Holeboard maze-learning deficits and brain monoaminergic neurotransmitter concentrations in rats after intracerebroventricular injection of 3-bromopyruvate
Identifieur interne : 000441 ( Main/Corpus ); précédent : 000440; suivant : 000442Holeboard maze-learning deficits and brain monoaminergic neurotransmitter concentrations in rats after intracerebroventricular injection of 3-bromopyruvate
Auteurs : L. Froelich ; A. Ding ; S. HoyerSource :
- Pharmacology, Biochemistry and Behavior [ 0091-3057 ] ; 1993.
Abstract
3-Bromopyruvate is a suicide inhibitor of pyruvate dehydrogenase complex in brain homogenates, and after intracerebral injection reduces acetylcholine tissue content and muscarinic cholinergic receptors in brain cortex and hippocampus for extended periods of time. A stereotaxic injection of 0.2 μmol 3-bromopyruvate was given twice into the cerebral ventricles of male Wistar rats. Ten weeks later, the animals were tested for learning deficits in a food-motivated complex holeboard test. 3-Bromopyruvate-treated rats showed an increased number of visits to nonfood-baited holes over a 5-day testing period (four trials per day) compared to sham-operated control rats, an increased number of visits to food-baited holes over the first 2 days of the testing period and an increased time for completing the task. There were no changes in brain monoaminergic neurotransmitter concentrations compared to controls. The results indicate that long-term learning deficits in a spatial discrimination paradigm are caused by 3-bromopyruvate, which might be related to a cholinergic deficit induced by a primary inhibition of brain glucose metabolism at the step of pyruvate dehydrogenase complex. This animal model may be useful for behavioral studies in relation to neurodegenerative diseases like dementia of Alzheimer type.
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DOI: 10.1016/0091-3057(95)00079-C
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Froelich</name><affiliation><mods:affiliation>Department of Psychiatry I, University of Frankfurt am Main, Heinrich-Hoffmanstr. 10, D-60528 Frankfurt am Main, Germany</mods:affiliation></affiliation></author><author><name sortKey="Ding, A" sort="Ding, A" uniqKey="Ding A" first="A." last="Ding">A. Ding</name><affiliation><mods:affiliation>Department of Pathochemistry and General Neurochemistry, University of Heidelberg, Heidelberg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hoyer, S" sort="Hoyer, S" uniqKey="Hoyer S" first="S." last="Hoyer">S. 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A stereotaxic injection of 0.2 μmol 3-bromopyruvate was given twice into the cerebral ventricles of male Wistar rats. Ten weeks later, the animals were tested for learning deficits in a food-motivated complex holeboard test. 3-Bromopyruvate-treated rats showed an increased number of visits to nonfood-baited holes over a 5-day testing period (four trials per day) compared to sham-operated control rats, an increased number of visits to food-baited holes over the first 2 days of the testing period and an increased time for completing the task. There were no changes in brain monoaminergic neurotransmitter concentrations compared to controls. The results indicate that long-term learning deficits in a spatial discrimination paradigm are caused by 3-bromopyruvate, which might be related to a cholinergic deficit induced by a primary inhibition of brain glucose metabolism at the step of pyruvate dehydrogenase complex. This animal model may be useful for behavioral studies in relation to neurodegenerative diseases like dementia of Alzheimer type.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>L. Froelich</name><affiliations><json:string>Department of Psychiatry I, University of Frankfurt am Main, Heinrich-Hoffmanstr. 10, D-60528 Frankfurt am Main, Germany</json:string></affiliations></json:item><json:item><name>A. Ding</name><affiliations><json:string>Department of Pathochemistry and General Neurochemistry, University of Heidelberg, Heidelberg, Germany</json:string></affiliations></json:item><json:item><name>S. Hoyer</name><affiliations><json:string>Department of Pathochemistry and General Neurochemistry, University of Heidelberg, Heidelberg, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>3-Bromopyruvate</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Pyruvate dehydrogenase complex</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Rats</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Holeboard maze</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Learning deficits</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Noradrenalin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Serotonin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dopamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Neurotransmitters</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cholinergic