Metabolic Control of Vesicular Glutamate Transport and Release
Fasting has been used to control epilepsy since antiquity, but the mechanism of coupling between metabolic state and excitatory neurotransmission remains unknown. Previous work has shown that the vesicular glutamate transporters (VGLUTs) required for exocytotic release of glutamate undergo an unusua...
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| Veröffentlicht in: | Neuron (Cambridge, Mass.) Mass.), 2010-10, Vol.68 (1), p.99-112 |
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| creator | Juge, Narinobu Gray, John A. Omote, Hiroshi Miyaji, Takaaki Inoue, Tsuyoshi Hara, Chiaki Uneyama, Hisayuki Edwards, Robert H. Nicoll, Roger A. Moriyama, Yoshinori |
| description | Fasting has been used to control epilepsy since antiquity, but the mechanism of coupling between metabolic state and excitatory neurotransmission remains unknown. Previous work has shown that the vesicular glutamate transporters (VGLUTs) required for exocytotic release of glutamate undergo an unusual form of regulation by Cl
−. Using functional reconstitution of the purified VGLUTs into proteoliposomes, we now show that Cl
− acts as an allosteric activator, and the ketone bodies that increase with fasting inhibit glutamate release by competing with Cl
− at the site of allosteric regulation. Consistent with these observations, acetoacetate reduced quantal size at hippocampal synapses and suppresses glutamate release and seizures evoked with 4-aminopyridine in the brain. The results indicate an unsuspected link between metabolic state and excitatory neurotransmission through anion-dependent regulation of VGLUT activity.
► Cl
− acts as an allosteric activator of VGLUTs ► Ketone bodies inhibited vesicular glutamate uptake by competing with Cl
− ► Acetoacetate reduced quantal size at hippocampal synapses ► Acetoacetate suppressed 4AP-evoked glutamate release and seizures |
| doi_str_mv | 10.1016/j.neuron.2010.09.002 |
| format | Article |
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−. Using functional reconstitution of the purified VGLUTs into proteoliposomes, we now show that Cl
− acts as an allosteric activator, and the ketone bodies that increase with fasting inhibit glutamate release by competing with Cl
− at the site of allosteric regulation. Consistent with these observations, acetoacetate reduced quantal size at hippocampal synapses and suppresses glutamate release and seizures evoked with 4-aminopyridine in the brain. The results indicate an unsuspected link between metabolic state and excitatory neurotransmission through anion-dependent regulation of VGLUT activity.
► Cl
− acts as an allosteric activator of VGLUTs ► Ketone bodies inhibited vesicular glutamate uptake by competing with Cl
− ► Acetoacetate reduced quantal size at hippocampal synapses ► Acetoacetate suppressed 4AP-evoked glutamate release and seizures</description><identifier>ISSN: 0896-6273</identifier><identifier>EISSN: 1097-4199</identifier><identifier>DOI: 10.1016/j.neuron.2010.09.002</identifier><identifier>PMID: 20920794</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>4-Aminopyridine - pharmacology ; Acetoacetates - pharmacology ; Animals ; Astrocytes - drug effects ; Astrocytes - physiology ; Behavior ; Behavior, Animal ; Brain research ; Cells, Cultured ; Chlorides - metabolism ; Chromatography, High Pressure Liquid - methods ; Disease Models, Animal ; Dopamine - metabolism ; Dose-Response Relationship, Drug ; Embryo, Mammalian ; Epilepsy ; Excitatory Postsynaptic Potentials - drug effects ; Exocytosis - drug effects ; Exocytosis - genetics ; Gene Expression Regulation ; Glutamic Acid - metabolism ; Hippocampus - cytology ; Humans ; In Vitro Techniques ; Ketone Bodies ; Membrane Potential, Mitochondrial - drug effects ; Membrane Potential, Mitochondrial - genetics ; Metabolites ; Mice ; Mice, Inbred C57BL ; Microdialysis - methods ; Models, Biological ; Neurons - drug effects ; Neurons - metabolism ; Patch-Clamp Techniques - methods ; Potassium Channel Blockers - pharmacology ; Rats ; Rodents ; Seizures - chemically induced ; Seizures - physiopathology ; Studies ; Synaptic Vesicles - metabolism ; Vesicular Glutamate Transport Protein 2 - chemistry ; Vesicular Glutamate Transport Protein 2 - genetics ; Vesicular Glutamate Transport Protein 2 - metabolism</subject><ispartof>Neuron (Cambridge, Mass.), 2010-10, Vol.68 (1), p.99-112</ispartof><rights>2010 Elsevier Inc.