Rab3a-mediated vesicle recruitment regulates short-term plasticity at the mouse diaphragm synapse
Rab3a is a small GTP-binding protein associated with presynaptic vesicles. We have measured the releasable pool in the neuromuscular junction of Rab3a(−) mice by recordings of the asynchronous release activity produced by local applications of hypertonic solutions and demonstrated that the releasabl...
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| Veröffentlicht in: | Molecular and cellular neuroscience 2009-06, Vol.41 (2), p.286-296 |
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| creator | Coleman, William L. Bykhovskaia, Maria |
| description | Rab3a is a small GTP-binding protein associated with presynaptic vesicles. We have measured the releasable pool in the neuromuscular junction of Rab3a(−) mice by recordings of the asynchronous release activity produced by local applications of hypertonic solutions and demonstrated that the releasable pool is significantly reduced in Rab3a(−) synapses. We found that the activity-dependent vesicle recruitment, as well as the synaptic enhancement associated with it, is disrupted in Rab3a(−) synapses. We employed Ca
2+ chelators and disruption of Ca
2+ sensitivity of fusion machinery by botulinum neurotoxin type-A microinjections, and demonstrated that local Ca
2+ elevation may overcome the Rab3a deficiency in maintaining the releasable pool. Rab3a(−) terminals demonstrated a small but significant low-frequency depression, probably due to insufficient refilling of the releasable pool. Our results, taken together, support the hypothesis that Rab3a maintains the pool of fusion competent vesicles tightly coupled to Ca
2+ channels. |
| doi_str_mv | 10.1016/j.mcn.2009.03.008 |
| format | Article |
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2+ chelators and disruption of Ca
2+ sensitivity of fusion machinery by botulinum neurotoxin type-A microinjections, and demonstrated that local Ca
2+ elevation may overcome the Rab3a deficiency in maintaining the releasable pool. Rab3a(−) terminals demonstrated a small but significant low-frequency depression, probably due to insufficient refilling of the releasable pool. Our results, taken together, support the hypothesis that Rab3a maintains the pool of fusion competent vesicles tightly coupled to Ca
2+ channels.</description><identifier>ISSN: 1044-7431</identifier><identifier>EISSN: 1095-9327</identifier><identifier>DOI: 10.1016/j.mcn.2009.03.008</identifier><identifier>PMID: 19348946</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Botulinum Toxins, Type A - metabolism ; Calcium - metabolism ; Diaphragm - innervation ; Diaphragm - metabolism ; Electric Stimulation ; Excitatory Postsynaptic Potentials - physiology ; Mice ; Mice, Knockout ; Neuronal Plasticity - physiology ; Presynaptic Terminals - metabolism ; rab3A GTP-Binding Protein - genetics ; rab3A GTP-Binding Protein - metabolism ; Synapses - metabolism ; Synaptic Vesicles - metabolism</subject><ispartof>Molecular and cellular neuroscience, 2009-06, Vol.41 (2), p.286-296</ispartof><rights>2009 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c382t-d2591e881427be44ed00229f3e7e9b210a16e0aabdbc6d0e201433d7c695f4d33</citedby><cites>FETCH-LOGICAL-c382t-d2591e881427be44ed00229f3e7e9b210a16e0aabdbc6d0e201433d7c695f4d33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1044743109000682$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19348946$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Coleman, William L.</creatorcontrib><creatorcontrib>Bykhovskaia, Maria</creatorcontrib><title>Rab3a-mediated vesicle recruitment regulates short-term plasticity at the mouse diaphragm synapse</title><title>Molecular and cellular neuroscience</title><addtitle>Mol Cell Neurosci</addtitle><description>Rab3a is a small GTP-binding protein associated with presynaptic vesicles. We have measured the releasable pool in the neuromuscular junction of Rab3a(−) mice by recordings of the asynchronous release activity produced by local applications of hypertonic solutions and demonstrated that the releasable pool is significantly reduced in Rab3a(−) synapses. We found that the activity-dependent vesicle recruitment, as well as the synaptic enhancement associated with it, is disrupted in Rab3a(−) synapses. We employed Ca
2+ chelators and disruption of Ca
2+ sensitivity of fusion machinery by botulinum neurotoxin type-A microinjections, and demonstrated that local Ca
2+ elevation may overcome the Rab3a deficiency in maintaining the releasable pool. Rab3a(−) terminals demonstrated a small but significant low-frequency depression, probably due to insufficient refilling of the releasable pool. Our results, taken together, support the hypothesis that Rab3a maintains the pool of fusion competent vesicles tightly coupled to Ca
