Similar post-lesion receptor readjustments following the unilateral 6-hydroxydopamine lesion of the dopaminergic mesotelencephalic system in neonatal and adult rats
Identifieur interne : 001855 ( Istex/Corpus ); précédent : 001854; suivant : 001856Similar post-lesion receptor readjustments following the unilateral 6-hydroxydopamine lesion of the dopaminergic mesotelencephalic system in neonatal and adult rats
Auteurs : D. N. Abrous ; J. M. Rivet ; M. Le Moal ; J. P. HermanSource :
- Brain Research [ 0006-8993 ] ; 1990.
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Abstract
Abstract: The ascending dopaminergic system of adult or 3-day-old rats has been unilaterally lesioned by the intraparenchymal injection of 6-hydroxydopamine aimed at the medial forebrain bundle at the level of the level of the lateral hypothalamus. Nigral dopaminergic neurons disappeared following the lesion on the lesioned side in both experimental groups while the depletion of the ventral tegmental area was less extensive, especially following the neonatal lesion. Striatal regions were markedly depleted of their dopaminergic innervation, although the magnitude of the depletion was slightly higher following the adult stage lesion as judged on the basis of biochemical measurements (99% vs. 96%). Amphetamine (5 mg/kg) evoked an identical ipsilateral rotational response in both experimental groups. Moreover, this rotational response was blocked both by the specific D1 receptor blocker SCH-23390 (0.1 mg/kg) and the specific D2 receptor antagonist raclopride (2 mg/kg). Likewise, contralateral rotational responses to the directly acting D1 and D2 dopamine receptor agonists SKF-38393 (2.5 mg/kg) and LY-171555 (0.15 mg/kg) were similar in both experimental groups, both qualitatively and quantitatively. These results confirm conclusions obtained in earlier works, and indicate that reported differences in behavioral deficits between animals lesioned as neonates or adults are not related to differing modifications of striatal DA receptor sensitivities.
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DOI: 10.1016/0006-8993(90)91221-2
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<front><div type="abstract" xml:lang="en">Abstract: The ascending dopaminergic system of adult or 3-day-old rats has been unilaterally lesioned by the intraparenchymal injection of 6-hydroxydopamine aimed at the medial forebrain bundle at the level of the level of the lateral hypothalamus. Nigral dopaminergic neurons disappeared following the lesion on the lesioned side in both experimental groups while the depletion of the ventral tegmental area was less extensive, especially following the neonatal lesion. Striatal regions were markedly depleted of their dopaminergic innervation, although the magnitude of the depletion was slightly higher following the adult stage lesion as judged on the basis of biochemical measurements (99% vs. 96%). Amphetamine (5 mg/kg) evoked an identical ipsilateral rotational response in both experimental groups. Moreover, this rotational response was blocked both by the specific D1 receptor blocker SCH-23390 (0.1 mg/kg) and the specific D2 receptor antagonist raclopride (2 mg/kg). Likewise, contralateral rotational responses to the directly acting D1 and D2 dopamine receptor agonists SKF-38393 (2.5 mg/kg) and LY-171555 (0.15 mg/kg) were similar in both experimental groups, both qualitatively and quantitatively. These results confirm conclusions obtained in earlier works, and indicate that reported differences in behavioral deficits between animals lesioned as neonates or adults are not related to differing modifications of striatal DA receptor sensitivities.</div>
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<abstract xml:lang="en"><p>Abstract: The ascending dopaminergic system of adult or 3-day-old rats has been unilaterally lesioned by the intraparenchymal injection of 6-hydroxydopamine aimed at the medial forebrain bundle at the level of the level of the lateral hypothalamus. Nigral dopaminergic neurons disappeared following the lesion on the lesioned side in both experimental groups while the depletion of the ventral tegmental area was less extensive, especially following the neonatal lesion. Striatal regions were markedly depleted of their dopaminergic innervation, although the magnitude of the depletion was slightly higher following the adult stage lesion as judged on the basis of biochemical measurements (99% vs. 96%). Amphetamine (5 mg/kg) evoked an identical ipsilateral rotational response in both experimental groups. Moreover, this rotational response was blocked both by the specific D1 receptor blocker SCH-23390 (0.1 mg/kg) and the specific D2 receptor antagonist raclopride (2 mg/kg). Likewise, contralateral rotational responses to the directly acting D1 and D2 dopamine receptor agonists SKF-38393 (2.5 mg/kg) and LY-171555 (0.15 mg/kg) were similar in both experimental groups, both qualitatively and quantitatively. These results confirm conclusions obtained in earlier works, and indicate that reported differences in behavioral deficits between animals lesioned as neonates or adults are not related to differing modifications of striatal DA receptor sensitivities.</p>
