv1xtfEATO9u2Cadms9mw5KONokzzP5Izosk</recordid><startdate>20040707</startdate><enddate>20040707</enddate><creator>Nishiki, Tei-ichi</creator><creator>Augustine, George J</creator><general>Soc Neuroscience</general><general>Society for Neuroscience</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20040707</creationdate><title>Synaptotagmin I Synchronizes Transmitter Release in Mouse Hippocampal Neurons</title><author>Nishiki, Tei-ichi ; Augustine, George J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c539t-a19fb76b8d000f1ea2dc5c036106f556743f1fec7766d5b3a893b82be35de1fa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Brief Communications</topic><topic>Calcium-Binding Proteins - genetics</topic><topic>Calcium-Binding Proteins - metabolism</topic><topic>Calcium-Binding Proteins - physiology</topic><topic>Cells, Cultured</topic><topic>Endocytosis - physiology</topic><topic>Excitatory Postsynaptic Potentials - physiology</topic><topic>Exocytosis - physiology</topic><topic>Fluorescent Dyes - pharmacokinetics</topic><topic>Hippocampus - cytology</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - physiology</topic><topic>Membrane Glycoproteins - genetics</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Membrane Glycoproteins - physiology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Nerve Tissue Proteins - physiology</topic><topic>Neurons - metabolism</topic><topic>Neurons - physiology</topic><topic>Neurotransmitter Agents - metabolism</topic><topic>Patch-Clamp Techniques</topic><topic>Stimulation, Chemical</topic><topic>Synaptic Transmission - physiology</topic><topic>Synaptotagmin I</topic><topic>Synaptotagmins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nishiki, Tei-ichi</creatorcontrib><creatorcontrib>Augustine, George J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nishiki, Tei-ichi</au><au>Augustine, George J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Synaptotagmin I Synchronizes Transmitter Release in Mouse Hippocampal Neurons</atitle><jtitle>The Journal of neuroscience</jtitle><addtitle>J Neurosci</addtitle><date>2004-07-07</date><risdate>2004</risdate><volume>24</volume><issue>27</issue><spage>6127</spage><epage>6132</epage><pages>6127-6132</pages><issn>0270-6474</issn><eissn>1529-2401</eissn><abstract>We have asked whether loss of the Ca2+ sensor protein synaptotagmin I influences the total amount of neurotransmitter released after a presynaptic action potential. Hippocampal neurons from synaptotagmin I knock-out mice had a greatly reduced fast synchronous component of glutamate release, as reported previously. However, the amount of glutamate released during the slow asynchronous component increased in these knock-out neurons. As a result of these changes in the kinetics of release, there was no significant difference between wild-type and knock-out neurons in the total amount of transmitter released within 400 msec after a presynaptic stimulus. Fluorescence imaging experiments demonstrated that wild-type and knock-out neurons take up and release similar amounts of FM dye after depolarization, indicating normal amounts of synaptic vesicle trafficking in the knock-out neurons. These results indicate that synaptotagmin I knock-out neurons are fully capable of releasing neurotransmitter, with the increased slow component of release serving to compensate for loss of the fast component. Thus, synaptotagmin I synchronizes the rapid release of neurotransmitters after Ca2+ entry into presynaptic terminals and also appears to suppress the slower, asynchronous form of transmitter release.</abstract><cop>United States</cop><pub>Soc Neuroscience</pub><pmid>15240804</pmid><doi>10.1523/JNEUROSCI.1563-04.2004</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Brief Communications Calcium-Binding Proteins - genetics Calcium-Binding Proteins - metabolism Calcium-Binding Proteins - physiology Cells, Cultured Endocytosis - physiology Excitatory Postsynaptic Potentials - physiology Exocytosis - physiology Fluorescent Dyes - pharmacokinetics Hippocampus - cytology Hippocampus - metabolism Hippocampus - physiology Membrane Glycoproteins - genetics Membrane Glycoproteins - metabolism Membrane Glycoproteins - physiology Mice Mice, Knockout Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Nerve Tissue Proteins - physiology Neurons - metabolism Neurons - physiology Neurotransmitter Agents - metabolism Patch-Clamp Techniques Stimulation, Chemical Synaptic Transmission - physiology Synaptotagmin I Synaptotagmins |
| title | Synaptotagmin I Synchronizes Transmitter Release in Mouse Hippocampal Neurons |
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