Locomotor effects of imidazoline I2-site-specific ligands and monoamine oxidase inhibitors in rats with a unilateral 6-hydroxydopamine lesion of the nigrostriatal pathway
Identifieur interne : 001167 ( Main/Exploration ); précédent : 001166; suivant : 001168Locomotor effects of imidazoline I2-site-specific ligands and monoamine oxidase inhibitors in rats with a unilateral 6-hydroxydopamine lesion of the nigrostriatal pathway
Auteurs : Nicholas Macinnes ; Susan DutySource :
- British Journal of Pharmacology [ 0007-1188 ] ; 2004.
Abstract
The present study examined the ability of the selective imidazoline I2-site ligands 2-(-2-benzofuranyl)-2-imidazoline (2-BFI) and 2-[4,5-dihydroimidaz-2-yl]-quinoline (BU224) and selected monoamine oxidase (MAO) inhibitors to evoke locomotor activity in rats bearing a lesion of the nigrostriatal pathway. Male Sprague–Dawley rats were injected with 12.5 Intraperitoneal (i.p.) administration of the irreversible MAO-B inhibitor deprenyl (20 mg kg−1) or the imidazoline I2-site ligands BU224 (14 mg kg−1) and 2-BFI (7 and 14 mg kg−1) produced significant increases in ipsiversive rotations compared to vehicle controls totaling, at the highest respective doses tested, 521±120, 131±37 and 92.5±16.3 net contraversive rotations in 30 (deprenyl) or 60 (BU224 and 2-BFI) min. In contrast, the reversible MAO-A inhibitor moclobemide (2.5–10 mg kg−1) and the reversible MAO-B inhibitor lazabemide (2.5–10 mg kg−1) failed to instigate significant rotational behaviour compared to vehicle. Coadministration of lazabemide (10 mg kg−1), moclobemide (10 mg kg−1) or 2-BFI (14 mg kg−1) with These data suggest that I2-specific ligands have dual effects in the 6-OHDA-lesioned rat model of Parkinson's disease; a first effect associated with an increase in activity in the intact hemisphere, probably
Url:
DOI: 10.1038/sj.bjp.0706019
PubMed: 15545290
PubMed Central: 1575965
Affiliations:
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Le document en format XML
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-site-specific ligands and monoamine oxidase inhibitors in rats with a unilateral 6-hydroxydopamine lesion of the nigrostriatal pathway</title>
<author><name sortKey="Macinnes, Nicholas" sort="Macinnes, Nicholas" uniqKey="Macinnes N" first="Nicholas" last="Macinnes">Nicholas Macinnes</name>
<affiliation><nlm:aff id="aff1"><sup>1</sup>
Wolfson Centre for Age-Related Diseases, G20 Wolfson Wing, Hodgkin Building, Guy's Campus, GKT School of Biomedical Sciences, King's College London, London SE1 1UL</nlm:aff>
<wicri:noCountry code="subfield">London SE1 1UL</wicri:noCountry>
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<author><name sortKey="Duty, Susan" sort="Duty, Susan" uniqKey="Duty S" first="Susan" last="Duty">Susan Duty</name>
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Wolfson Centre for Age-Related Diseases, G20 Wolfson Wing, Hodgkin Building, Guy's Campus, GKT School of Biomedical Sciences, King's College London, London SE1 1UL</nlm:aff>
<wicri:noCountry code="subfield">London SE1 1UL</wicri:noCountry>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Locomotor effects of imidazoline I<sub>2</sub>
-site-specific ligands and monoamine oxidase inhibitors in rats with a unilateral 6-hydroxydopamine lesion of the nigrostriatal pathway</title>
<author><name sortKey="Macinnes, Nicholas" sort="Macinnes, Nicholas" uniqKey="Macinnes N" first="Nicholas" last="Macinnes">Nicholas Macinnes</name>
<affiliation><nlm:aff id="aff1"><sup>1</sup>
