Serotonergic regulation of the GABAergic transmission in the rat basal ganglia.
Identifieur interne : 001073 ( PubMed/Corpus ); précédent : 001072; suivant : 001074Serotonergic regulation of the GABAergic transmission in the rat basal ganglia.
Auteurs : Benjamin Di Cara ; Denise Samuel ; Pascal Salin ; Lydia Kerkerian-Le Goff ; Annie DaszutaSource :
- Synapse (New York, N.Y.) [ 0887-4476 ] ; 2003.
English descriptors
- KwdEn :
- 5,7-Dihydroxytryptamine, Animals, Basal Ganglia (metabolism), Extracellular Fluid (metabolism), Female, Glutamate Decarboxylase (genetics), Glutamate Decarboxylase (metabolism), Isoenzymes (genetics), Isoenzymes (metabolism), Membrane Potentials (physiology), Neural Inhibition (physiology), Neural Pathways (enzymology), Neurons (metabolism), Parkinson Disease (enzymology), Parkinson Disease (physiopathology), RNA Processing, Post-Transcriptional (physiology), RNA, Messenger (metabolism), Rats, Rats, Wistar, Serotonin (deficiency), Synaptic Transmission (physiology), gamma-Aminobutyric Acid (biosynthesis).
- MESH :
- chemical , biosynthesis : gamma-Aminobutyric Acid.
- chemical , deficiency : Serotonin.
- chemical , genetics : Glutamate Decarboxylase, Isoenzymes.
- chemical , metabolism : Glutamate Decarboxylase, Isoenzymes, RNA, Messenger.
- chemical : 5,7-Dihydroxytryptamine.
- enzymology : Neural Pathways, Parkinson Disease.
- metabolism : Basal Ganglia, Extracellular Fluid, Neurons.
- physiology : Membrane Potentials, Neural Inhibition, RNA Processing, Post-Transcriptional, Synaptic Transmission.
- physiopathology : Parkinson Disease.
- Animals, Female, Rats, Rats, Wistar.
Abstract
The GABAergic neurons represent a major neuronal population in the basal ganglia. Although alterations in serotonin (5-HT) transmission are associated with neurodegenerative diseases involving these regions, the influence exerted by 5-HT afferents on GABAergic populations remains poorly understood. Here, we examined the consequences of 5,7-dihydroxytryptamine-induced lesion of 5-HT neurons on glutamic acid decarboxylase (GAD) activity, mRNA expression of the two isoforms of the enzyme, GAD65 and GAD67, GABA uptake, and extracellular GABA levels in the striatum. The 5-HT depletion produced an increase in GAD activity without modifying GAD65 and GAD67 mRNA levels, suggesting that 5-HT acts at the posttranscriptional level to regulate striatal GABA synthesis. No change in GAD activity was measured in the main striatal target structures, the globus pallidus and substantia nigra. Striatal GABA uptake and extracellular levels of GABA measured under basal conditions in freely moving rats were maintained in a normal range following 5-HT deprivation. By contrast, depolarization-induced increases in extracellular levels of GABA were larger in the striatum of 5-HT-deprived rats than in controls, which may be accounted for by an increase in a releasable pool of GABA due to increased synthesis rate. Together, these results suggest that 5-HT afferents may exert a phasic inhibitory control on striatal GABA transmission. Therefore, a decrease in striatal 5-HT transmission in disease states, such as Parkinson's disease, may contribute to pathological changes in striatal GABA neuron activity by increasing their reactivity to depolarizing stimuli.
