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
Links to Exploration step
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<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>
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<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>
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<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>
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<term xml:id="k5">In Situ Hybridization</term>
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<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>
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<contentMeta><unparsedEditorialHistory>Received for publication December 19, 2000; accepted April 3, 2001.</unparsedEditorialHistory>
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<titleGroup><title type="main">Altered GABA<sub>A</sub>
Receptor Subunit and Splice Variant Expression in Rats Treated With Chronic Intermittent Ethanol</title>
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<creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Jennifer</givenNames>
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<creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Rachel F.</givenNames>
<familyName>Tyndale</familyName>
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<creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Maenghee Kang</givenNames>
<familyName>Park</familyName>
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<creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>Michael</givenNames>
<familyName>Fanselow</familyName>
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<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>
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<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>
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<noteGroup><note xml:id="n-fnt-1" numbered="no"><p>Supported by NIH grant AA07680 (RWO).</p>
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<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>
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<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>
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<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>
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<name type="personal"><namePart type="given">Richard W.</namePart>
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<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>
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<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>
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<physicalDescription><extent unit="references">55</extent>
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<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. 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>
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<topic>Dependence</topic>
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<topic>Plasticity</topic>
<topic>RT‐PCR</topic>
<topic>In Situ Hybridization</topic>
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<identifier type="ISSN">0145-6008</identifier>
<identifier type="eISSN">1530-0277</identifier>
<identifier type="DOI">10.1111/(ISSN)1530-0277</identifier>
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