Altered GABAA Receptor Subunit and Splice Variant Expression in Rats Treated With Chronic Intermittent Ethanol
Identifieur interne : 001C02 ( Istex/Corpus ); précédent : 001C01; suivant : 001C03Altered GABAA Receptor Subunit and Splice Variant Expression in Rats Treated With Chronic Intermittent Ethanol
Auteurs : Jennifer Petrie ; Douglas W. Sapp ; Rachel F. Tyndale ; Maenghee Kang Park ; Michael Fanselow ; Richard W. OlsenSource :
- Alcoholism: Clinical and Experimental Research [ 0145-6008 ] ; 2001-06.
Abstract
Background: Intermittent chronic administration of ethanol to rats has been shown previously to produce a hyperexcitable, kindling‐like state, accompanied by reduced inhibitory synaptic transmission in the hippocampus and changes in γ‐aminobutyric acid type A (GABAA) receptors. Further information is needed on the detailed changes in GABAA receptors and their time course and persistence, as is comparison to changes after chronic, continuous ethanol. Methods: GABAA receptors were analyzed in the rat brain after chronic intermittent ethanol (CIE) by using radioligand binding, photoaffinity labeling of polypeptides, and estimates of messenger RNA (mRNA) levels of receptor subunits by reverse transcriptase–polymerase chain reaction (RT‐PCR) and in situ hybridization. Results: CIE rats were confirmed to have increased GABAA receptor binding of the benzodiazepine partial inverse agonist and ethanol antidote ligand Ro15‐4513, due to increased expression of the α6 subunit polypeptide in the cerebellum, shown by photoaffinity labeling. Estimates of mRNA levels by use of RT‐PCR did not reveal any significant increase in α6 or in several other receptor subunits in several brain regions, but a decrease in the ratio of the long and short splice variants (L/S) of the γ2 subunit was detected in the hippocampus, especially the CA1 region. Conclusions: Changes in GABAA receptors were found in rats given CIE. Increased α6 subunit in the cerebellum was demonstrated by using both the binding to diazepam‐insensitive sites for [3H]Ro15‐4513 and increased levels of the 57‐kDa α6 polypeptide after photoaffinity labeling with this ligand. This increase appeared after 30 doses of ethanol and decayed to normal 1 week after ethanol was discontinued. The transient change in cerebellar α6 subunit‐containing receptors, also reportedly seen after chronic continuous ethanol, is thus unlikely to account for the persistently hyperexcitable, kindled, seizure‐susceptible state seen in CIE. However, the significant decrease in γ2 subunit L/S splice variant ratio in the hippocampus implies changes in GABAA receptor function, possibly involving protein phosphorylation by protein kinase C. Altered receptor trafficking and turnover associated with synaptic plasticity may contribute to the observed reduced inhibition in the hippocampus and other signs of alcohol dependence produced by CIE.