DOI: 10.1002/syn.10252
PubMed: 12923817
Links to Exploration step
pubmed:12923817Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Serotonergic regulation of the GABAergic transmission in the rat basal ganglia.</title><author><name sortKey="Di Cara, Benjamin" sort="Di Cara, Benjamin" uniqKey="Di Cara B" first="Benjamin" last="Di Cara">Benjamin Di Cara</name><affiliation><nlm:affiliation>Laboratoire de Neurobiology Cellulaire et Fonctionnelle, CNRS, Marseille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Samuel, Denise" sort="Samuel, Denise" uniqKey="Samuel D" first="Denise" last="Samuel">Denise Samuel</name></author><author><name sortKey="Salin, Pascal" sort="Salin, Pascal" uniqKey="Salin P" first="Pascal" last="Salin">Pascal Salin</name></author><author><name sortKey="Kerkerian Le Goff, Lydia" sort="Kerkerian Le Goff, Lydia" uniqKey="Kerkerian Le Goff L" first="Lydia" last="Kerkerian-Le Goff">Lydia Kerkerian-Le Goff</name></author><author><name sortKey="Daszuta, Annie" sort="Daszuta, Annie" uniqKey="Daszuta A" first="Annie" last="Daszuta">Annie Daszuta</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2003">2003</date><idno type="RBID">pubmed:12923817</idno><idno type="pmid">12923817</idno><idno type="doi">10.1002/syn.10252</idno><idno type="wicri:Area/PubMed/Corpus">001073</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001073</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Serotonergic regulation of the GABAergic transmission in the rat basal ganglia.</title><author><name sortKey="Di Cara, Benjamin" sort="Di Cara, Benjamin" uniqKey="Di Cara B" first="Benjamin" last="Di Cara">Benjamin Di Cara</name><affiliation><nlm:affiliation>Laboratoire de Neurobiology Cellulaire et Fonctionnelle, CNRS, Marseille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Samuel, Denise" sort="Samuel, Denise" uniqKey="Samuel D" first="Denise" last="Samuel">Denise Samuel</name></author><author><name sortKey="Salin, Pascal" sort="Salin, Pascal" uniqKey="Salin P" first="Pascal" last="Salin">Pascal Salin</name></author><author><name sortKey="Kerkerian Le Goff, Lydia" sort="Kerkerian Le Goff, Lydia" uniqKey="Kerkerian Le Goff L" first="Lydia" last="Kerkerian-Le Goff">Lydia Kerkerian-Le Goff</name></author><author><name sortKey="Daszuta, Annie" sort="Daszuta, Annie" uniqKey="Daszuta A" first="Annie" last="Daszuta">Annie Daszuta</name></author></analytic><series><title level="j">Synapse (New York, N.Y.)</title><idno type="ISSN">0887-4476</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>5,7-Dihydroxytryptamine</term><term>Animals</term><term>Basal Ganglia (metabolism)</term><term>Extracellular Fluid (metabolism)</term><term>Female</term><term>Glutamate Decarboxylase (genetics)</term><term>Glutamate Decarboxylase (metabolism)</term><term>Isoenzymes (genetics)</term><term>Isoenzymes (metabolism)</term><term>Membrane Potentials (physiology)</term><term>Neural Inhibition (physiology)</term><term>Neural Pathways (enzymology)</term><term>Neurons (metabolism)</term><term>Parkinson Disease (enzymology)</term><term>Parkinson Disease (physiopathology)</term><term>RNA Processing, Post-Transcriptional (physiology)</term><term>RNA, Messenger (metabolism)</term><term>Rats</term><term>Rats, Wistar</term><term>Serotonin (deficiency)</term><term>Synaptic Transmission (physiology)</term><term>gamma-Aminobutyric Acid (biosynthesis)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>gamma-Aminobutyric Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Serotonin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutamate Decarboxylase</term><term>Isoenzymes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutamate Decarboxylase</term><term>Isoenzymes</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>5,7-Dihydroxytryptamine</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Neural Pathways</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Basal Ganglia</term><term>Extracellular Fluid</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Membrane Potentials</term><term>Neural Inhibition</term><term>RNA Processing, Post-Transcriptional</term><term>Synaptic Transmission</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Rats</term><term>Rats, Wistar</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The GABAergic neurons represent a major neuronal population in the basal ganglia. Although alterations in serotonin (5-HT) transmission are associated with neurodegenerative diseases involving these regions, the influence exerted by 5-HT afferents on GABAergic populations remains poorly understood. Here, we examined the consequences of 5,7-dihydroxytryptamine-induced lesion of 5-HT neurons on glutamic acid decarboxylase (GAD) activity, mRNA expression of the two isoforms of the enzyme, GAD65 and GAD67, GABA uptake, and extracellular GABA levels in the striatum. The 5-HT depletion produced an increase in GAD activity without modifying GAD65 and GAD67 mRNA levels, suggesting that 5-HT acts at the posttranscriptional level to regulate striatal GABA synthesis. No change in GAD activity was measured in the main striatal target structures, the globus pallidus and substantia nigra. Striatal GABA uptake and extracellular levels of GABA measured under basal conditions in freely moving rats were maintained in a normal range following 5-HT deprivation. By contrast, depolarization-induced increases in extracellular levels of GABA were larger in the striatum of 5-HT-deprived rats than in controls, which may be accounted for by an increase in a releasable pool of GABA due to increased synthesis rate. Together, these results suggest that 5-HT afferents may exert a phasic inhibitory control on striatal GABA transmission. Therefore, a decrease in striatal 5-HT transmission in disease states, such as Parkinson's disease, may contribute to pathological changes in striatal GABA neuron activity by increasing their reactivity to depolarizing stimuli.