Role of pedunculopontine cholinergic neurons in the vulnerability of nigral dopaminergic neurons in Parkinson's disease.
Identifieur interne : 000168 ( Main/Exploration ); précédent : 000167; suivant : 000169Role of pedunculopontine cholinergic neurons in the vulnerability of nigral dopaminergic neurons in Parkinson's disease.
Auteurs : Manale Bensaid [France] ; Patrick P. Michel [France] ; Stewart D. Clark [États-Unis] ; Etienne C. Hirsch [France] ; Chantal François [France]Source :
- Experimental neurology [ 1090-2430 ] ; 2016.
English descriptors
- KwdEn :
- MESH :
- chemical : Oxidopamine.
- pathology : Cholinergic Neurons, Dopaminergic Neurons, Parkinson Disease, Pedunculopontine Tegmental Nucleus, Substantia Nigra.
- Animals, Macaca fascicularis, Male, Rats, Rats, Sprague-Dawley.
- mix :
Abstract
Pedunculopontine nucleus (PPN) cholinergic neurons, which exert excitatory nicotinic control over substantia nigra dopaminergic neurons, degenerate in Parkinson's disease (PD). This finding and other studies showing that nicotine, the preferential agonist of nicotinic acetylcholine receptors, is neuroprotective in experimental models of PD suggest that a deficit in PPN excitatory cholinergic inputs might contribute to the death of nigral dopaminergic neurons in PD. To explore this possibility, we used lesion paradigms of dopaminergic and/or cholinergic systems in rats and monkeys. Consistent with our hypothesis, we observed that stereotaxic lesioning of PPN cholinergic neurons with diphtheria toxin coupled to urotensin II resulted in a significant loss of nigral dopaminergic neurons in rats and induced morphological changes in these neurons in macaques. Unexpectedly, a lesion of dopaminergic neurons induced by unilateral striatal injection of 6-hydroxydopamine (6-OHDA) in rats, or by repeated systemic injections of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in macaques, led to a 29% and 7% loss of PPN cholinergic neurons, respectively. Lastly, when the PPN cholinergic lesion was performed in rats in which the dopaminergic lesion induced by 6-OHDA was in progress, loss of cholinergic neurons was more drastic than when each neurotransmitter system was lesioned separately. Thus, our results suggest that strong PPN cholinergic and dopaminergic interactions may be an important mechanism in the pathophysiology of PD.
Url:
DOI: 10.1016/j.expneurol.2015.11.004
PubMed: 26571193
Affiliations:
- France, États-Unis
- État de New York, Île-de-France
- Buffalo (New York), Paris
- Université d'État de New York à Buffalo
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Le document en format XML
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Michel</name><affiliation wicri:level="3"><nlm:affiliation>Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, UM75, U1127, UMR 7225, ICM, F-75013 Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, UM75, U1127, UMR 7225, ICM, F-75013 Paris</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Clark, Stewart D" sort="Clark, Stewart D" uniqKey="Clark S" first="Stewart D" last="Clark">Stewart D. Clark</name><affiliation wicri:level="4"><nlm:affiliation>Department of Pharmacology and Toxicology, University at Buffalo, Buffalo, New York 14214, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pharmacology and Toxicology, University at Buffalo, Buffalo, New York 14214</wicri:regionArea><orgName type="university">Université d'État de New York à Buffalo</orgName><placeName><settlement type="city">Buffalo (New York)</settlement><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name><affiliation wicri:level="3"><nlm:affiliation>Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, UM75, U1127, UMR 7225, ICM, F-75013 Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, UM75, U1127, UMR 7225, ICM, F-75013 Paris</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Francois, Chantal" sort="Francois, Chantal" uniqKey="Francois C" first="Chantal" last="François">Chantal François</name><affiliation wicri:level="3"><nlm:affiliation>Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, UM75, U1127, UMR 7225, ICM, F-75013 Paris, France. Electronic address: Chantal.francois@upmc.fr.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, UM75, U1127, UMR 7225, ICM, F-75013 Paris</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author></analytic><series><title level="j">Experimental neurology</title><idno type="eISSN">1090-2430</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cholinergic Neurons (pathology)</term><term>Dopaminergic Neurons (pathology)</term><term>Macaca fascicularis</term><term>Male</term><term>Oxidopamine</term><term>Parkinson Disease (pathology)</term><term>Pedunculopontine Tegmental Nucleus (pathology)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Substantia Nigra (pathology)</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Oxidopamine</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cholinergic Neurons</term><term>Dopaminergic Neurons</term><term>Parkinson Disease</term><term>Pedunculopontine Tegmental Nucleus</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Macaca fascicularis</term><term>Male</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords><keywords scheme="mix" xml:lang="en"><term>6-OHDA</term><term>Cholinergic</term><term>Diphtheria toxin-urotensin II</term><term>Dopamine</term><term>Mptp</term><term>Parkinson's disease</term><term>Pedunculopontine nucleus</term><term>Substantia nigra</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Pedunculopontine nucleus (PPN) cholinergic neurons, which exert excitatory nicotinic control over substantia nigra dopaminergic neurons, degenerate in Parkinson's disease (PD). This finding and other studies showing that nicotine, the preferential agonist of nicotinic acetylcholine receptors, is neuroprotective in experimental models of PD suggest that a deficit in PPN excitatory cholinergic inputs might contribute to the death of nigral dopaminergic neurons in PD. To explore this possibility, we used lesion paradigms of dopaminergic and/or cholinergic systems in rats and monkeys. Consistent with our hypothesis, we observed that stereotaxic lesioning of PPN cholinergic neurons with diphtheria toxin coupled to urotensin II resulted in a significant loss of nigral dopaminergic neurons in rats and induced morphological changes in these neurons in macaques. Unexpectedly, a lesion of dopaminergic neurons induced by unilateral striatal injection of 6-hydroxydopamine (6-OHDA) in rats, or by repeated systemic injections of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in macaques, led to a 29% and 7% loss of PPN cholinergic neurons, respectively. Lastly, when the PPN cholinergic lesion was performed in rats in which the dopaminergic lesion induced by 6-OHDA was in progress, loss of cholinergic neurons was more drastic than when each neurotransmitter system was lesioned separately. Thus, our results suggest that strong PPN cholinergic and dopaminergic interactions may be an important mechanism in the pathophysiology of PD.</div></front></TEI><affiliations><list><country><li>France</li><li>États-Unis</li></country><region><li>État de New York</li><li>Île-de-France</li></region><settlement><li>Buffalo (New York)</li><li>Paris</li></settlement><orgName><li>Université d'État de New York à Buffalo</li></orgName></list><tree><country name="France"><region name="Île-de-France"><name sortKey="Bensaid, Manale" sort="Bensaid, Manale" uniqKey="Bensaid M" first="Manale" last="Bensaid">Manale Bensaid</name></region><name sortKey="Francois, Chantal" sort="Francois, Chantal" uniqKey="Francois C" first="Chantal" last="François">Chantal François</name><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name><name sortKey="Michel, Patrick P" sort="Michel, Patrick P" uniqKey="Michel P" first="Patrick P" last="Michel">Patrick P. Michel</name></country><country name="États-Unis"><region name="État de New York"><name sortKey="Clark, Stewart D" sort="Clark, Stewart D" uniqKey="Clark S" first="Stewart D" last="Clark">Stewart D. Clark</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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