Increasing levels of the endocannabinoid 2-AG is neuroprotective in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease.
Identifieur interne : 000376 ( PubMed/Corpus ); précédent : 000375; suivant : 000377Increasing levels of the endocannabinoid 2-AG is neuroprotective in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease.
Auteurs : Ross B. Mounsey ; Sarah Mustafa ; Lianne Robinson ; Ruth A. Ross ; Gernot Riedel ; Roger G. Pertwee ; Peter TeismannSource :
- Experimental neurology [ 1090-2430 ] ; 2015.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology), Animals, Arachidonic Acids (therapeutic use), Benzodioxoles (therapeutic use), Brain (drug effects), Brain (metabolism), Brain (pathology), Cell Death (drug effects), Cyclooxygenase 2 (metabolism), Disease Models, Animal, Dose-Response Relationship, Drug, Endocannabinoids (therapeutic use), Enzyme Inhibitors (pharmacology), Furans (therapeutic use), Gait Disorders, Neurologic (drug therapy), Gait Disorders, Neurologic (etiology), Glycerides (therapeutic use), Male, Mice, Mice, Inbred C57BL, Motor Activity (drug effects), Neuroprotective Agents (therapeutic use), Neurotoxins (toxicity), Parkinson Disease (complications), Parkinson Disease (diet therapy), Parkinson Disease (etiology), Parkinson Disease (pathology), Piperidines (therapeutic use), Time Factors, Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , metabolism : Cyclooxygenase 2, Tyrosine 3-Monooxygenase.
- chemical , pharmacology : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Enzyme Inhibitors.
- chemical , therapeutic use : Arachidonic Acids, Benzodioxoles, Endocannabinoids, Furans, Glycerides, Neuroprotective Agents, Piperidines.
- complications : Parkinson Disease.
- diet therapy : Parkinson Disease.
- drug effects : Brain, Cell Death, Motor Activity.
- drug therapy : Gait Disorders, Neurologic.
- etiology : Gait Disorders, Neurologic, Parkinson Disease.
- metabolism : Brain.
- pathology : Brain, Parkinson Disease.
- chemical , toxicity : Neurotoxins.
- Animals, Disease Models, Animal, Dose-Response Relationship, Drug, Male, Mice, Mice, Inbred C57BL, Time Factors.
Abstract
Parkinson's disease (PD) is a common chronic neurodegenerative disorder, usually of idiopathic origin. Symptoms including tremor, bradykinesia, rigidity and postural instability are caused by the progressive loss of dopaminergic neurons in the nigrostriatal region of the brain. Symptomatic therapies are available but no treatment slows or prevents the loss of neurons. Neuroinflammation has been implicated in its pathogenesis. To this end, the present study utilises the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin to reproduce the pattern of cell death evident in PD patients. Herein, the role of a potential regulator of an immune response, the endocannabinoid system (ECS), is investigated. The most prevalent endocannabinoid, 2-arachidonoylglycerol (2-AG) (3 and 5mg/kg), was added exogenously and its enzymatic degradation inhibited to provide protection against MPTP-induced cell death. Furthermore, the addition of DFU (25mg/kg), a selective inhibitor of inflammatory mediator cyclooxygenase-2 (COX-2), potentiated these effects. Levels of 2-AG were shown to be upregulated in a time- and region-specific manner following MPTP administration, indicating that the ECS represents a natural defence mechanism against inflammation, potentiation of which could provide therapeutic benefits. The results expand the current understanding of the role that this signalling system has and its potential influence in PD.