deficit</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dementia of Alzheimer type</value></json:item></subject><language><json:string>eng</json:string></language><abstract>3-Bromopyruvate is a suicide inhibitor of pyruvate dehydrogenase complex in brain homogenates, and after intracerebral injection reduces acetylcholine tissue content and muscarinic cholinergic receptors in brain cortex and hippocampus for extended periods of time. A stereotaxic injection of 0.2 μmol 3-bromopyruvate was given twice into the cerebral ventricles of male Wistar rats. Ten weeks later, the animals were tested for learning deficits in a food-motivated complex holeboard test. 3-Bromopyruvate-treated rats showed an increased number of visits to nonfood-baited holes over a 5-day testing period (four trials per day) compared to sham-operated control rats, an increased number of visits to food-baited holes over the first 2 days of the testing period and an increased time for completing the task. There were no changes in brain monoaminergic neurotransmitter concentrations compared to controls. The results indicate that long-term learning deficits in a spatial discrimination paradigm are caused by 3-bromopyruvate, which might be related to a cholinergic deficit induced by a primary inhibition of brain glucose metabolism at the step of pyruvate dehydrogenase complex. 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A stereotaxic injection of 0.2 μmol 3-bromopyruvate was given twice into the cerebral ventricles of male Wistar rats. Ten weeks later, the animals were tested for learning deficits in a food-motivated complex holeboard test. 3-Bromopyruvate-treated rats showed an increased number of visits to nonfood-baited holes over a 5-day testing period (four trials per day) compared to sham-operated control rats, an increased number of visits to food-baited holes over the first 2 days of the testing period and an increased time for completing the task. There were no changes in brain monoaminergic neurotransmitter concentrations compared to controls. The results indicate that long-term learning deficits in a spatial discrimination paradigm are caused by 3-bromopyruvate, which might be related to a cholinergic deficit induced by a primary inhibition of brain glucose metabolism at the step of pyruvate dehydrogenase complex. This animal model may be useful for behavioral studies in relation to neurodegenerative diseases like dementia of Alzheimer type.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>3-Bromopyruvate</term></item><item><term>Pyruvate dehydrogenase complex</term></item><item><term>Rats</term></item><item><term>Holeboard maze</term></item><item><term>Learning deficits</term></item><item><term>Noradrenalin</term></item><item><term>Serotonin</term></item><item><term>Dopamine</term></item><item><term>Neurotransmitters</term></item><item><term>Cholinergic deficit</term></item><item><term>Dementia of Alzheimer type</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1993-06-23">Received</change><change when="1993">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/35B33AE2293849F14FB357BCEEF44A5510E2E881/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>PBB</jid><aid>9500079C</aid><ce:pii>0091-3057(95)00079-C</ce:pii><ce:doi>10.1016/0091-3057(95)00079-C</ce:doi><ce:copyright type="unknown" year="1995"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Article</ce:textfn></ce:dochead><ce:title>Holeboard maze-learning deficits and brain monoaminergic neurotransmitter concentrations in rats after intracerebroventricular injection of 3-bromopyruvate</ce:title><ce:author-group><ce:author><ce:given-name>L.</ce:given-name><ce:surname>Froelich</ce:surname><ce:cross-ref refid="COR1"><ce:sup>1</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>A.</ce:given-name><ce:surname>Ding</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>‡</ce:sup></ce:cross-ref><ce:cross-ref refid="FN1"><ce:sup>2</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>S.</ce:given-name><ce:surname>Hoyer</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>‡</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>∗</ce:label><ce:textfn>Department of Psychiatry I, University of Frankfurt am Main, Heinrich-Hoffmanstr. 10, D-60528 Frankfurt am Main, Germany</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>‡</ce:label><ce:textfn>Department of Pathochemistry and General Neurochemistry, University of Heidelberg, Heidelberg, Germany</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>1</ce:label><ce:text>To whom requests for reprints should be addressed.</ce:text></ce:correspondence><ce:footnote id="FN1"><ce:label>2</ce:label><ce:note-para>Present address is: Boehringer Ingelheim KG, Ingelheim, Germany.