Imaging in Vivo Glutamate Fluctuations with [11C]ABP688: A GLT-1 Challenge with Ceftriaxone
Molecular imaging offers unprecedented opportunities for investigating dynamic changes underlying neuropsychiatric conditions. Here, we evaluated whether [11C]ABP688, a positron emission tomography (PET) ligand that binds to the allosteric site of the metabotropic glutamate receptor type 5 (mGluR5),...
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| Veröffentlicht in: | Journal of cerebral blood flow and metabolism 2015-07, Vol.35 (7), p.1169-1174 |
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| container_title | Journal of cerebral blood flow and metabolism |
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| creator | Zimmer, Eduardo R Parent, Maxime J Leuzy, Antoine Aliaga, Antonio Aliaga, Arturo Moquin, Luc Schirrmacher, Esther S Soucy, Jean-Paul Skelin, Ivan Gratton, Alain Gauthier, Serge Rosa-Neto, Pedro |
| description | Molecular imaging offers unprecedented opportunities for investigating dynamic changes underlying neuropsychiatric conditions. Here, we evaluated whether [11C]ABP688, a positron emission tomography (PET) ligand that binds to the allosteric site of the metabotropic glutamate receptor type 5 (mGluR5), is sensitive to glutamate fluctuations after a pharmacological challenge. For this, we used ceftriaxone (CEF) administration in rats, an activator of the GLT-1 transporter (EAAT2), which is known to decrease extracellular levels of glutamate. MicroPET [11C]ABP688 dynamic acquisitions were conducted in rats after a venous injection of either saline (baseline) or CEF 200 mg/kg (challenge). Binding potentials (BPND) were obtained using the simplified reference tissue method. Between-condition statistical parametric maps indicating brain regions showing the highest CEF effects guided placement of microdialysis probes for subsequent assessment of extracellular levels of glutamate. The CEF administration increased [11C]ABP688 BPND in the thalamic ventral anterior (VA) nucleus bilaterally. Subsequent microdialysis assessment revealed declines in extracellular glutamate concentrations in the VA. The present results support the concept that availability of mGluR5 allosteric binding sites is sensitive to extracellular concentrations of glutamate. This interesting property of mGluR5 allosteric binding sites has potential applications for assessing the role of glutamate in the pathogenesis of neuropsychiatric conditions. |
| doi_str_mv | 10.1038/jcbfm.2015.35 |
| format | Article |
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Here, we evaluated whether [11C]ABP688, a positron emission tomography (PET) ligand that binds to the allosteric site of the metabotropic glutamate receptor type 5 (mGluR5), is sensitive to glutamate fluctuations after a pharmacological challenge. For this, we used ceftriaxone (CEF) administration in rats, an activator of the GLT-1 transporter (EAAT2), which is known to decrease extracellular levels of glutamate. MicroPET [11C]ABP688 dynamic acquisitions were conducted in rats after a venous injection of either saline (baseline) or CEF 200 mg/kg (challenge). Binding potentials (BPND) were obtained using the simplified reference tissue method. Between-condition statistical parametric maps indicating brain regions showing the highest CEF effects guided placement of microdialysis probes for subsequent assessment of extracellular levels of glutamate. The CEF administration increased [11C]ABP688 BPND in the thalamic ventral anterior (VA) nucleus bilaterally. Subsequent microdialysis assessment revealed declines in extracellular glutamate concentrations in the VA. The present results support the concept that availability of mGluR5 allosteric binding sites is sensitive to extracellular concentrations of glutamate. This interesting property of mGluR5 allosteric binding sites has potential applications for assessing the role of glutamate in the pathogenesis of neuropsychiatric conditions.