DOI: 10.1016/j.expneurol.2015.07.024
PubMed: 26244281
Links to Exploration step
pubmed:26244281Le document en format XML
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<term>Animals</term>
<term>Arachidonic Acids (therapeutic use)</term>
<term>Benzodioxoles (therapeutic use)</term>
<term>Brain (drug effects)</term>
<term>Brain (metabolism)</term>
<term>Brain (pathology)</term>
<term>Cell Death (drug effects)</term>
<term>Cyclooxygenase 2 (metabolism)</term>
<term>Disease Models, Animal</term>
<term>Dose-Response Relationship, Drug</term>
<term>Endocannabinoids (therapeutic use)</term>
<term>Enzyme Inhibitors (pharmacology)</term>
<term>Furans (therapeutic use)</term>
<term>Gait Disorders, Neurologic (drug therapy)</term>
<term>Gait Disorders, Neurologic (etiology)</term>
<term>Glycerides (therapeutic use)</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Motor Activity (drug effects)</term>
<term>Neuroprotective Agents (therapeutic use)</term>
<term>Neurotoxins (toxicity)</term>
<term>Parkinson Disease (complications)</term>
<term>Parkinson Disease (diet therapy)</term>
<term>Parkinson Disease (etiology)</term>
<term>Parkinson Disease (pathology)</term>
<term>Piperidines (therapeutic use)</term>
<term>Time Factors</term>
<term>Tyrosine 3-Monooxygenase (metabolism)</term>
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<term>Tyrosine 3-Monooxygenase</term>
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<term>Enzyme Inhibitors</term>
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<term>Benzodioxoles</term>
<term>Endocannabinoids</term>
<term>Furans</term>
<term>Glycerides</term>
<term>Neuroprotective Agents</term>
<term>Piperidines</term>
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<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="diet therapy" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
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<term>Cell Death</term>
<term>Motor Activity</term>
</keywords>
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<term>Disease Models, Animal</term>
<term>Dose-Response Relationship, Drug</term>
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<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a common chronic neurodegenerative disorder, usually of idiopathic origin. Symptoms including tremor, bradykinesia, rigidity and postural instability are caused by the progressive loss of dopaminergic neurons in the nigrostriatal region of the brain. Symptomatic therapies are available but no treatment slows or prevents the loss of neurons. Neuroinflammation has been implicated in its pathogenesis. To this end, the present study utilises the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin to reproduce the pattern of cell death evident in PD patients. Herein, the role of a potential regulator of an immune response, the endocannabinoid system (ECS), is investigated. The most prevalent endocannabinoid, 2-arachidonoylglycerol (2-AG) (3 and 5mg/kg), was added exogenously and its enzymatic degradation inhibited to provide protection against MPTP-induced cell death. Furthermore, the addition of DFU (25mg/kg), a selective inhibitor of inflammatory mediator cyclooxygenase-2 (COX-2), potentiated these effects. Levels of 2-AG were shown to be upregulated in a time- and region-specific manner following MPTP administration, indicating that the ECS represents a natural defence mechanism against inflammation, potentiation of which could provide therapeutic benefits. The results expand the current understanding of the role that this signalling system has and its potential influence in PD.</div>
</front>
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<Abstract><AbstractText>Parkinson's disease (PD) is a common chronic neurodegenerative disorder, usually of idiopathic origin. Symptoms including tremor, bradykinesia, rigidity and postural instability are caused by the progressive loss of dopaminergic neurons in the nigrostriatal region of the brain. Symptomatic therapies are available but no treatment slows or prevents the loss of neurons. Neuroinflammation has been implicated in its pathogenesis. To this end, the present study utilises the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin to reproduce the pattern of cell death evident in PD patients. Herein, the role of a potential regulator of an immune response, the endocannabinoid system (ECS), is investigated. The most prevalent endocannabinoid, 2-arachidonoylglycerol (2-AG) (3 and 5mg/kg), was added exogenously and its enzymatic degradation inhibited to provide protection against MPTP-induced cell death. Furthermore, the addition of DFU (25mg/kg), a selective inhibitor of inflammatory mediator cyclooxygenase-2 (COX-2), potentiated these effects. Levels of 2-AG were shown to be upregulated in a time- and region-specific manner following MPTP administration, indicating that the ECS represents a natural defence mechanism against inflammation, potentiation of which could provide therapeutic benefits. The results expand the current understanding of the role that this signalling system has and its potential influence in PD.</AbstractText>
<CopyrightInformation>Copyright © 2015. Published by Elsevier Inc.</CopyrightInformation>
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