MovDisordV3, Main, Exploration, bibRecord, 004F74

Kappa‐opioid receptor agonists increase locomotor activity in the monoamine‐depleted rat model of parkinsonism

Identifieur interne : 004F74 ( Main/Exploration ); précédent : 004F73; suivant : 004F75

Kappa‐opioid receptor agonists increase locomotor activity in the monoamine‐depleted rat model of parkinsonism

Auteurs : Neill R. Hughes [Royaume-Uni] ; Alexander T. Mcknight [Royaume-Uni] ; Geoffrey N. Woodruff [Royaume-Uni] ; Michael P. Hill [Royaume-Uni] ; Alan R. Crossman [Royaume-Uni] ; Brotchie [Royaume-Uni]

Source :

Movement Disorders [ 0885-3185 ] ; 1998-03.

RBID : ISTEX:2E85DAD4A21FF1D7C14D8CF7E9EB962A9EBF6C58

Descripteurs français

Pascal (Inist)
- Agoniste, Animal, Antiparkinsonien, Chimiothérapie, Effet biologique, Enadoline, Locomotion, Lévodopa, Mâle, Mécanisme action, Parkinson maladie, Parkinsonisme, Rat, Relation dose réponse, Récepteur opiacé κ, Traitement, U69,593, Voie intrapéritonéale.

English descriptors

KwdEn :
- Agonist, Animal, Animals, Antiparkinson Agents (pharmacology), Antiparkinson agent, Benzeneacetamides, Benzofurans (pharmacology), Biological effect, Chemotherapy, Dose activity relation, Dose-Response Relationship, Drug, Drug Synergism, Enadoline, Intraperitoneal administration, Kappa opioid receptor, Levodopa, Levodopa (pharmacology), Locomotion, Male, Mechanism of action, Motor Activity (drug effects), Motor Activity (physiology), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (physiopathology), Parkinson disease, Parkinson's disease, Parkinsonism, Pyrrolidines (pharmacology), Rat, Rats, Rats, Sprague-Dawley, Receptors, Opioid, kappa (agonists), Receptors, Opioid, kappa (physiology), Reserpine, Treatment, alpha-Methyltyrosine, κ Opioid receptor.
MESH :
- chemical , agonists : Receptors, Opioid, kappa.
- chemical , pharmacology : Antiparkinson Agents, Benzofurans, Levodopa, Pyrrolidines.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Motor Activity.
- physiology : Motor Activity, Receptors, Opioid, kappa.
- physiopathology : Parkinson Disease, Secondary.
- Animals, Benzeneacetamides, Dose-Response Relationship, Drug, Drug Synergism, Male, Rats, Rats, Sprague-Dawley, Reserpine, alpha-Methyltyrosine.

Abstract

Excessive glutamate transmission in the basal ganglia is a major factor in the neural mechanisms underlying parkinsonian akinesia. Activation of K opioid receptors causes a presynaptic reduction in glutamate release. K opioid receptors are concentrated in those regions of the basal ganglia associated with increased glutamate transmission in parkinsonism. In this study, we use the α‐methyl‐p‐tyrosine and reserpine‐treated rat model of parkinsonism to investigate whether systemic administration of the K opioid agonists enadoline (CI‐977) and U69,593 can alleviate the symptoms of parkinsonism either alone or in conjunction with dopamine replacement therapy. We report that, when administered alone, both enadoline and U69,593 can increase locomotion in monoamine‐depleted rats. No increase in locomotor activity was seen after K opioid agonist administration in non‐parkinsonian rats. The responses to K opioid agonists were blocked by co‐administration of either the nonspecific opioid receptor antagonist naloxone or the selective K opioid receptor antagonist nor‐binaltorphimine (nor‐BNI). An important finding is that when enadoline and L‐dopa administered togethe, their anti‐akinetic properties are synergistic. Thus, the doses of enadoline and L‐dopa required to alleviate akinesia when administered together are lower than either administered alone. These data illustrate the importance of K opioid receptors in the neural mechanisms controlling voluntary movement and suggest that K opioid agonists may have a role as adjuncts to dopamine replacement in the management of Parkinson's disease.

Url:

https://api.istex.fr/document/2E85DAD4A21FF1D7C14D8CF7E9EB962A9EBF6C58/fulltext/pdf

DOI: 10.1002/mds.870130206

Affiliations:

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<term>Antiparkinson agent</term>
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<front><div type="abstract" xml:lang="en">Excessive glutamate transmission in the basal ganglia is a major factor in the neural mechanisms underlying parkinsonian akinesia. Activation of K opioid receptors causes a presynaptic reduction in glutamate release. K opioid receptors are concentrated in those regions of the basal ganglia associated with increased glutamate transmission in parkinsonism. In this study, we use the α‐methyl‐p‐tyrosine and reserpine‐treated rat model of parkinsonism to investigate whether systemic administration of the K opioid agonists enadoline (CI‐977) and U69,593 can alleviate the symptoms of parkinsonism either alone or in conjunction with dopamine replacement therapy. We report that, when administered alone, both enadoline and U69,593 can increase locomotion in monoamine‐depleted rats. No increase in locomotor activity was seen after K opioid agonist administration in non‐parkinsonian rats. The responses to K opioid agonists were blocked by co‐administration of either the nonspecific opioid receptor antagonist naloxone or the selective K opioid receptor antagonist nor‐binaltorphimine (nor‐BNI). An important finding is that when enadoline and L‐dopa administered togethe, their anti‐akinetic properties are synergistic. Thus, the doses of enadoline and L‐dopa required to alleviate akinesia when administered together are lower than either administered alone. These data illustrate the importance of K opioid receptors in the neural mechanisms controlling voluntary movement and suggest that K opioid agonists may have a role as adjuncts to dopamine replacement in the management of Parkinson's disease.</div>
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Movement Disorders (revue)

Kappa‐opioid receptor agonists increase locomotor activity in the monoamine‐depleted rat model of parkinsonism

Kappa‐opioid receptor agonists increase locomotor activity in the monoamine‐depleted rat model of parkinsonism

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

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Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

	Movement Disorders (revue)
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