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<item><term>Dopamine D1 receptor</term>
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<item><term>Dopamine D2 receptor</term>
</item>
<item><term>Dopamine</term>
</item>
<item><term>6-Hydroxydopamine</term>
</item>
<item><term>Neonatal lesion</term>
</item>
<item><term>Receptor hypersensitivity</term>
</item>
<item><term>Turning behavior</term>
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<item><term>Striatum</term>
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<head><ce:title>Similar post-lesion receptor readjustments following the unilateral 6-hydroxydopamine lesion of the dopaminergic mesotelencephalic system in neonatal and adult rats</ce:title>
<ce:author-group><ce:author><ce:given-name>D.N.</ce:given-name>
<ce:surname>Abrous</ce:surname>
</ce:author>
<ce:author><ce:given-name>J.M.</ce:given-name>
<ce:surname>Rivet</ce:surname>
</ce:author>
<ce:author><ce:given-name>M.</ce:given-name>
<ce:surname>Le Moal</ce:surname>
</ce:author>
<ce:author><ce:given-name>J.P.</ce:given-name>
<ce:surname>Herman</ce:surname>
<ce:cross-ref refid="cor1"><ce:sup loc="post">*</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:affiliation><ce:textfn>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</ce:textfn>
</ce:affiliation>
<ce:correspondence id="cor1"><ce:label>*</ce:label>
<ce:text><ce:italic>Correspondence:</ce:italic>
J.P. Herman, Inserm U-259-Universite´de Bordeaux II, Domaine de Carreire, rue Camille Saint-Sae¨ns, 33077 Bordeaux Cedex, France.</ce:text>
</ce:correspondence>
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<ce:date-accepted day="27" month="2" year="1990"></ce:date-accepted>
<ce:abstract id="ab1" class="author" xml:lang="en"><ce:section-title>Abstract</ce:section-title>
<ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">The ascending dopaminergic system of adult or 3-day-old rats has been unilaterally lesioned by the intraparenchymal injection of 6-hydroxydopamine aimed at the medial forebrain bundle at the level of the level of the lateral hypothalamus. Nigral dopaminergic neurons disappeared following the lesion on the lesioned side in both experimental groups while the depletion of the ventral tegmental area was less extensive, especially following the neonatal lesion. Striatal regions were markedly depleted of their dopaminergic innervation, although the magnitude of the depletion was slightly higher following the adult stage lesion as judged on the basis of biochemical measurements (99% vs. 96%). Amphetamine (5 mg/kg) evoked an identical ipsilateral rotational response in both experimental groups. Moreover, this rotational response was blocked both by the specific D<ce:inf loc="post">1</ce:inf>
receptor blocker SCH-23390 (0.1 mg/kg) and the specific D<ce:inf loc="post">2</ce:inf>
receptor antagonist raclopride (2 mg/kg). Likewise, contralateral rotational responses to the directly acting D<ce:inf loc="post">1</ce:inf>
and D<ce:inf loc="post">2</ce:inf>
dopamine receptor agonists SKF-38393 (2.5 mg/kg) and LY-171555 (0.15 mg/kg) were similar in both experimental groups, both qualitatively and quantitatively. These results confirm conclusions obtained in earlier works, and indicate that reported differences in behavioral deficits between animals lesioned as neonates or adults are not related to differing modifications of striatal DA receptor sensitivities.</ce:simple-para>
</ce:abstract-sec>
</ce:abstract>
<ce:keywords class="keyword" xml:lang="en"><ce:section-title>Keywords</ce:section-title>
<ce:keyword><ce:text>Dopamine D<ce:inf loc="post">1</ce:inf>
receptor</ce:text>
</ce:keyword>
<ce:keyword><ce:text>Dopamine D<ce:inf loc="post">2</ce:inf>
receptor</ce:text>
</ce:keyword>
<ce:keyword><ce:text>Dopamine</ce:text>
</ce:keyword>
<ce:keyword><ce:text>6-Hydroxydopamine</ce:text>
</ce:keyword>
<ce:keyword><ce:text>Neonatal lesion</ce:text>
</ce:keyword>
<ce:keyword><ce:text>Receptor hypersensitivity</ce:text>
</ce:keyword>
<ce:keyword><ce:text>Turning behavior</ce:text>