</rights><rights>Copyright © 2010 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Oct 6, 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c588t-35592eef666fddf3a7485a8d848ebe82de2b9b47e4f3295a37b40ee7300405743</citedby><cites>FETCH-LOGICAL-c588t-35592eef666fddf3a7485a8d848ebe82de2b9b47e4f3295a37b40ee7300405743</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0896627310007191$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20920794$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Juge, Narinobu</creatorcontrib><creatorcontrib>Gray, John A.</creatorcontrib><creatorcontrib>Omote, Hiroshi</creatorcontrib><creatorcontrib>Miyaji, Takaaki</creatorcontrib><creatorcontrib>Inoue, Tsuyoshi</creatorcontrib><creatorcontrib>Hara, Chiaki</creatorcontrib><creatorcontrib>Uneyama, Hisayuki</creatorcontrib><creatorcontrib>Edwards, Robert H.</creatorcontrib><creatorcontrib>Nicoll, Roger A.</creatorcontrib><creatorcontrib>Moriyama, Yoshinori</creatorcontrib><title>Metabolic Control of Vesicular Glutamate Transport and Release</title><title>Neuron (Cambridge, Mass.)</title><addtitle>Neuron</addtitle><description>Fasting has been used to control epilepsy since antiquity, but the mechanism of coupling between metabolic state and excitatory neurotransmission remains unknown. Previous work has shown that the vesicular glutamate transporters (VGLUTs) required for exocytotic release of glutamate undergo an unusual form of regulation by Cl
−. Using functional reconstitution of the purified VGLUTs into proteoliposomes, we now show that Cl
− acts as an allosteric activator, and the ketone bodies that increase with fasting inhibit glutamate release by competing with Cl
− at the site of allosteric regulation. Consistent with these observations, acetoacetate reduced quantal size at hippocampal synapses and suppresses glutamate release and seizures evoked with 4-aminopyridine in the brain. The results indicate an unsuspected link between metabolic state and excitatory neurotransmission through anion-dependent regulation of VGLUT activity.
► Cl
− acts as an allosteric activator of VGLUTs ► Ketone bodies inhibited vesicular glutamate uptake by competing with Cl
− ► Acetoacetate reduced quantal size at hippocampal synapses ► Acetoacetate suppressed 4AP-evoked glutamate release and seizures</description><subject>4-Aminopyridine - pharmacology</subject><subject>Acetoacetates - pharmacology</subject><subject>Animals</subject><subject>Astrocytes - drug effects</subject><subject>Astrocytes - physiology</subject><subject>Behavior</subject><subject>Behavior, Animal</subject><subject>Brain research</subject><subject>Cells, Cultured</subject><subject>Chlorides - metabolism</subject><subject>Chromatography, High Pressure Liquid - methods</subject><subject>Disease Models, Animal</subject><subject>Dopamine - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Embryo, Mammalian</subject><subject>Epilepsy</subject><subject>Excitatory Postsynaptic Potentials - drug effects</subject><subject>Exocytosis - drug effects</subject><subject>Exocytosis - genetics</subject><subject>Gene Expression Regulation</subject><subject>Glutamic Acid - metabolism</subject><subject>Hippocampus - cytology</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Ketone Bodies</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Membrane Potential, Mitochondrial - genetics</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microdialysis - methods</subject><subject>Models, Biological</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Patch-Clamp Techniques - methods</subject><subject>Potassium Channel Blockers - pharmacology</subject><subject>Rats</subject><subject>Rodents</subject><subject>Seizures - chemically induced</subject><subject>Seizures - physiopathology</subject><subject>Studies</subject><subject>Synaptic Vesicles - metabolism</subject><subject>Vesicular Glutamate Transport Protein 2 - chemistry</subject><subject>Vesicular Glutamate Transport Protein 2 - genetics</subject><subject>Vesicular Glutamate Transport Protein 2 - metabolism</subject><issn>0896-6273</issn><issn>1097-4199</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kV9rFTEQxYNY7LX6DUQWfPBpbyfZ_H0pyKW2QktBqq8hm53VXHI312S34Lc35dZWffApMDlzZs78CHlDYU2BytPtesIlp2nNoJbArAHYM7KiYFTLqTHPyQq0ka1kqjsmL0vZAlAuDH1BjhkYBsrwFTm7xtn1KQbfbNI05xSbNDZfsQS_RJebi7jMbudmbG6zm8o-5blx09B8xoiu4CtyNLpY8PXDe0K-fDy_3Vy2VzcXnzYfrlovtJ7bTgjDEEcp5TgMY-cU18LpQXONPWo2IOtNzxXysWNGuE71HBBVB8BBKN6dkLOD737pdzh4rKu6aPc57Fz-aZML9u-fKXy339KdZUZpKmQ1eP9gkNOPBctsd6F4jNFNmJZitVSKG81FVb77R7lNS55qOksFdJpzkLqq-EHlcyol4_i4CwV7z8du7YGPvedjwdjKp7a9_TPHY9NvIE9BsV7zLmC2xQecPA4ho5_tkML_J_wCCK6jfw</recordid><startdate>20101006</startdate><enddate>20101006</enddate><creator>Juge, Narinobu</creator><creator>Gray, John A.</creator><creator>Omote, Hiroshi</creator><creator>Miyaji, Takaaki</creator><creator>Inoue, Tsuyoshi</creator><creator>Hara, Chiaki</creator><creator>Uneyama, Hisayuki</creator><creator>Edwards, Robert H.</creator><creator>Nicoll, Roger A.</creator><creator>Moriyama, Yoshinori</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><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>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20101006</creationdate><title>Metabolic Control of Vesicular Glutamate Transport and Release</title><author>Juge, Narinobu ; Gray, John A. ; Omote, Hiroshi ; Miyaji, Takaaki ; Inoue, Tsuyoshi ; Hara, Chiaki ; Uneyama, Hisayuki ; Edwards, Robert H. ; Nicoll, Roger A. ; Moriyama, Yoshinori</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c588t-35592eef666fddf3a7485a8d848ebe82de2b9b47e4f3295a37b40ee7300405743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>4-Aminopyridine - pharmacology</topic><topic>Acetoacetates - pharmacology</topic><topic>Animals</topic><topic>Astrocytes - drug effects</topic><topic>Astrocytes - physiology</topic><topic>Behavior</topic><topic>Behavior, Animal</topic><topic>Brain research</topic><topic>Cells, Cultured</topic><topic>Chlorides - metabolism</topic><topic>Chromatography, High Pressure Liquid - methods</topic><topic>Disease Models, Animal</topic><topic>Dopamine - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Embryo, Mammalian</topic><topic>Epilepsy</topic><topic>Excitatory Postsynaptic Potentials - drug effects</topic><topic>Exocytosis - drug effects</topic><topic>Exocytosis - genetics</topic><topic>Gene Expression Regulation</topic><topic>Glutamic Acid - metabolism</topic><topic>Hippocampus - cytology</topic><topic>Humans</topic><topic>In Vitro Techniques</topic><topic>Ketone Bodies</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Membrane Potential, Mitochondrial - genetics</topic><topic>Metabolites</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microdialysis - methods</topic><topic>Models, Biological</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Patch-Clamp Techniques - methods</topic><topic>Potassium Channel Blockers - pharmacology</topic><topic>Rats</topic><topic>Rodents</topic><topic>Seizures - chemically induced</topic><topic>Seizures - physiopathology</topic><topic>Studies</topic><topic>Synaptic Vesicles - metabolism</topic><topic>Vesicular Glutamate Transport Protein 2 - chemistry</topic><topic>Vesicular Glutamate Transport Protein 2 - genetics</topic><topic>Vesicular Glutamate Transport Protein 2 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Juge, Narinobu</creatorcontrib><creatorcontrib>Gray, John A.