Url:
DOI: 10.1111/j.1530-0277.2001.tb02285.x
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Sapp</name><affiliation><mods:affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</mods:affiliation></affiliation></author><author><name sortKey="Tyndale, Rachel F" sort="Tyndale, Rachel F" uniqKey="Tyndale R" first="Rachel F." last="Tyndale">Rachel F. Tyndale</name><affiliation><mods:affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</mods:affiliation></affiliation></author><author><name sortKey="Park, Maenghee Kang" sort="Park, Maenghee Kang" uniqKey="Park M" first="Maenghee Kang" last="Park">Maenghee Kang Park</name><affiliation><mods:affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</mods:affiliation></affiliation></author><author><name sortKey="Fanselow, Michael" sort="Fanselow, Michael" uniqKey="Fanselow M" first="Michael" last="Fanselow">Michael Fanselow</name><affiliation><mods:affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</mods:affiliation></affiliation></author><author><name sortKey="Olsen, Richard W" sort="Olsen, Richard W" uniqKey="Olsen R" first="Richard W." last="Olsen">Richard W. Olsen</name><affiliation><mods:affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: rolsen@mednet.ucla.edu</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:9E9282EFE9CDAF874DCB86920298CA4C096B7B51</idno><date when="2001" year="2001">2001</date><idno type="doi">10.1111/j.1530-0277.2001.tb02285.x</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-L7ZDWW0L-L/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001C02</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001C02</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Altered GABAA Receptor Subunit and Splice Variant Expression in Rats Treated With Chronic Intermittent Ethanol</title><author><name sortKey="Petrie, Jennifer" sort="Petrie, Jennifer" uniqKey="Petrie J" first="Jennifer" last="Petrie">Jennifer Petrie</name><affiliation><mods:affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</mods:affiliation></affiliation></author><author><name sortKey="Sapp, Douglas W" sort="Sapp, Douglas W" uniqKey="Sapp D" first="Douglas W." last="Sapp">Douglas W. Sapp</name><affiliation><mods:affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</mods:affiliation></affiliation></author><author><name sortKey="Tyndale, Rachel F" sort="Tyndale, Rachel F" uniqKey="Tyndale R" first="Rachel F." last="Tyndale">Rachel F. Tyndale</name><affiliation><mods:affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</mods:affiliation></affiliation></author><author><name sortKey="Park, Maenghee Kang" sort="Park, Maenghee Kang" uniqKey="Park M" first="Maenghee Kang" last="Park">Maenghee Kang Park</name><affiliation><mods:affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</mods:affiliation></affiliation></author><author><name sortKey="Fanselow, Michael" sort="Fanselow, Michael" uniqKey="Fanselow M" first="Michael" last="Fanselow">Michael Fanselow</name><affiliation><mods:affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</mods:affiliation></affiliation></author><author><name sortKey="Olsen, Richard W" sort="Olsen, Richard W" uniqKey="Olsen R" first="Richard W." last="Olsen">Richard W. Olsen</name><affiliation><mods:affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: rolsen@mednet.ucla.edu</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Alcoholism: Clinical and Experimental Research</title><title level="j" type="alt">ALCOHOLISM CLINICAL EXPERIMENTAL RESEARCH</title><idno type="ISSN">0145-6008</idno><idno type="eISSN">1530-0277</idno><imprint><biblScope unit="vol">25</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="819">819</biblScope><biblScope unit="page" to="828">828</biblScope><biblScope unit="page-count">10</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2001-06">2001-06</date></imprint><idno type="ISSN">0145-6008</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0145-6008</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background: Intermittent chronic administration of ethanol to rats has been shown previously to produce a hyperexcitable, kindling‐like state, accompanied by reduced inhibitory synaptic transmission in the hippocampus and changes in γ‐aminobutyric acid type A (GABAA) receptors. Further information is needed on the detailed changes in GABAA receptors and their time course and persistence, as is comparison to changes after chronic, continuous ethanol. Methods: GABAA receptors were analyzed in the rat brain after chronic intermittent ethanol (CIE) by using radioligand binding, photoaffinity labeling of polypeptides, and estimates of messenger RNA (mRNA) levels of receptor subunits by reverse transcriptase–polymerase chain reaction (RT‐PCR) and in situ hybridization. Results: CIE rats were confirmed to have increased GABAA receptor binding of the benzodiazepine partial inverse agonist and ethanol