</description><identifier>ISSN: 0271-678X</identifier><identifier>EISSN: 1559-7016</identifier><identifier>DOI: 10.1038/jcbfm.2015.35</identifier><identifier>PMID: 25806702</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Animals ; Carbon Radioisotopes - metabolism ; Ceftriaxone - pharmacology ; Excitatory Amino Acid Transporter 2 - metabolism ; Glutamic Acid - analysis ; Glutamic Acid - metabolism ; Original ; Oximes - metabolism ; Positron-Emission Tomography ; Pyridines - metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor, Metabotropic Glutamate 5 - metabolism ; Thalamus - metabolism</subject><ispartof>Journal of cerebral blood flow and metabolism, 2015-07, Vol.35 (7), p.1169-1174</ispartof><rights>2015 ISCBFM</rights><rights>Copyright Nature Publishing Group Jul 2015</rights><rights>Copyright © 2015 International Society for Cerebral Blood Flow & Metabolism, Inc. 2015 International Society for Cerebral Blood Flow & Metabolism, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c553t-2054d537aec45b7aa21a0f638cfa1806312104d23506479fc3eac3170f47ac1f3</citedby><cites>FETCH-LOGICAL-c553t-2054d537aec45b7aa21a0f638cfa1806312104d23506479fc3eac3170f47ac1f3</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/PMC4640271/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4640271/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,21819,27924,27925,43621,43622,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25806702$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zimmer, Eduardo R</creatorcontrib><creatorcontrib>Parent, Maxime J</creatorcontrib><creatorcontrib>Leuzy, Antoine</creatorcontrib><creatorcontrib>Aliaga, Antonio</creatorcontrib><creatorcontrib>Aliaga, Arturo</creatorcontrib><creatorcontrib>Moquin, Luc</creatorcontrib><creatorcontrib>Schirrmacher, Esther S</creatorcontrib><creatorcontrib>Soucy, Jean-Paul</creatorcontrib><creatorcontrib>Skelin, Ivan</creatorcontrib><creatorcontrib>Gratton, Alain</creatorcontrib><creatorcontrib>Gauthier, Serge</creatorcontrib><creatorcontrib>Rosa-Neto, Pedro</creatorcontrib><title>Imaging in Vivo Glutamate Fluctuations with [11C]ABP688: A GLT-1 Challenge with Ceftriaxone</title><title>Journal of cerebral blood flow and metabolism</title><addtitle>J Cereb Blood Flow Metab</addtitle><description>Molecular imaging offers unprecedented opportunities for investigating dynamic changes underlying neuropsychiatric conditions. Here, we evaluated whether [11C]ABP688, a positron emission tomography (PET) ligand that binds to the allosteric site of the metabotropic glutamate receptor type 5 (mGluR5), is sensitive to glutamate fluctuations after a pharmacological challenge. For this, we used ceftriaxone (CEF) administration in rats, an activator of the GLT-1 transporter (EAAT2), which is known to decrease extracellular levels of glutamate. MicroPET [11C]ABP688 dynamic acquisitions were conducted in rats after a venous injection of either saline (baseline) or CEF 200 mg/kg (challenge). Binding potentials (BPND) were obtained using the simplified reference tissue method. Between-condition statistical parametric maps indicating brain regions showing the highest CEF effects guided placement of microdialysis probes for subsequent assessment of extracellular levels of glutamate. The CEF administration increased [11C]ABP688 BPND in the thalamic ventral anterior (VA) nucleus bilaterally. Subsequent microdialysis assessment revealed declines in extracellular glutamate concentrations in the VA. The present results support the concept that availability of mGluR5 allosteric binding sites is sensitive to extracellular concentrations of glutamate. This interesting property of mGluR5 allosteric binding sites has potential applications for assessing the role of glutamate in the pathogenesis of neuropsychiatric conditions.