Absence of synapsin I and II is accompanied by decreases in vesicular transport of specific neurotransmitters
Studies of synapsin‐deficient mice have shown decreases in the number of synaptic vesicles but knowledge about the consequences of this decrease, and which classes of vesicles are being affected, has been lacking. In this study, glutamatergic, GABAergic and dopaminergic transport has been analysed i...
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| Veröffentlicht in: | Journal of neurochemistry 2006-03, Vol.96 (5), p.1458-1466 |
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| container_title | Journal of neurochemistry |
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| creator | Bogen, Inger Lise Boulland, Jean‐Luc Mariussen, Espen Wright, Marianne S. Fonnum, Frode Kao, Hung‐Teh Walaas, S. Ivar |
| description | Studies of synapsin‐deficient mice have shown decreases in the number of synaptic vesicles but knowledge about the consequences of this decrease, and which classes of vesicles are being affected, has been lacking. In this study, glutamatergic, GABAergic and dopaminergic transport has been analysed in animals where the genes encoding synapsin I and II were inactivated. The levels of the vesicular glutamate transporter (VGLUT) 1, VGLUT2 and the vesicular GABA transporter (VGAT) were decreased by approximately 40% in adult forebrain from mice devoid of synapsin I and II, while vesicular monoamine transporter (VMAT) 2 and VGLUT3 were present in unchanged amounts compared with wild‐type mice. Functional studies on synaptic vesicles showed that the vesicular uptake of glutamate and GABA was decreased by 41 and 23%, respectively, while uptake of dopamine was unaffected by the lack of synapsin I and II. Double‐labelling studies showed that VGLUT1 and VGLUT2 colocalized fully with synapsin I and/or II in the hippocampus and neostriatum, respectively. VGAT showed partial colocalization, while VGLUT3 and VMAT2 did not colocalize with either synapsin I or II in the brain areas studied. In conclusion, distinct vesicular transporters show a variable degree of colocalization with synapsin proteins and, hence, distinct sensitivities to inactivation of the genes encoding synapsin I and II. |
| doi_str_mv | 10.1111/j.1471-4159.2005.03636.x |
| format | Article |
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Ivar</creator><creatorcontrib>Bogen, Inger Lise ; Boulland, Jean‐Luc ; Mariussen, Espen ; Wright, Marianne S. ; Fonnum, Frode ; Kao, Hung‐Teh ; Walaas, S. Ivar</creatorcontrib><description>Studies of synapsin‐deficient mice have shown decreases in the number of synaptic vesicles but knowledge about the consequences of this decrease, and which classes of vesicles are being affected, has been lacking. In this study, glutamatergic, GABAergic and dopaminergic transport has been analysed in animals where the genes encoding synapsin I and II were inactivated. The levels of the vesicular glutamate transporter (VGLUT) 1, VGLUT2 and the vesicular GABA transporter (VGAT) were decreased by approximately 40% in adult forebrain from mice devoid of synapsin I and II, while vesicular monoamine transporter (VMAT) 2 and VGLUT3 were present in unchanged amounts compared with wild‐type mice. Functional studies on synaptic vesicles showed that the vesicular uptake of glutamate and GABA was decreased by 41 and 23%, respectively, while uptake of dopamine was unaffected by the lack of synapsin I and II. Double‐labelling studies showed that VGLUT1 and VGLUT2 colocalized fully with synapsin I and/or II in the hippocampus and neostriatum, respectively. VGAT showed partial colocalization, while VGLUT3 and VMAT2 did not colocalize with either synapsin I or II in the brain areas studied. In conclusion, distinct vesicular transporters show a variable degree of colocalization with synapsin proteins and, hence, distinct sensitivities to inactivation of the genes encoding synapsin I and II.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.2005.03636.x</identifier><identifier>PMID: 16478532</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Biochemistry and metabolism ; Biological and medical sciences ; Cell physiology ; Central nervous system ; colocalization ; Fluorescent Antibody Technique - methods ; Fundamental and applied biological sciences. Psychology ; Gene Expression - genetics ; Genes ; Glial Fibrillary Acidic Protein - metabolism ; knockout ; Membrane and intracellular transports ; Mice ; Mice, Knockout ; Microscopy, Confocal - methods ; Molecular and cellular biology ; Neurotransmitter Agents - metabolism ; neurotransmitter transport ; Neurotransmitters ; Proteins ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - metabolism ; Rodents ; Subcellular Fractions - metabolism ; synapsin ; Synapsins - deficiency ; Synapsins - physiology ; synaptic vesicles ; Synaptosomes - metabolism ; Vertebrates: nervous system and sense organs ; Vesicular Neurotransmitter Transport Proteins - classification ; Vesicular Neurotransmitter Transport Proteins - metabolism ; vesicular transporters</subject><ispartof>Journal of neurochemistry, 2006-03, Vol.96 (5), p.1458-1466</ispartof><rights>2006 INIST-CNRS</rights><rights>2006 The Authors Journal Compilation 2006 International Society for Neurochemistry</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5716-7924b79fbd9f0cffd57e573f8f8ac1ae80dfb116abe9ce5c6a606c0f1426b2a73</citedby><cites>FETCH-LOGICAL-c5716-7924b79fbd9f0cffd57e573f8f8ac1ae80dfb116abe9ce5c6a606c0f1426b2a73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1471-4159.2005.03636.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1471-4159.2005.03636.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,1428,27905,27906,45555,45556,46390,46814</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17534698$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16478532$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bogen, Inger Lise</creatorcontrib><creatorcontrib>Boulland, Jean‐Luc</creatorcontrib><creatorcontrib>Mariussen, Espen</creatorcontrib><creatorcontrib>Wright, Marianne S.</creatorcontrib><creatorcontrib>Fonnum, Frode</creatorcontrib><creatorcontrib>Kao, Hung‐Teh</creatorcontrib><creatorcontrib>Walaas, S. Ivar</creatorcontrib><title>Absence of synapsin I and II is accompanied by decreases in vesicular transport of specific neurotransmitters</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>Studies of synapsin‐deficient mice have shown decreases in the number of synaptic vesicles but knowledge about the consequences of this decrease, and which classes of vesicles are being affected, has been lacking. In this study, glutamatergic, GABAergic and dopaminergic transport has been analysed in animals where the genes encoding synapsin I and II were inactivated. The levels of the vesicular glutamate transporter (VGLUT) 1, VGLUT2 and the vesicular GABA transporter (VGAT) were decreased by approximately 40% in adult forebrain from mice devoid of synapsin I and II, while vesicular monoamine transporter (VMAT) 2 and VGLUT3 were present in unchanged amounts compared with wild‐type mice. Functional studies on synaptic vesicles showed that the vesicular uptake of glutamate and GABA was decreased by 41 and 23%, respectively, while uptake of dopamine was unaffected by the lack of synapsin I and II. Double‐labelling studies showed that VGLUT1 and VGLUT2 colocalized fully with synapsin I and/or II in the hippocampus and neostriatum, respectively. VGAT showed partial colocalization, while VGLUT3 and VMAT2 did not colocalize with either synapsin I or II in the brain areas studied. In conclusion, distinct vesicular transporters show a variable degree of colocalization with synapsin proteins and, hence, distinct sensitivities to inactivation of the genes encoding synapsin I and II.</description><subject>Animals</subject><subject>Biochemistry and metabolism</subject><subject>Biological and medical sciences</subject><subject>Cell physiology</subject><subject>Central nervous system</subject><subject>colocalization</subject><subject>Fluorescent Antibody Technique - methods</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression - genetics</subject><subject>Genes</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>knockout</subject><subject>Membrane and intracellular transports</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Microscopy, Confocal - methods</subject><subject>Molecular and cellular biology</subject><subject>Neurotransmitter Agents - metabolism</subject><subject>neurotransmitter transport</subject><subject>Neurotransmitters</subject><subject>Proteins</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Subcellular Fractions - metabolism</subject><subject>synapsin</subject><subject>Synapsins - deficiency</subject><subject>Synapsins - physiology</subject><subject>synaptic vesicles</subject><subject>Synaptosomes - metabolism</subject><subject>Vertebrates: nervous system and sense organs</subject><subject>Vesicular Neurotransmitter Transport Proteins - classification</subject><subject>Vesicular Neurotransmitter Transport Proteins - metabolism</subject><subject>vesicular transporters</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1v1DAQhi0EotvCX0AWEtyS-iO2kwOHagVlq4peytlynLHkVb7wJND99yS7KypxAV_G0jzzyuOHEMpZzpdzvc95YXhWcFXlgjGVM6mlzp9ekM2fxkuyYUyITLJCXJBLxD1jXBeavyYXSzWlkmJDupsaofdAh0Dx0LsRY0931PUN3e1oROq8H7rR9REaWh9oAz6BQ0C6cD8Bo59bl-iUXI_jkKZjzgg-huhpD3Majq0uThMkfENeBdcivD3XK_L9y-fH7dfs_uF2t725z7wyXGemEkVtqlA3VWA-hEYZUEaGMpTOcwcla0LNuXY1VB6U104z7VnghdC1cEZekY-n3DENP2bAyXYRPbSt62GY0WqjteC8_CfIDVdGlGvi-7_A_TCnflnCCqZVUZVSLlB5gnwaEBMEO6bYuXSwnNlVnN3b1Y9d_dhVnD2Ks0_L6Ltz_lx30DwPnk0twIcz4NC7Niy_6iM-c0bJQlfrRp9O3K_YwuG_H2Dvvm3Xm_wNRgS01w</recordid><startdate>200603</startdate><enddate>200603</enddate><creator>Bogen, Inger Lise</creator><creator>Boulland, Jean‐Luc</creator><creator>Mariussen, Espen</creator><creator>Wright, Marianne S.