antidote ligand Ro15‐4513, due to increased expression of the α6 subunit polypeptide in the cerebellum, shown by photoaffinity labeling. Estimates of mRNA levels by use of RT‐PCR did not reveal any significant increase in α6 or in several other receptor subunits in several brain regions, but a decrease in the ratio of the long and short splice variants (L/S) of the γ2 subunit was detected in the hippocampus, especially the CA1 region. Conclusions: Changes in GABAA receptors were found in rats given CIE. Increased α6 subunit in the cerebellum was demonstrated by using both the binding to diazepam‐insensitive sites for [3H]Ro15‐4513 and increased levels of the 57‐kDa α6 polypeptide after photoaffinity labeling with this ligand. This increase appeared after 30 doses of ethanol and decayed to normal 1 week after ethanol was discontinued. The transient change in cerebellar α6 subunit‐containing receptors, also reportedly seen after chronic continuous ethanol, is thus unlikely to account for the persistently hyperexcitable, kindled, seizure‐susceptible state seen in CIE. However, the significant decrease in γ2 subunit L/S splice variant ratio in the hippocampus implies changes in GABAA receptor function, possibly involving protein phosphorylation by protein kinase C. Altered receptor trafficking and turnover associated with synaptic plasticity may contribute to the observed reduced inhibition in the hippocampus and other signs of alcohol dependence produced by CIE.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>subunit</json:string><json:string>receptor</json:string><json:string>ethanol</json:string><json:string>gabaa</json:string><json:string>mrna</json:string><json:string>hippocampus</json:string><json:string>cerebellum</json:string><json:string>benzodiazepine</json:string><json:string>gabaa receptor</json:string><json:string>pharmacol</json:string><json:string>kang</json:string><json:string>chronic ethanol</json:string><json:string>ticku</json:string><json:string>hippocampal</json:string><json:string>hybridization</json:string><json:string>agonist</json:string><json:string>devaud</json:string><json:string>photoaffinity</json:string><json:string>mhatre</json:string><json:string>kokka</json:string><json:string>bmax</json:string><json:string>neurosci</json:string><json:string>kindling</json:string><json:string>pharmacology</json:string><json:string>polypeptide</json:string><json:string>control animal</json:string><json:string>diazepam</json:string><json:string>splice variant</json:string><json:string>chronic intermittent ethanol</json:string><json:string>splice</json:string><json:string>mckernan</json:string><json:string>hippocampal formation</json:string><json:string>sapp</json:string><json:string>mahmoudi</json:string><json:string>alcohol clin</json:string><json:string>chronic ethanol administration</json:string><json:string>olsen</json:string><json:string>neuron</json:string><json:string>dos</json:string><json:string>subunit mrna</json:string><json:string>alcohol dependence</json:string><json:string>cerebral cortex</json:string><json:string>total binding</json:string><json:string>binding site</json:string><json:string>brain region</json:string><json:string>significant increase</json:string><json:string>morrow</json:string><json:string>pyramidal cell</json:string><json:string>subunit expression</json:string><json:string>rat change gabaa receptor</json:string><json:string>benzodiazepine agonist</json:string><json:string>neuroactive steroid</json:string><json:string>scatchard analysis</json:string><json:string>significant decrease</json:string><json:string>protein kinase</json:string><json:string>aminobutyric acid type</json:string><json:string>significant change</json:string><json:string>mrna level</json:string><json:string>ethanol withdrawal</json:string><json:string>subunit mrna level</json:string><json:string>chronic intermittent ethanol treatment</json:string><json:string>rat</json:string><json:string>intermittent</json:string><json:string>chronic</json:string><json:string>homogenate</json:string></teeft></keywords><author><json:item><name>Jennifer Petrie</name><affiliations><json:string>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</json:string></affiliations></json:item><json:item><name>Douglas W. Sapp</name><affiliations><json:string>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</json:string></affiliations></json:item><json:item><name>Rachel F. Tyndale</name><affiliations><json:string>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</json:string></affiliations></json:item><json:item><name>Maenghee Kang Park</name><affiliations><json:string>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</json:string></affiliations></json:item><json:item><name>Michael Fanselow</name><affiliations><json:string>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</json:string></affiliations></json:item><json:item><name>Richard