</ce:keyword>
<ce:keyword><ce:text>Striatum</ce:text>
</ce:keyword>
</ce:keywords>
</head>
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<mods version="3.6"><titleInfo lang="en"><title>Similar post-lesion receptor readjustments following the unilateral 6-hydroxydopamine lesion of the dopaminergic mesotelencephalic system in neonatal and adult rats</title>
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<titleInfo type="alternative" lang="en" contentType="CDATA"><title>Similar post-lesion receptor readjustments following the unilateral 6-hydroxydopamine lesion of the dopaminergic mesotelencephalic system in neonatal and adult rats</title>
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<name type="personal"><namePart type="given">D.N.</namePart>
<namePart type="family">Abrous</namePart>
<affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</affiliation>
<role><roleTerm type="text">author</roleTerm>
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</name>
<name type="personal"><namePart type="given">J.M.</namePart>
<namePart type="family">Rivet</namePart>
<affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</affiliation>
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<name type="personal"><namePart type="given">M.</namePart>
<namePart type="family">Le Moal</namePart>
<affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<name type="personal"><namePart type="given">J.P.</namePart>
<namePart type="family">Herman</namePart>
<affiliation>INSERM U-259-Universite´de Bordeaux II, Bordeaux France</affiliation>
<description>Correspondence: J.P. Herman, Inserm U-259-Universite´de Bordeaux II, Domaine de Carreire, rue Camille Saint-Sae¨ns, 33077 Bordeaux Cedex, France.</description>
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<abstract lang="en">Abstract: The ascending dopaminergic system of adult or 3-day-old rats has been unilaterally lesioned by the intraparenchymal injection of 6-hydroxydopamine aimed at the medial forebrain bundle at the level of the level of the lateral hypothalamus. Nigral dopaminergic neurons disappeared following the lesion on the lesioned side in both experimental groups while the depletion of the ventral tegmental area was less extensive, especially following the neonatal lesion. Striatal regions were markedly depleted of their dopaminergic innervation, although the magnitude of the depletion was slightly higher following the adult stage lesion as judged on the basis of biochemical measurements (99% vs. 96%). Amphetamine (5 mg/kg) evoked an identical ipsilateral rotational response in both experimental groups. Moreover, this rotational response was blocked both by the specific D1 receptor blocker SCH-23390 (0.1 mg/kg) and the specific D2 receptor antagonist raclopride (2 mg/kg). Likewise, contralateral rotational responses to the directly acting D1 and D2 dopamine receptor agonists SKF-38393 (2.5 mg/kg) and LY-171555 (0.15 mg/kg) were similar in both experimental groups, both qualitatively and quantitatively. These results confirm conclusions obtained in earlier works, and indicate that reported differences in behavioral deficits between animals lesioned as neonates or adults are not related to differing modifications of striatal DA receptor sensitivities.</abstract>
<subject lang="en"><genre>Keywords</genre>
<topic>Dopamine D1 receptor</topic>
<topic>Dopamine D2 receptor</topic>
<topic>Dopamine</topic>
<topic>6-Hydroxydopamine</topic>
<topic>Neonatal lesion</topic>
<topic>Receptor hypersensitivity</topic>
<topic>Turning behavior</topic>
<topic>Striatum</topic>
</subject>
<relatedItem type="host"><titleInfo><title>Brain Research</title>
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<titleInfo type="abbreviated"><title>BRES</title>
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<originInfo><dateIssued encoding="w3cdtf">19900903</dateIssued>
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<identifier type="ISSN">0006-8993</identifier>
<identifier type="PII">S0006-8993(00)X0710-X</identifier>
<part><date>19900903</date>
<detail type="volume"><number>526</number>
<caption>vol.</caption>
</detail>
<detail type="issue"><number>2</number>
<caption>no.</caption>
</detail>
<extent unit="issue pages"><start>181</start>
<end>362</end>
</extent>
<extent unit="pages"><start>195</start>
<end>202</end>
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<identifier type="DOI">10.1016/0006-8993(90)91221-2</identifier>
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<identifier type="ArticleID">90912212</identifier>
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