</description><subject>Animals</subject><subject>Carbon Radioisotopes - metabolism</subject><subject>Ceftriaxone - pharmacology</subject><subject>Excitatory Amino Acid Transporter 2 - metabolism</subject><subject>Glutamic Acid - analysis</subject><subject>Glutamic Acid - metabolism</subject><subject>Original</subject><subject>Oximes - metabolism</subject><subject>Positron-Emission Tomography</subject><subject>Pyridines - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Metabotropic Glutamate 5 - metabolism</subject><subject>Thalamus - metabolism</subject><issn>0271-678X</issn><issn>1559-7016</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqF0c9rFDEUB_Agit1Wj14l4KUUZvteMklmPQjbwa6FhXqoIhQJb7OZ2Szzo05mqv73znZrqSJ4yiEfvi95X8ZeIUwRZHa6dauingpANZXqCZugUrPEAOqnbALCYKJN9uWAHca4BYBMKvWcHQiVgTYgJuz6oqYyNCUPDf8cblu-qIaeauo9P68G1w_Uh7aJ_HvoN_waMf86P_uos-wtn_PF8ipBnm-oqnxT-r3JfdF3gX60jX_BnhVURf_y_jxin87fX-UfkuXl4iKfLxOnlOwTASpdK2nIu1StDJFAgkLLzBWE4zslCoR0LaQCnZpZ4aQnJ9FAkRpyWMgj9m6fezOsar92vuk7quxNF2rqftqWgv3zpgkbW7a3NtXpbkVjwPF9QNd-G3zsbR2i81VFjW-HaMdZqEAq1P-neiaMEphmI33zF922Q9eMm7hTAMpoMapkr1zXxtj54uHdCHbXsL1r2O4atlKN_vXjzz7o35WO4GQPIpX-0ch_pv0Cy6StMA</recordid><startdate>20150701</startdate><enddate>20150701</enddate><creator>Zimmer, Eduardo R</creator><creator>Parent, Maxime J</creator><creator>Leuzy, Antoine</creator><creator>Aliaga, Antonio</creator><creator>Aliaga, Arturo</creator><creator>Moquin, Luc</creator><creator>Schirrmacher, Esther S</creator><creator>Soucy, Jean-Paul</creator><creator>Skelin, Ivan</creator><creator>Gratton, Alain</creator><creator>Gauthier, Serge</creator><creator>Rosa-Neto, Pedro</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><general>Nature Publishing Group</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>20150701</creationdate><title>Imaging in Vivo Glutamate Fluctuations with [11C]ABP688: A GLT-1 Challenge with Ceftriaxone</title><author>Zimmer, Eduardo R ; 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Here, we evaluated whether [11C]ABP688, a positron emission tomography (PET) ligand that binds to the allosteric site of the metabotropic glutamate receptor type 5 (mGluR5), is sensitive to glutamate fluctuations after a pharmacological challenge. For this, we used ceftriaxone (CEF) administration in rats, an activator of the GLT-1 transporter (EAAT2), which is known to decrease extracellular levels of glutamate. MicroPET [11C]ABP688 dynamic acquisitions were conducted in rats after a venous injection of either saline (baseline) or CEF 200 mg/kg (challenge). Binding potentials (BPND) were obtained using the simplified reference tissue method. Between-condition statistical parametric maps indicating brain regions showing the highest CEF effects guided placement of microdialysis probes for subsequent assessment of extracellular levels of glutamate. The CEF administration increased [11C]ABP688 BPND in the thalamic ventral anterior (VA) nucleus bilaterally. Subsequent microdialysis assessment revealed declines in extracellular glutamate concentrations in the VA. The present results support the concept that availability of mGluR5 allosteric binding sites is sensitive to extracellular concentrations of glutamate. This interesting property of mGluR5 allosteric binding sites has potential applications for assessing the role of glutamate in the pathogenesis of neuropsychiatric conditions.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>25806702</pmid><doi>10.1038/jcbfm.2015.35</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Carbon Radioisotopes - metabolism Ceftriaxone - pharmacology Excitatory Amino Acid Transporter 2 - metabolism Glutamic Acid - analysis Glutamic Acid - metabolism Original Oximes - metabolism Positron-Emission Tomography Pyridines - metabolism Rats Rats, Sprague-Dawley Receptor, Metabotropic Glutamate 5 - metabolism Thalamus - metabolism |
| title | Imaging in Vivo Glutamate Fluctuations with [11C]ABP688: A GLT-1 Challenge with Ceftriaxone |
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