W. Olsen</name><affiliations><json:string>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</json:string><json:string>E-mail: rolsen@mednet.ucla.edu</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Dependence</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Kindling</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Plasticity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>RT‐PCR</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>In Situ Hybridization</value></json:item></subject><articleId><json:string>ACER819</json:string></articleId><arkIstex>ark:/67375/WNG-L7ZDWW0L-L</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Background: Intermittent chronic administration of ethanol to rats has been shown previously to produce a hyperexcitable, kindling‐like state, accompanied by reduced inhibitory synaptic transmission in the hippocampus and changes in γ‐aminobutyric acid type A (GABAA) receptors. Further information is needed on the detailed changes in GABAA receptors and their time course and persistence, as is comparison to changes after chronic, continuous ethanol. Methods: GABAA receptors were analyzed in the rat brain after chronic intermittent ethanol (CIE) by using radioligand binding, photoaffinity labeling of polypeptides, and estimates of messenger RNA (mRNA) levels of receptor subunits by reverse transcriptase–polymerase chain reaction (RT‐PCR) and in situ hybridization. Results: CIE rats were confirmed to have increased GABAA receptor binding of the benzodiazepine partial inverse agonist and ethanol antidote ligand Ro15‐4513, due to increased expression of the α6 subunit polypeptide in the cerebellum, shown by photoaffinity labeling. Estimates of mRNA levels by use of RT‐PCR did not reveal any significant increase in α6 or in several other receptor subunits in several brain regions, but a decrease in the ratio of the long and short splice variants (L/S) of the γ2 subunit was detected in the hippocampus, especially the CA1 region. Conclusions: Changes in GABAA receptors were found in rats given CIE. Increased α6 subunit in the cerebellum was demonstrated by using both the binding to diazepam‐insensitive sites for [3H]Ro15‐4513 and increased levels of the 57‐kDa α6 polypeptide after photoaffinity labeling with this ligand. This increase appeared after 30 doses of ethanol and decayed to normal 1 week after ethanol was discontinued. The transient change in cerebellar α6 subunit‐containing receptors, also reportedly seen after chronic continuous ethanol, is thus unlikely to account for the persistently hyperexcitable, kindled, seizure‐susceptible state seen in CIE. However, the significant decrease in γ2 subunit L/S splice variant ratio in the hippocampus implies changes in GABAA receptor function, possibly involving protein phosphorylation by protein kinase C. Altered receptor trafficking and turnover associated with synaptic plasticity may contribute to the observed reduced inhibition in the hippocampus and other signs of alcohol dependence produced by CIE.</abstract><qualityIndicators><score>10</score><pdfWordCount>7362</pdfWordCount><pdfCharCount>44516</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>10</pdfPageCount><pdfPageSize>585 x 781 pts</pdfPageSize><pdfWordsPerPage>736</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>342</abstractWordCount><abstractCharCount>2389</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Altered GABAA Receptor Subunit and Splice Variant Expression in Rats Treated With Chronic Intermittent Ethanol</title><pmid><json:string>11410716</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Alcoholism: Clinical and Experimental Research</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1530-0277</json:string></doi><issn><json:string>0145-6008</json:string></issn><eissn><json:string>1530-0277</json:string></eissn><publisherId><json:string>ACER</json:string></publisherId><volume>25</volume><issue>6</issue><pages><first>819</first><last>828</last><total>10</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2001</json:string><json:string>35S</json:string></date><geogName></geogName><orgName><json:string>University of Toronto</json:string><json:string>DWS</json:string><json:string>Department of Neurology, Duke University, Durham, North Carolina</json:string><json:string>Department of Molecular</json:string><json:string>Department of Neuroscience, University of Rochester, Rochester, New York</json:string><json:string>University of California, Los Angeles</json:string><json:string>Department of Pharmacology</json:string><json:string>Gemini Biotechnology</json:string><json:string>Research Society on Alcoholism</json:string><json:string>JP</json:string><json:string>Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Jennifer Petrie</json:string><json:string>E. Hoffman</json:string><json:string>Time