Endogenous GABA mediates presynaptic inhibition of spontaneous and evoked excitatory synaptic potentials in the rat neostriatum
Identifieur interne : 000C36 ( Istex/Corpus ); précédent : 000C35; suivant : 000C37Endogenous GABA mediates presynaptic inhibition of spontaneous and evoked excitatory synaptic potentials in the rat neostriatum
Auteurs : P. Calabresi ; N. B. Mercuri ; M. De Murtas ; G. BernardiSource :
- Neuroscience Letters [ 0304-3940 ] ; 1990.
Abstract
The effect of the blockade of the γ-aminobutyric acid (GABA) uptake system on the amplitude of glutamatergic synaptic potentials was studied by using a corticostriatal slice preparation. Nipecotic acid (0.1–1 mM), a GABA uptake blocker, produced a dose-dependent decrease of the amplitude of kynurenate-sensitive excitatory synaptic potentials recorded in the neostriatum following cortical stimulation. Nipecotic acid did not affect the postsynaptic responses to exogenously applied glutamate. The presynaptic effect of endogenous GABA was bicuculline-resistant and was mimicked by baclofen (0.3–3 μM). This effect was not blocked by phaclofen (0.5–1 mM). These findings show that phaclofen-insensitive GABAB receptors, activated by endogenous GABA, mediate presynaptic inhibition of cortical glutamatergic inputs in the neostriatum.
Url:
DOI: 10.1016/0304-3940(90)90258-B
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Sanità, 2a Università di Roma, Rome Italy</mods:affiliation></affiliation></author><author><name sortKey="Mercuri, N B" sort="Mercuri, N B" uniqKey="Mercuri N" first="N. B." last="Mercuri">N. B. Mercuri</name><affiliation><mods:affiliation>Clinica Neurologica, Dip. Sanità, 2a Università di Roma, Rome Italy</mods:affiliation></affiliation></author><author><name sortKey="De Murtas, M" sort="De Murtas, M" uniqKey="De Murtas M" first="M." last="De Murtas">M. De Murtas</name><affiliation><mods:affiliation>Clinica Neurologica, Dip. Sanità, 2a Università di Roma, Rome Italy</mods:affiliation></affiliation></author><author><name sortKey="Bernardi, G" sort="Bernardi, G" uniqKey="Bernardi G" first="G." last="Bernardi">G. Bernardi</name><affiliation><mods:affiliation>Clinica Neurologica, Dip. 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Nipecotic acid (0.1–1 mM), a GABA uptake blocker, produced a dose-dependent decrease of the amplitude of kynurenate-sensitive excitatory synaptic potentials recorded in the neostriatum following cortical stimulation. Nipecotic acid did not affect the postsynaptic responses to exogenously applied glutamate. The presynaptic effect of endogenous GABA was bicuculline-resistant and was mimicked by baclofen (0.3–3 μM). This effect was not blocked by phaclofen (0.5–1 mM). These findings show that phaclofen-insensitive GABAB receptors, activated by endogenous GABA, mediate presynaptic inhibition of cortical glutamatergic inputs in the neostriatum.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>P. Calabresi</name><affiliations><json:string>Clinica Neurologica, Dip. Sanità, 2a Università di Roma, Rome Italy</json:string></affiliations></json:item><json:item><name>N.B. Mercuri</name><affiliations><json:string>Clinica Neurologica, Dip. 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Nipecotic acid (0.1–1 mM), a GABA uptake blocker, produced a dose-dependent decrease of the amplitude of kynurenate-sensitive excitatory synaptic potentials recorded in the neostriatum following cortical stimulation. Nipecotic acid did not affect the postsynaptic responses to exogenously applied glutamate. The presynaptic effect of endogenous GABA was bicuculline-resistant and was mimicked by baclofen (0.3–3 μM). This effect was not blocked by phaclofen (0.5–1 mM). 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Calabresi, Clinica Neurologica, Dip. Sanità Publica, 2a Università di Roma, Via O. Raimondo 00173, Rome, Italy.</p></note><affiliation>Clinica Neurologica, Dip. Sanità, 2a Università di Roma, Rome Italy</affiliation></author><author xml:id="author-2"><persName><forename type="first">N.B.</forename><surname>Mercuri</surname></persName><affiliation>Clinica Neurologica, Dip. Sanità, 2a Università di Roma, Rome Italy</affiliation></author><author xml:id="author-3"><persName><forename type="first">M.