</creator><creator>Fonnum, Frode</creator><creator>Kao, Hung‐Teh</creator><creator>Walaas, S. 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Psychology</topic><topic>Gene Expression - genetics</topic><topic>Genes</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>knockout</topic><topic>Membrane and intracellular transports</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Microscopy, Confocal - methods</topic><topic>Molecular and cellular biology</topic><topic>Neurotransmitter Agents - metabolism</topic><topic>neurotransmitter transport</topic><topic>Neurotransmitters</topic><topic>Proteins</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - methods</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Subcellular Fractions - metabolism</topic><topic>synapsin</topic><topic>Synapsins - deficiency</topic><topic>Synapsins - physiology</topic><topic>synaptic vesicles</topic><topic>Synaptosomes - metabolism</topic><topic>Vertebrates: nervous system and sense organs</topic><topic>Vesicular Neurotransmitter Transport Proteins - classification</topic><topic>Vesicular Neurotransmitter Transport Proteins - metabolism</topic><topic>vesicular transporters</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bogen, Inger Lise</creatorcontrib><creatorcontrib>Boulland, Jean‐Luc</creatorcontrib><creatorcontrib>Mariussen, Espen</creatorcontrib><creatorcontrib>Wright, Marianne S.</creatorcontrib><creatorcontrib>Fonnum, Frode</creatorcontrib><creatorcontrib>Kao, Hung‐Teh</creatorcontrib><creatorcontrib>Walaas, S. 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Ivar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Absence of synapsin I and II is accompanied by decreases in vesicular transport of specific neurotransmitters</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2006-03</date><risdate>2006</risdate><volume>96</volume><issue>5</issue><spage>1458</spage><epage>1466</epage><pages>1458-1466</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>Studies of synapsin‐deficient mice have shown decreases in the number of synaptic vesicles but knowledge about the consequences of this decrease, and which classes of vesicles are being affected, has been lacking. In this study, glutamatergic, GABAergic and dopaminergic transport has been analysed in animals where the genes encoding synapsin I and II were inactivated. The levels of the vesicular glutamate transporter (VGLUT) 1, VGLUT2 and the vesicular GABA transporter (VGAT) were decreased by approximately 40% in adult forebrain from mice devoid of synapsin I and II, while vesicular monoamine transporter (VMAT) 2 and VGLUT3 were present in unchanged amounts compared with wild‐type mice. Functional studies on synaptic vesicles showed that the vesicular uptake of glutamate and GABA was decreased by 41 and 23%, respectively, while uptake of dopamine was unaffected by the lack of synapsin I and II. Double‐labelling studies showed that VGLUT1 and VGLUT2 colocalized fully with synapsin I and/or II in the hippocampus and neostriatum, respectively. VGAT showed partial colocalization, while VGLUT3 and VMAT2 did not colocalize with either synapsin I or II in the brain areas studied. In conclusion, distinct vesicular transporters show a variable degree of colocalization with synapsin proteins and, hence, distinct sensitivities to inactivation of the genes encoding synapsin I and II.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>16478532</pmid><doi>10.1111/j.1471-4159.2005.03636.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biochemistry and metabolism Biological and medical sciences Cell physiology Central nervous system colocalization Fluorescent Antibody Technique - methods Fundamental and applied biological sciences. Psychology Gene Expression - genetics Genes Glial Fibrillary Acidic Protein - metabolism knockout Membrane and intracellular transports Mice Mice, Knockout Microscopy, Confocal - methods Molecular and cellular biology Neurotransmitter Agents - metabolism neurotransmitter transport Neurotransmitters Proteins Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - metabolism Rodents Subcellular Fractions - metabolism synapsin Synapsins - deficiency Synapsins - physiology synaptic vesicles Synaptosomes - metabolism Vertebrates: nervous system and sense organs Vesicular Neurotransmitter Transport Proteins - classification Vesicular Neurotransmitter Transport Proteins - metabolism vesicular transporters |
| title | Absence of synapsin I and II is accompanied by decreases in vesicular transport of specific neurotransmitters |
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