Dependence</json:string><json:string>Bmax</json:string><json:string>Rachel F. Tyndale</json:string><json:string>Michael Fanselow</json:string><json:string>Charles Young</json:string><json:string>S. Levels</json:string><json:string>Douglas W. Sapp</json:string><json:string>Kang Park</json:string><json:string>A.J. Tobin</json:string><json:string>Richard W. Olsen</json:string></persName><placeName><json:string>Rochester</json:string><json:string>Germany</json:string><json:string>NY</json:string><json:string>St. Catherines</json:string><json:string>IN</json:string><json:string>Pittsburgh</json:string><json:string>Canada</json:string><json:string>Boston</json:string><json:string>Toronto</json:string><json:string>Los Angeles</json:string><json:string>CA</json:string><json:string>MA</json:string><json:string>Alachua</json:string><json:string>FL</json:string><json:string>Indianapolis</json:string><json:string>PA</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Turner et al., 1991</json:string><json:string>Wang et al., 1999</json:string><json:string>Devaud et al., 1996</json:string><json:string>Montpied et al., 1991</json:string><json:string>Mihic et al., 1997</json:string><json:string>Connolly et al., 1999</json:string><json:string>Morrow et al., 1992</json:string><json:string>Hu and Ticku, 1997</json:string><json:string>Kang et al., 1996, 1998</json:string><json:string>Devaud et al., 1995, 1997</json:string><json:string>Sapp et al., 1992</json:string><json:string>Mhatre et al., 1988</json:string><json:string>Devaud et al. 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the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</addrLine><country key="CA" xml:lang="en">CANADA</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Douglas W.</forename><surname>Sapp</surname></persName><affiliation><orgName type="division">Departments of Molecular and Medical Pharmacology (JP</orgName><address><addrLine>DWS</addrLine><addrLine>RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</addrLine><country key="CA" xml:lang="en">CANADA</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Rachel F.</forename><surname>Tyndale</surname></persName><affiliation><orgName type="division">Departments of Molecular and Medical Pharmacology (JP</orgName><address><addrLine>DWS</addrLine><addrLine>RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</addrLine><country key="CA" xml:lang="en">CANADA</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Maenghee Kang</forename><surname>Park</surname></persName><affiliation><orgName type="division">Departments of Molecular and Medical Pharmacology (JP</orgName><address><addrLine>DWS</addrLine><addrLine>RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</addrLine><country key="CA" xml:lang="en">CANADA</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Michael</forename><surname>Fanselow</surname></persName><affiliation><orgName type="division">Departments of Molecular and Medical Pharmacology (JP</orgName><address><addrLine>DWS</addrLine><addrLine>RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</addrLine><country key="CA" xml:lang="en">CANADA</country></address></affiliation></author><author xml:id="author-0005" role="corresp"><persName><forename type="first">Richard W.</forename><surname>Olsen</surname></persName><affiliation><orgName type="division">Departments of Molecular and Medical Pharmacology (JP</orgName><address><addrLine>DWS</addrLine><addrLine>RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</addrLine><country key="CA" xml:lang="en">CANADA</country></address></affiliation></author><idno type="istex">9E9282EFE9CDAF874DCB86920298CA4C096B7B51</idno><idno type="ark">ark:/67375/WNG-L7ZDWW0L-L</idno><idno type="DOI">10.1111/j.1530-0277.2001.tb02285.x</idno><idno type="unit">ACER819</idno><idno type="toTypesetVersion">file:ACER.ACER819.pdf</idno></analytic><monogr><title level="j" type="main">Alcoholism: Clinical and Experimental Research</title><title level="j" type="alt">ALCOHOLISM CLINICAL EXPERIMENTAL RESEARCH</title><idno type="pISSN">0145-6008</idno><idno type="eISSN">1530-0277</idno><idno type="book-DOI">10.1111/(ISSN)1530-0277</idno><idno type="book-part-DOI">10.1111/acer.2001.25.issue-6</idno><idno type="product">ACER</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">25</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="819">819</biblScope><biblScope unit="page" to="828">828</biblScope><biblScope unit="page-count">10</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2001-06"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><encodingDesc><schemaRef type="ODD" url="https://xml-schema.delivery.istex.fr/tei-istex.odd"></schemaRef><appInfo><application ident="pub2tei" version="1.0.10" when="2019-12-20"><label>pub2TEI-ISTEX</label><desc>A set of style sheets for converting XML documents encoded in various scientific publisher formats into a common TEI format.