Wolfson Centre for Age-Related Diseases, G20 Wolfson Wing, Hodgkin Building, Guy's Campus, GKT School of Biomedical Sciences, King's College London, London SE1 1UL</nlm:aff>
<wicri:noCountry code="subfield">London SE1 1UL</wicri:noCountry>
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<author><name sortKey="Duty, Susan" sort="Duty, Susan" uniqKey="Duty S" first="Susan" last="Duty">Susan Duty</name>
<affiliation><nlm:aff id="aff1"><sup>1</sup>
Wolfson Centre for Age-Related Diseases, G20 Wolfson Wing, Hodgkin Building, Guy's Campus, GKT School of Biomedical Sciences, King's College London, London SE1 1UL</nlm:aff>
<wicri:noCountry code="subfield">London SE1 1UL</wicri:noCountry>
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<series><title level="j">British Journal of Pharmacology</title>
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<front><div type="abstract" xml:lang="en"><p><list list-type="order"><list-item><p>The present study examined the ability of the selective imidazoline I<sub>2</sub>
-site ligands 2-(-2-benzofuranyl)-2-imidazoline (2-BFI) and 2-[4,5-dihydroimidaz-2-yl]-quinoline (BU224) and selected monoamine oxidase (MAO) inhibitors to evoke locomotor activity in rats bearing a lesion of the nigrostriatal pathway.</p>
</list-item>
<list-item><p>Male Sprague–Dawley rats were injected with 12.5 <italic>μ</italic>
g 6-hydroxydopamine (6-OHDA) into the right median forebrain bundle to induce a unilateral lesion of the nigrostriatal tract. After 6 weeks, test drugs were administered either alone or in combination with <sc>L</sc>
-DOPA (<sc>L</sc>
-3,4-dihydroxyphenylamine) and the circling behaviour of animals was monitored as an index of anti-Parkinsonian activity.</p>
</list-item>
<list-item><p>Intraperitoneal (i.p.) administration of the irreversible MAO-B inhibitor deprenyl (20 mg kg<sup>−1</sup>
) or the imidazoline I<sub>2</sub>
-site ligands BU224 (14 mg kg<sup>−1</sup>
) and 2-BFI (7 and 14 mg kg<sup>−1</sup>
) produced significant increases in ipsiversive rotations compared to vehicle controls totaling, at the highest respective doses tested, 521±120, 131±37 and 92.5±16.3 net contraversive rotations in 30 (deprenyl) or 60 (BU224 and 2-BFI) min. In contrast, the reversible MAO-A inhibitor moclobemide (2.5–10 mg kg<sup>−1</sup>
) and the reversible MAO-B inhibitor lazabemide (2.5–10 mg kg<sup>−1</sup>
) failed to instigate significant rotational behaviour compared to vehicle.</p>
</list-item>
<list-item><p>Coadministration of lazabemide (10 mg kg<sup>−1</sup>
), moclobemide (10 mg kg<sup>−1</sup>
) or 2-BFI (14 mg kg<sup>−1</sup>
) with <sc>L</sc>
-DOPA (20 mg kg<sup>−1</sup>
) significantly increased either the duration or total number of contraversive rotations emitted over the testing period in comparison to <sc>L</sc>
-DOPA alone.</p>
</list-item>
<list-item><p>These data suggest that I<sub>2</sub>
-specific ligands have dual effects in the 6-OHDA-lesioned rat model of Parkinson's disease; a first effect associated with an increase in activity in the intact hemisphere, probably <italic>via</italic>
an increase in striatal dopamine content, and a secondary action which, through the previously documented inhibition of MAO-A and/or MAO-B, increases the availability of dopamine produced by <sc>L</sc>
-DOPA.</p>
</list-item>
</list>
</p>
</div>
</front>
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<affiliations><list></list>
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<name sortKey="Macinnes, Nicholas" sort="Macinnes, Nicholas" uniqKey="Macinnes N" first="Nicholas" last="Macinnes">Nicholas Macinnes</name>
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