2+ channels.</description><subject>Animals</subject><subject>Botulinum Toxins, Type A - metabolism</subject><subject>Calcium - metabolism</subject><subject>Diaphragm - innervation</subject><subject>Diaphragm - metabolism</subject><subject>Electric Stimulation</subject><subject>Excitatory Postsynaptic Potentials - physiology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Neuronal Plasticity - physiology</subject><subject>Presynaptic Terminals - metabolism</subject><subject>rab3A GTP-Binding Protein - genetics</subject><subject>rab3A GTP-Binding Protein - metabolism</subject><subject>Synapses - metabolism</subject><subject>Synaptic Vesicles - metabolism</subject><issn>1044-7431</issn><issn>1095-9327</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM1LJDEQxcOirDr6B-xlyclbt5WP6e7gSURXYUAQ9xzSSc1Mhv4ySQvz32-GGfC2p3pQ7z2qfoT8YlAyYNXdruztUHIAVYIoAZof5JKBWhZK8PrsoKUsainYBbmKcQcAS67ET3LBlJCNktUlMe-mFabo0XmT0NEvjN52SAPaMPvU45Cy3sxd3kYat2NIRcLQ06kzMXnr056aRNMWaT_OEWnumbbBbHoa94OZIl6T87XpIt6c5oL8fX76eHwpVm9_Xh8fVoUVDU-F40vFsGmY5HWLUqID4FytBdaoWs7AsArBmNa1tnKAHJgUwtW2Usu1dEIsyO2xdwrj54wx6d5Hi11nBsyXaQ4Vr5lQ2ciORhvGGAOu9RR8b8JeM9AHrnqnM1d94KpB6Mw1Z36fyuc2s_pOnEBmw_3RgPnFL49BR-txsJlrRpm0G_1_6v8BHGiKGA</recordid><startdate>20090601</startdate><enddate>20090601</enddate><creator>Coleman, William L.</creator><creator>Bykhovskaia, Maria</creator><general>Elsevier Inc</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></search><sort><creationdate>20090601</creationdate><title>Rab3a-mediated vesicle recruitment regulates short-term plasticity at the mouse diaphragm synapse</title><author>Coleman, William L. ; Bykhovskaia, Maria</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c382t-d2591e881427be44ed00229f3e7e9b210a16e0aabdbc6d0e201433d7c695f4d33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Botulinum Toxins, Type A - metabolism</topic><topic>Calcium - metabolism</topic><topic>Diaphragm - innervation</topic><topic>Diaphragm - metabolism</topic><topic>Electric Stimulation</topic><topic>Excitatory Postsynaptic Potentials - physiology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Neuronal Plasticity - physiology</topic><topic>Presynaptic Terminals - metabolism</topic><topic>rab3A GTP-Binding Protein - genetics</topic><topic>rab3A GTP-Binding Protein - metabolism</topic><topic>Synapses - metabolism</topic><topic>Synaptic Vesicles - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Coleman, William L.</creatorcontrib><creatorcontrib>Bykhovskaia, Maria</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><jtitle>Molecular and cellular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Coleman, William L.</au><au>Bykhovskaia, Maria</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Rab3a-mediated vesicle recruitment regulates short-term plasticity at the mouse diaphragm synapse</atitle><jtitle>Molecular and cellular neuroscience</jtitle><addtitle>Mol Cell Neurosci</addtitle><date>2009-06-01</date><risdate>2009</risdate><volume>41</volume><issue>2</issue><spage>286</spage><epage>296</epage><pages>286-296</pages><issn>1044-7431</issn><eissn>1095-9327</eissn><abstract>Rab3a is a small GTP-binding protein associated with presynaptic vesicles. We have measured the releasable pool in the neuromuscular junction of Rab3a(−) mice by recordings of the asynchronous release activity produced by local applications of hypertonic solutions and demonstrated that the releasable pool is significantly reduced in Rab3a(−) synapses. We found that the activity-dependent vesicle recruitment, as well as the synaptic enhancement associated with it, is disrupted in Rab3a(−) synapses. We employed Ca
2+ chelators and disruption of Ca
2+ sensitivity of fusion machinery by botulinum neurotoxin type-A microinjections, and demonstrated that local Ca
2+ elevation may overcome the Rab3a deficiency in maintaining the releasable pool. Rab3a(−) terminals demonstrated a small but significant low-frequency depression, probably due to insufficient refilling of the releasable pool. Our results, taken together, support the hypothesis that Rab3a maintains the pool of fusion competent vesicles tightly coupled to Ca
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| ispartof | Molecular and cellular neuroscience, 2009-06, Vol.41 (2), p.286-296 |
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| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Botulinum Toxins, Type A - metabolism Calcium - metabolism Diaphragm - innervation Diaphragm - metabolism Electric Stimulation Excitatory Postsynaptic Potentials - physiology Mice Mice, Knockout Neuronal Plasticity - physiology Presynaptic Terminals - metabolism rab3A GTP-Binding Protein - genetics rab3A GTP-Binding Protein - metabolism Synapses - metabolism Synaptic Vesicles - metabolism |
| title | Rab3a-mediated vesicle recruitment regulates short-term plasticity at the mouse diaphragm synapse |
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