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="23" month="6" year="1993"></ce:date-received><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>3-Bromopyruvate is a suicide inhibitor of pyruvate dehydrogenase complex in brain homogenates, and after intracerebral injection reduces acetylcholine tissue content and muscarinic cholinergic receptors in brain cortex and hippocampus for extended periods of time. A stereotaxic injection of 0.2 μmol 3-bromopyruvate was given twice into the cerebral ventricles of male Wistar rats. Ten weeks later, the animals were tested for learning deficits in a food-motivated complex holeboard test. 3-Bromopyruvate-treated rats showed an increased number of visits to nonfood-baited holes over a 5-day testing period (four trials per day) compared to sham-operated control rats, an increased number of visits to food-baited holes over the first 2 days of the testing period and an increased time for completing the task. There were no changes in brain monoaminergic neurotransmitter concentrations compared to controls. The results indicate that long-term learning deficits in a spatial discrimination paradigm are caused by 3-bromopyruvate, which might be related to a cholinergic deficit induced by a primary inhibition of brain glucose metabolism at the step of pyruvate dehydrogenase complex. This animal model may be useful for behavioral studies in relation to neurodegenerative diseases like dementia of Alzheimer type.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>3-Bromopyruvate</ce:text></ce:keyword><ce:keyword><ce:text>Pyruvate dehydrogenase complex</ce:text></ce:keyword><ce:keyword><ce:text>Rats</ce:text></ce:keyword><ce:keyword><ce:text>Holeboard maze</ce:text></ce:keyword><ce:keyword><ce:text>Learning deficits</ce:text></ce:keyword><ce:keyword><ce:text>Noradrenalin</ce:text></ce:keyword><ce:keyword><ce:text>Serotonin</ce:text></ce:keyword><ce:keyword><ce:text>Dopamine</ce:text></ce:keyword><ce:keyword><ce:text>Neurotransmitters</ce:text></ce:keyword><ce:keyword><ce:text>Cholinergic deficit</ce:text></ce:keyword><ce:keyword><ce:text>Dementia of Alzheimer type</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Holeboard maze-learning deficits and brain monoaminergic neurotransmitter concentrations in rats after intracerebroventricular injection of 3-bromopyruvate</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Holeboard maze-learning deficits and brain monoaminergic neurotransmitter concentrations in rats after intracerebroventricular injection of 3-bromopyruvate</title></titleInfo><name type="personal"><namePart type="given">L.</namePart><namePart type="family">Froelich</namePart><affiliation>Department of Psychiatry I, University of Frankfurt am Main, Heinrich-Hoffmanstr. 10, D-60528 Frankfurt am Main, Germany</affiliation><description>To whom requests for reprints should be addressed.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Ding</namePart><affiliation>Department of Pathochemistry and General Neurochemistry, University of Heidelberg, Heidelberg, Germany</affiliation><description>Present address is: Boehringer Ingelheim KG, Ingelheim, Germany.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Hoyer</namePart><affiliation>Department of Pathochemistry and General Neurochemistry, University of Heidelberg, Heidelberg, Germany</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">1993</dateIssued><dateCaptured encoding="w3cdtf">1993-06-23</dateCaptured><copyrightDate encoding="w3cdtf">1995</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">3-Bromopyruvate is a suicide inhibitor of pyruvate dehydrogenase complex in brain homogenates, and after intracerebral injection reduces acetylcholine tissue content and muscarinic cholinergic receptors in brain cortex and hippocampus for extended periods of time. A stereotaxic injection of 0.2 μmol 3-bromopyruvate was given twice into the cerebral ventricles of male Wistar rats. Ten weeks later, the animals were tested for learning deficits in a food-motivated complex holeboard test. 3-Bromopyruvate-treated rats showed an increased number of visits to nonfood-baited holes over a 5-day testing period (four trials per day) compared to sham-operated control rats, an increased number of visits to food-baited holes over the first 2 days of the testing period and an increased time for completing the task. There were no changes in brain monoaminergic neurotransmitter concentrations compared to controls. The results indicate that long-term learning deficits in a spatial discrimination paradigm are caused by 3-bromopyruvate, which might be related to a cholinergic deficit induced by a primary inhibition of brain glucose metabolism at the step of pyruvate dehydrogenase complex. 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