<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract xml:lang="en" style="main"><p><hi rend="bold">Background: </hi> Intermittent chronic administration of ethanol to rats has been shown previously to produce a hyperexcitable, kindling‐like state, accompanied by reduced inhibitory synaptic transmission in the hippocampus and changes in γ‐aminobutyric acid type A (GABA<hi rend="subscript">A</hi>) receptors. Further information is needed on the detailed changes in GABA<hi rend="subscript">A</hi> receptors and their time course and persistence, as is comparison to changes after chronic, continuous ethanol.</p><p><hi rend="bold">Methods: </hi> GABA<hi rend="subscript">A</hi> receptors were analyzed in the rat brain after chronic intermittent ethanol (CIE) by using radioligand binding, photoaffinity labeling of polypeptides, and estimates of messenger RNA (mRNA) levels of receptor subunits by reverse transcriptase–polymerase chain reaction (RT‐PCR) and in situ hybridization.</p><p><hi rend="bold">Results: </hi> CIE rats were confirmed to have increased GABA<hi rend="subscript">A</hi> receptor binding of the benzodiazepine partial inverse agonist and ethanol antidote ligand Ro15‐4513, due to increased expression of the α6 subunit polypeptide in the cerebellum, shown by photoaffinity labeling. Estimates of mRNA levels by use of RT‐PCR did not reveal any significant increase in α6 or in several other receptor subunits in several brain regions, but a decrease in the ratio of the long and short splice variants (L/S) of the γ2 subunit was detected in the hippocampus, especially the CA1 region.</p><p><hi rend="bold">Conclusions: </hi> Changes in GABA<hi rend="subscript">A</hi> receptors were found in rats given CIE. Increased α6 subunit in the cerebellum was demonstrated by using both the binding to diazepam‐insensitive sites for [<hi rend="superscript">3</hi>H]Ro15‐4513 and increased levels of the 57‐kDa α6 polypeptide after photoaffinity labeling with this ligand. This increase appeared after 30 doses of ethanol and decayed to normal 1 week after ethanol was discontinued. The transient change in cerebellar α6 subunit‐containing receptors, also reportedly seen after chronic continuous ethanol, is thus unlikely to account for the persistently hyperexcitable, kindled, seizure‐susceptible state seen in CIE. However, the significant decrease in γ2 subunit L/S splice variant ratio in the hippocampus implies changes in GABA<hi rend="subscript">A</hi> receptor function, possibly involving protein phosphorylation by protein kinase C. Altered receptor trafficking and turnover associated with synaptic plasticity may contribute to the observed reduced inhibition in the hippocampus and other signs of alcohol dependence produced by CIE.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">Dependence</term><term xml:id="k2">Kindling</term><term xml:id="k3">Plasticity</term><term xml:id="k4">RT‐PCR</term><term xml:id="k5">In Situ Hybridization</term></keywords><keywords rend="tocHeading1"><term>Genetics and Molecular Biology</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-L7ZDWW0L-L/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1530-0277</doi><issn type="print">0145-6008</issn><issn type="electronic">1530-0277</issn><idGroup><id type="product" value="ACER"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ALCOHOLISM CLINICAL EXPERIMENTAL RESEARCH">Alcoholism: Clinical and Experimental Research</title></titleGroup></publicationMeta><publicationMeta level="part" position="06006"><doi origin="wiley">10.1111/acer.2001.25.issue-6</doi><numberingGroup><numbering type="journalVolume" number="25">25</numbering><numbering type="journalIssue" number="6">6</numbering></numberingGroup><coverDate startDate="2001-06">June 2001</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0081900" status="forIssue"><doi origin="wiley">10.1111/j.1530-0277.2001.tb02285.x</doi><idGroup><id type="unit" value="ACER819"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="tocHeading1">Genetics and Molecular Biology</title></titleGroup><eventGroup><event type="firstOnline" date="2006-04-11"></event><event type="publishedOnlineFinalForm" date="2006-04-11"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-02"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2013-12-31"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="819">819</numbering><numbering type="pageLast" number="828">828</numbering></numberingGroup><correspondenceTo>Reprint requests: Richard W. Olsen, Department of Molecular & Medical Pharmacology, UCLA School of Medicine, Room CHS 23‐120, 650 Charles Young Dr., Los Angeles, CA 90095‐1735; Fax: 310‐267‐2003; E‐mail: <email>rolsen@mednet.ucla.