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12923817</PMID><DateCreated><Year>2003</Year><Month>08</Month><Day>18</Day></DateCreated><DateCompleted><Year>2004</Year><Month>02</Month><Day>24</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0887-4476</ISSN><JournalIssue CitedMedium="Print"><Volume>50</Volume><Issue>2</Issue><PubDate><Year>2003</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Synapse (New York, N.Y.)</Title><ISOAbbreviation>Synapse</ISOAbbreviation></Journal><ArticleTitle>Serotonergic regulation of the GABAergic transmission in the rat basal ganglia.</ArticleTitle><Pagination><MedlinePgn>144-50</MedlinePgn></Pagination><Abstract><AbstractText>The GABAergic neurons represent a major neuronal population in the basal ganglia. Although alterations in serotonin (5-HT) transmission are associated with neurodegenerative diseases involving these regions, the influence exerted by 5-HT afferents on GABAergic populations remains poorly understood. Here, we examined the consequences of 5,7-dihydroxytryptamine-induced lesion of 5-HT neurons on glutamic acid decarboxylase (GAD) activity, mRNA expression of the two isoforms of the enzyme, GAD65 and GAD67, GABA uptake, and extracellular GABA levels in the striatum. The 5-HT depletion produced an increase in GAD activity without modifying GAD65 and GAD67 mRNA levels, suggesting that 5-HT acts at the posttranscriptional level to regulate striatal GABA synthesis. No change in GAD activity was measured in the main striatal target structures, the globus pallidus and substantia nigra. Striatal GABA uptake and extracellular levels of GABA measured under basal conditions in freely moving rats were maintained in a normal range following 5-HT deprivation. By contrast, depolarization-induced increases in extracellular levels of GABA were larger in the striatum of 5-HT-deprived rats than in controls, which may be accounted for by an increase in a releasable pool of GABA due to increased synthesis rate. Together, these results suggest that 5-HT afferents may exert a phasic inhibitory control on striatal GABA transmission. Therefore, a decrease in striatal 5-HT transmission in disease states, such as Parkinson's disease, may contribute to pathological changes in striatal GABA neuron activity by increasing their reactivity to depolarizing stimuli.</AbstractText><CopyrightInformation>Copyright 2003 Wiley-Liss, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Di Cara</LastName><ForeName>Benjamin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Laboratoire de Neurobiology Cellulaire et Fonctionnelle, CNRS, Marseille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Samuel</LastName><ForeName>Denise</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Salin</LastName><ForeName>Pascal</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Kerkerian-Le Goff</LastName><ForeName>Lydia</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Daszuta</LastName><ForeName>Annie</ForeName><Initials>A</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Synapse</MedlineTA><NlmUniqueID>8806914</NlmUniqueID><ISSNLinking>0887-4476</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007527">Isoenzymes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>31363-74-3</RegistryNumber><NameOfSubstance UI="D015116">5,7-Dihydroxytryptamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>333DO1RDJY</RegistryNumber><NameOfSubstance UI="D012701">Serotonin</NameOfSubstance></Chemical><Chemical><RegistryNumber>56-12-2</RegistryNumber><NameOfSubstance UI="D005680">gamma-Aminobutyric Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 4.1.1.15</RegistryNumber><NameOfSubstance UI="D005968">Glutamate Decarboxylase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 4.1.1.15</RegistryNumber><NameOfSubstance UI="C402565">glutamate decarboxylase 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 4.1.1.15</RegistryNumber><NameOfSubstance UI="C401141">glutamate decarboxylase 2</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015116" MajorTopicYN="N">5,7-Dihydroxytryptamine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001479" MajorTopicYN="N">Basal Ganglia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045604" MajorTopicYN="N">Extracellular Fluid</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005968" MajorTopicYN="N">Glutamate Decarboxylase</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007527" MajorTopicYN="N">Isoenzymes</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008564" MajorTopicYN="N">Membrane Potentials</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009433" MajorTopicYN="N">Neural Inhibition</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009434" MajorTopicYN="N">Neural Pathways</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012323" MajorTopicYN="N">RNA Processing, Post-Transcriptional</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017208" MajorTopicYN="N">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012701" MajorTopicYN="N">Serotonin</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="Y">deficiency</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009435" MajorTopicYN="N">Synaptic Transmission</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005680" MajorTopicYN="N">gamma-Aminobutyric Acid</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2003</Year><Month>8</Month><Day>19</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2004</Year><Month>2</Month><Day>26</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2003</Year><Month>8</Month><Day>19</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12923817</ArticleId><ArticleId IdType="doi">10.1002/syn.10252</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001073 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 001073 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonFranceV1
|flux= PubMed
|étape= Corpus
|type= RBID
|clé= pubmed:12923817
|texte= Serotonergic regulation of the GABAergic transmission in the rat basal ganglia.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:12923817" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonFranceV1
| This area was generated with Dilib version V0.6.29. |  |