</creatorcontrib><creatorcontrib>Omote, Hiroshi</creatorcontrib><creatorcontrib>Miyaji, Takaaki</creatorcontrib><creatorcontrib>Inoue, Tsuyoshi</creatorcontrib><creatorcontrib>Hara, Chiaki</creatorcontrib><creatorcontrib>Uneyama, Hisayuki</creatorcontrib><creatorcontrib>Edwards, Robert H.</creatorcontrib><creatorcontrib>Nicoll, Roger A.</creatorcontrib><creatorcontrib>Moriyama, Yoshinori</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neuron (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Juge, Narinobu</au><au>Gray, John A.</au><au>Omote, Hiroshi</au><au>Miyaji, Takaaki</au><au>Inoue, Tsuyoshi</au><au>Hara, Chiaki</au><au>Uneyama, Hisayuki</au><au>Edwards, Robert H.</au><au>Nicoll, Roger A.</au><au>Moriyama, Yoshinori</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metabolic Control of Vesicular Glutamate Transport and Release</atitle><jtitle>Neuron (Cambridge, Mass.)</jtitle><addtitle>Neuron</addtitle><date>2010-10-06</date><risdate>2010</risdate><volume>68</volume><issue>1</issue><spage>99</spage><epage>112</epage><pages>99-112</pages><issn>0896-6273</issn><eissn>1097-4199</eissn><abstract>Fasting has been used to control epilepsy since antiquity, but the mechanism of coupling between metabolic state and excitatory neurotransmission remains unknown. Previous work has shown that the vesicular glutamate transporters (VGLUTs) required for exocytotic release of glutamate undergo an unusual form of regulation by Cl
−. Using functional reconstitution of the purified VGLUTs into proteoliposomes, we now show that Cl
− acts as an allosteric activator, and the ketone bodies that increase with fasting inhibit glutamate release by competing with Cl
− at the site of allosteric regulation. Consistent with these observations, acetoacetate reduced quantal size at hippocampal synapses and suppresses glutamate release and seizures evoked with 4-aminopyridine in the brain. The results indicate an unsuspected link between metabolic state and excitatory neurotransmission through anion-dependent regulation of VGLUT activity.
► Cl
− acts as an allosteric activator of VGLUTs ► Ketone bodies inhibited vesicular glutamate uptake by competing with Cl
− ► Acetoacetate reduced quantal size at hippocampal synapses ► Acetoacetate suppressed 4AP-evoked glutamate release and seizures</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>20920794</pmid><doi>10.1016/j.neuron.2010.09.002</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Cell Press Free Archives; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | 4-Aminopyridine - pharmacology Acetoacetates - pharmacology Animals Astrocytes - drug effects Astrocytes - physiology Behavior Behavior, Animal Brain research Cells, Cultured Chlorides - metabolism Chromatography, High Pressure Liquid - methods Disease Models, Animal Dopamine - metabolism Dose-Response Relationship, Drug Embryo, Mammalian Epilepsy Excitatory Postsynaptic Potentials - drug effects Exocytosis - drug effects Exocytosis - genetics Gene Expression Regulation Glutamic Acid - metabolism Hippocampus - cytology Humans In Vitro Techniques Ketone Bodies Membrane Potential, Mitochondrial - drug effects Membrane Potential, Mitochondrial - genetics Metabolites Mice Mice, Inbred C57BL Microdialysis - methods Models, Biological Neurons - drug effects Neurons - metabolism Patch-Clamp Techniques - methods Potassium Channel Blockers - pharmacology Rats Rodents Seizures - chemically induced Seizures - physiopathology Studies Synaptic Vesicles - metabolism Vesicular Glutamate Transport Protein 2 - chemistry Vesicular Glutamate Transport Protein 2 - genetics Vesicular Glutamate Transport Protein 2 - metabolism |
| title | Metabolic Control of Vesicular Glutamate Transport and Release |
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