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ACER.ACER819.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received for publication December 19, 2000; accepted April 3, 2001.</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="55"></count><count type="linksCrossRef" number="7"></count></countGroup><titleGroup><title type="main">Altered GABA<sub>A</sub> Receptor Subunit and Splice Variant Expression in Rats Treated With Chronic Intermittent Ethanol</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Jennifer</givenNames><familyName>Petrie</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Douglas W.</givenNames><familyName>Sapp</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Rachel F.</givenNames><familyName>Tyndale</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Maenghee Kang</givenNames><familyName>Park</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>Michael</givenNames><familyName>Fanselow</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1" corresponding="yes"><personName><givenNames>Richard W.</givenNames><familyName>Olsen</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="CA"><unparsedAffiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Dependence</keyword><keyword xml:id="k2">Kindling</keyword><keyword xml:id="k3">Plasticity</keyword><keyword xml:id="k4">RT‐PCR</keyword><keyword xml:id="k5">In Situ Hybridization</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>Background: </b> Intermittent chronic administration of ethanol to rats has been shown previously to produce a hyperexcitable, kindling‐like state, accompanied by reduced inhibitory synaptic transmission in the hippocampus and changes in γ‐aminobutyric acid type A (GABA<sub>A</sub>) receptors. Further information is needed on the detailed changes in GABA<sub>A</sub> receptors and their time course and persistence, as is comparison to changes after chronic, continuous ethanol.</p><p><b>Methods: </b> GABA<sub>A</sub> receptors were analyzed in the rat brain after chronic intermittent ethanol (CIE) by using radioligand binding, photoaffinity labeling of polypeptides, and estimates of messenger RNA (mRNA) levels of receptor subunits by reverse transcriptase–polymerase chain reaction (RT‐PCR) and in situ hybridization.</p><p><b>Results: </b> CIE rats were confirmed to have increased GABA<sub>A</sub> receptor binding of the benzodiazepine partial inverse agonist and ethanol antidote ligand Ro15‐4513, due to increased expression of the α6 subunit polypeptide in the cerebellum, shown by photoaffinity labeling. Estimates of mRNA levels by use of RT‐PCR did not reveal any significant increase in α6 or in several other receptor subunits in several brain regions, but a decrease in the ratio of the long and short splice variants (L/S) of the γ2 subunit was detected in the hippocampus, especially the CA1 region.</p><p><b>Conclusions: </b> Changes in GABA<sub>A</sub> receptors were found in rats given CIE. Increased α6 subunit in the cerebellum was demonstrated by using both the binding to diazepam‐insensitive sites for [<sup>3</sup>H]Ro15‐4513 and increased levels of the 57‐kDa α6 polypeptide after photoaffinity labeling with this ligand. This increase appeared after 30 doses of ethanol and decayed to normal 1 week after ethanol was discontinued. The transient change in cerebellar α6 subunit‐containing receptors, also reportedly seen after chronic continuous ethanol, is thus unlikely to account for the persistently hyperexcitable, kindled, seizure‐susceptible state seen in CIE. However, the significant decrease in γ2 subunit L/S splice variant ratio in the hippocampus implies changes in GABA<sub>A</sub> receptor function, possibly involving protein phosphorylation by protein kinase C. Altered receptor trafficking and turnover associated with synaptic plasticity may contribute to the observed reduced inhibition in the hippocampus and other signs of alcohol dependence produced by CIE.