</forename><surname>De Murtas</surname></persName><affiliation>Clinica Neurologica, Dip. Sanità, 2a Università di Roma, Rome Italy</affiliation></author><author xml:id="author-4"><persName><forename type="first">G.</forename><surname>Bernardi</surname></persName><affiliation>Clinica Neurologica, Dip. Sanità, 2a Università di Roma, Rome Italy</affiliation></author></analytic><monogr><title level="j">Neuroscience Letters</title><title level="j" type="abbrev">NSL</title><idno type="pISSN">0304-3940</idno><idno type="PII">S0304-3940(00)X0540-X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1990"></date><biblScope unit="volume">118</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="99">99</biblScope><biblScope unit="page" to="102">102</biblScope></imprint></monogr><idno type="istex">A2C8A98AE03CBBD344735B1CBA4B311F9368D061</idno><idno type="DOI">10.1016/0304-3940(90)90258-B</idno><idno type="PII">0304-3940(90)90258-B</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1990</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The effect of the blockade of the γ-aminobutyric acid (GABA) uptake system on the amplitude of glutamatergic synaptic potentials was studied by using a corticostriatal slice preparation. Nipecotic acid (0.1–1 mM), a GABA uptake blocker, produced a dose-dependent decrease of the amplitude of kynurenate-sensitive excitatory synaptic potentials recorded in the neostriatum following cortical stimulation. Nipecotic acid did not affect the postsynaptic responses to exogenously applied glutamate. The presynaptic effect of endogenous GABA was bicuculline-resistant and was mimicked by baclofen (0.3–3 μM). This effect was not blocked by phaclofen (0.5–1 mM). These findings show that phaclofen-insensitive GABAB receptors, activated by endogenous GABA, mediate presynaptic inhibition of cortical glutamatergic inputs in the neostriatum.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>GABAB receptor</term></item><item><term>Nipecotic acid</term></item><item><term>Glutamate</term></item><item><term>Neostriatum</term></item><item><term>Intracellular recording</term></item><item><term>Huntington's disease</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1990-06-15">Modified</change><change when="1990">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/A2C8A98AE03CBBD344735B1CBA4B311F9368D061/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>NSL</jid><aid>9090258B</aid><ce:pii>0304-3940(90)90258-B</ce:pii><ce:doi>10.1016/0304-3940(90)90258-B</ce:doi><ce:copyright type="unknown" year="1990"></ce:copyright></item-info><head><ce:title>Endogenous GABA mediates presynaptic inhibition of spontaneous and evoked excitatory synaptic potentials in the rat neostriatum</ce:title><ce:author-group><ce:author><ce:given-name>P.</ce:given-name><ce:surname>Calabresi</ce:surname><ce:cross-ref refid="COR1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>N.B.</ce:given-name><ce:surname>Mercuri</ce:surname></ce:author><ce:author><ce:given-name>M.</ce:given-name><ce:surname>De Murtas</ce:surname></ce:author><ce:author><ce:given-name>G.</ce:given-name><ce:surname>Bernardi</ce:surname></ce:author><ce:affiliation><ce:textfn>Clinica Neurologica, Dip. Sanità, 2<ce:sup>a</ce:sup> Università di Roma, Rome Italy</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>1</ce:label><ce:text>Correspondence: P. Calabresi, Clinica Neurologica, Dip. Sanità Publica, 2<ce:sup>a</ce:sup> Università di Roma, Via O. Raimondo 00173, Rome, Italy.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="25" month="4" year="1990"></ce:date-received><ce:date-revised day="15" month="6" year="1990"></ce:date-revised><ce:date-accepted day="18" month="6" year="1990"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The effect of the blockade of the γ-aminobutyric acid (GABA) uptake system on the amplitude of glutamatergic synaptic potentials was studied by using a corticostriatal slice preparation. Nipecotic acid (0.1–1 mM), a GABA uptake blocker, produced a dose-dependent decrease of the amplitude of kynurenate-sensitive excitatory synaptic potentials recorded in the neostriatum following cortical stimulation. Nipecotic acid did not affect the postsynaptic responses to exogenously applied glutamate. The presynaptic effect of endogenous GABA was bicuculline-resistant and was mimicked by baclofen (0.3–3 μM). This effect was not blocked by phaclofen (0.5–1 mM). These findings show that phaclofen-insensitive GABA<ce:inf>B</ce:inf> receptors, activated by endogenous GABA, mediate presynaptic inhibition of cortical glutamatergic inputs in the neostriatum.