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Subthalamic Nucleus Lesion in Rats Prevents Dopaminergic Nigral Neuron Degeneration After Striatal 6‐OHDA Injection: Behavioural and Immunohistochemical Studies

Identifieur interne : 003165 ( Main/Corpus ); précédent : 003164; suivant : 003166

Subthalamic Nucleus Lesion in Rats Prevents Dopaminergic Nigral Neuron Degeneration After Striatal 6‐OHDA Injection: Behavioural and Immunohistochemical Studies

Auteurs : Brigitte Piallat ; Abdelhamid Benazzouz ; Alim Louis Benabid

Source :

RBID : ISTEX:DCFAC59007BA9B17DB0CC3E22F6A46001793F2C5

English descriptors

Abstract

Several studies have shown that antagonists of N‐methyl‐D‐aspartate receptors provide protection of the dopaminergic nigrostriatal pathway in animal models of Parkinson's disease. Since the substantia nigra compacta receives a moderate glutamatergic innervation from the subthalamic nucleus, we tried to determine whether subthalamic nucleus lesion could prevent the toxicity of the selective dopaminergic neurotoxin 6‐hydroxydopamine (6‐OHDA). Experiments were carried out on four groups of rats. Group 1 (n= 10) received a unilateral injection of 6‐hydroxydopamine in the striatum and group 2 (n= 10) received kainic acid in the subthalamic nucleus. Group 3 (n= 10) received an injection of kainic acid in the subthalamic nucleus and 1 week later an injection of 6‐OHDA in the striatum. Group 4 (n= 5) received the same treatment but kainic acid was replaced by saline. Apomorphine induced an ipsilateral rotation in rats of groups 2 and 3 and a contralateral rotation in rats of groups 1 and 4. The number of tyrosine hydroxylase‐immunoreactive cells in the pars compacta of the substantia nigra was not significantly different between injected and non‐injected sides in rats of groups 2 and 3, but was significantly decreased on the side ipsilateral to 6‐OHDA striatal injection in rats of groups 1 and 4. These results show that subthalamic nucleus lesion provides neuroprotection of the dopaminergic nigrostriatal pathway against 6‐OHDA toxicity and opens a new way for slowing or stopping the progression of Parkinson's disease.

Url:
DOI: 10.1111/j.1460-9568.1996.tb01603.x

Links to Exploration step

ISTEX:DCFAC59007BA9B17DB0CC3E22F6A46001793F2C5

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<affiliation>Laboratoire de Neurobiologie Préclinique, INSERM U.318, CHU, Pavillon B, BP 217, 38043 Grenoble Cedex 09, France</affiliation>
<description>Correspondence: B. Piallat, as above</description>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Abdelhamid</namePart>
<namePart type="family">Benazzouz</namePart>
<affiliation>Laboratoire de Neurobiologie Préclinique, INSERM U.318, CHU, Pavillon B, BP 217, 38043 Grenoble Cedex 09, France</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Alim Louis</namePart>
<namePart type="family">Benabid</namePart>
<affiliation>Laboratoire de Neurobiologie Préclinique, INSERM U.318, CHU, Pavillon B, BP 217, 38043 Grenoble Cedex 09, France</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<typeOfResource>text</typeOfResource>
<genre type="article" displayLabel="article"></genre>
<originInfo>
<publisher>Blackwell Publishing Ltd</publisher>
<place>
<placeTerm type="text">Oxford, UK</placeTerm>
</place>
<dateIssued encoding="w3cdtf">1996-07</dateIssued>
<edition>Received 31 July 1995, revised 29 January 1996, accepted 5 February 1996</edition>
<copyrightDate encoding="w3cdtf">1996</copyrightDate>
</originInfo>
<language>
<languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
</language>
<physicalDescription>
<internetMediaType>text/html</internetMediaType>
<extent unit="references">40</extent>
</physicalDescription>
<abstract lang="en">Several studies have shown that antagonists of N‐methyl‐D‐aspartate receptors provide protection of the dopaminergic nigrostriatal pathway in animal models of Parkinson's disease. Since the substantia nigra compacta receives a moderate glutamatergic innervation from the subthalamic nucleus, we tried to determine whether subthalamic nucleus lesion could prevent the toxicity of the selective dopaminergic neurotoxin 6‐hydroxydopamine (6‐OHDA). Experiments were carried out on four groups of rats. Group 1 (n= 10) received a unilateral injection of 6‐hydroxydopamine in the striatum and group 2 (n= 10) received kainic acid in the subthalamic nucleus. Group 3 (n= 10) received an injection of kainic acid in the subthalamic nucleus and 1 week later an injection of 6‐OHDA in the striatum. Group 4 (n= 5) received the same treatment but kainic acid was replaced by saline. Apomorphine induced an ipsilateral rotation in rats of groups 2 and 3 and a contralateral rotation in rats of groups 1 and 4. The number of tyrosine hydroxylase‐immunoreactive cells in the pars compacta of the substantia nigra was not significantly different between injected and non‐injected sides in rats of groups 2 and 3, but was significantly decreased on the side ipsilateral to 6‐OHDA striatal injection in rats of groups 1 and 4. These results show that subthalamic nucleus lesion provides neuroprotection of the dopaminergic nigrostriatal pathway against 6‐OHDA toxicity and opens a new way for slowing or stopping the progression of Parkinson's disease.</abstract>
<subject lang="en">
<genre>Keywords</genre>
<topic>substantia nigra</topic>
<topic>cell death</topic>
<topic>neuroprotection</topic>
<topic>Parkinson's disease</topic>
</subject>
<relatedItem type="host">
<titleInfo>
<title>European Journal of Neuroscience</title>
</titleInfo>
<genre type="Journal">journal</genre>
<identifier type="ISSN">0953-816X</identifier>
<identifier type="eISSN">1460-9568</identifier>
<identifier type="DOI">10.1111/(ISSN)1460-9568</identifier>
<identifier type="PublisherID">EJN</identifier>
<part>
<date>1996</date>
<detail type="volume">
<caption>vol.</caption>
<number>8</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>7</number>
</detail>
<extent unit="pages">
<start>1408</start>
<end>1414</end>
<total>7</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">DCFAC59007BA9B17DB0CC3E22F6A46001793F2C5</identifier>
<identifier type="DOI">10.1111/j.1460-9568.1996.tb01603.x</identifier>
<identifier type="ArticleID">EJN1408</identifier>
<recordInfo>
<recordContentSource>WILEY</recordContentSource>
<recordOrigin>Blackwell Publishing Ltd</recordOrigin>
</recordInfo>
</mods>
</metadata>
<serie></serie>
</istex>
</record>

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