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="n-fnt-1" numbered="no"><p>Supported by NIH grant AA07680 (RWO).</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Altered GABAA Receptor Subunit and Splice Variant Expression in Rats Treated With Chronic Intermittent Ethanol</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Altered GABAA Receptor Subunit and Splice Variant Expression in Rats Treated With Chronic Intermittent Ethanol</title></titleInfo><name type="personal"><namePart type="given">Jennifer</namePart><namePart type="family">Petrie</namePart><affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Douglas W.</namePart><namePart type="family">Sapp</namePart><affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rachel F.</namePart><namePart type="family">Tyndale</namePart><affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Maenghee Kang</namePart><namePart type="family">Park</namePart><affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Fanselow</namePart><affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Richard W.</namePart><namePart type="family">Olsen</namePart><affiliation>Departments of Molecular and Medical Pharmacology (JP, DWS, RFT, MKP, RWO) and Psychology (JP, MF), University of California, Los Angeles, California; the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania (JP); the Department of Neuroscience, University of Rochester, Rochester, New York (DWS); the Department of Pharmacology and the Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada (RFT); and the Department of Neurology, Duke University, Durham, North Carolina.</affiliation><affiliation>E-mail: rolsen@mednet.ucla.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2001-06</dateIssued><edition>Received for publication December 19, 2000; accepted April 3, 2001.</edition><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="references">55</extent><extent unit="linksCrossRef">7</extent></physicalDescription><abstract lang="en">Background: Intermittent chronic administration of ethanol to rats has been shown previously to produce a hyperexcitable, kindling‐like state, accompanied by reduced inhibitory synaptic transmission in the hippocampus and changes in γ‐aminobutyric acid type A (GABAA) receptors. Further information is needed on the detailed changes in GABAA receptors and their time course and persistence, as is comparison to changes after chronic, continuous ethanol. Methods: GABAA receptors were analyzed in the rat brain after chronic intermittent ethanol (CIE) by using radioligand binding, photoaffinity labeling of polypeptides, and estimates of messenger RNA (mRNA) levels of receptor subunits by reverse transcriptase–polymerase chain reaction (RT‐PCR) and in situ hybridization. Results: CIE rats were confirmed to have increased GABAA receptor binding of the benzodiazepine partial inverse agonist and ethanol antidote ligand Ro15‐4513, due to increased expression of the α6 subunit polypeptide in the cerebellum, shown by photoaffinity labeling. Estimates of mRNA levels by use of RT‐PCR did not reveal any significant increase in α6 or in several other receptor subunits in several brain regions, but a decrease in the ratio of the long and short splice variants (L/S) of the γ2 subunit was detected in the hippocampus, especially the CA1 region. Conclusions: Changes in GABAA receptors were found in rats given CIE. Increased α6 subunit in the cerebellum was demonstrated by using both the binding to diazepam‐insensitive sites for [3H]Ro15‐4513 and increased levels of the 57‐kDa α6 polypeptide after photoaffinity labeling with this ligand. This increase appeared after 30 doses of ethanol and decayed to normal 1 week after ethanol was discontinued. The transient change in cerebellar α6 subunit‐containing receptors, also reportedly seen after chronic continuous ethanol, is thus unlikely to account for the persistently hyperexcitable, kindled, seizure‐susceptible state seen in CIE. However, the significant decrease in γ2 subunit L/S splice variant ratio in the hippocampus implies changes in GABAA receptor function, possibly involving protein phosphorylation by protein kinase C. 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|texte= Altered GABAA Receptor Subunit and Splice Variant Expression in Rats Treated With Chronic Intermittent Ethanol
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