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>GABA<ce:inf>B</ce:inf> receptor</ce:text></ce:keyword><ce:keyword><ce:text>Nipecotic acid</ce:text></ce:keyword><ce:keyword><ce:text>Glutamate</ce:text></ce:keyword><ce:keyword><ce:text>Neostriatum</ce:text></ce:keyword><ce:keyword><ce:text>Intracellular recording</ce:text></ce:keyword><ce:keyword><ce:text>Huntington's disease</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Endogenous GABA mediates presynaptic inhibition of spontaneous and evoked excitatory synaptic potentials in the rat neostriatum</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Endogenous GABA mediates presynaptic inhibition of spontaneous and evoked excitatory synaptic potentials in the rat neostriatum</title></titleInfo><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Calabresi</namePart><affiliation>Clinica Neurologica, Dip. Sanità, 2a Università di Roma, Rome Italy</affiliation><description>Correspondence: P. Calabresi, Clinica Neurologica, Dip. Sanità Publica, 2a Università di Roma, Via O. Raimondo 00173, Rome, Italy.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.B.</namePart><namePart type="family">Mercuri</namePart><affiliation>Clinica Neurologica, Dip. Sanità, 2a Università di Roma, Rome Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">De Murtas</namePart><affiliation>Clinica Neurologica, Dip. Sanità, 2a Università di Roma, Rome Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Bernardi</namePart><affiliation>Clinica Neurologica, Dip. Sanità, 2a Università di Roma, Rome Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1990</dateIssued><dateModified encoding="w3cdtf">1990-06-15</dateModified><copyrightDate encoding="w3cdtf">1990</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">The effect of the blockade of the γ-aminobutyric acid (GABA) uptake system on the amplitude of glutamatergic synaptic potentials was studied by using a corticostriatal slice preparation. Nipecotic acid (0.1–1 mM), a GABA uptake blocker, produced a dose-dependent decrease of the amplitude of kynurenate-sensitive excitatory synaptic potentials recorded in the neostriatum following cortical stimulation. Nipecotic acid did not affect the postsynaptic responses to exogenously applied glutamate. The presynaptic effect of endogenous GABA was bicuculline-resistant and was mimicked by baclofen (0.3–3 μM). This effect was not blocked by phaclofen (0.5–1 mM). These findings show that phaclofen-insensitive GABAB receptors, activated by endogenous GABA, mediate presynaptic inhibition of cortical glutamatergic inputs in the neostriatum.</abstract><subject><genre>Keywords</genre><topic>GABAB receptor</topic><topic>Nipecotic acid</topic><topic>Glutamate</topic><topic>Neostriatum</topic><topic>Intracellular recording</topic><topic>Huntington's disease</topic></subject><relatedItem type="host"><titleInfo><title>Neuroscience Letters</title></titleInfo><titleInfo type="abbreviated"><title>NSL</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">19901002</dateIssued></originInfo><identifier type="ISSN">0304-3940</identifier><identifier type="PII">S0304-3940(00)X0540-X</identifier><part><date>19901002</date><detail type="volume"><number>118</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>140</end></extent><extent unit="pages"><start>99</start><end>102</end></extent></part></relatedItem><identifier type="istex">A2C8A98AE03CBBD344735B1CBA4B311F9368D061</identifier><identifier type="DOI">10.1016/0304-3940(90)90258-B</identifier><identifier type="PII">0304-3940(90)90258-B</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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