A Therapeutic Role For Melatonin Antagonism in Experimental Models of Parkinson’s Disease

To determine the effects of endogenous and exogenous melatonin on experimental models of Parkinson’s disease (PD), Sprague–Dawley rats were exposed to intracerebroventricular implants of slow release melatonin, pinealectomy (PX), or constant light (LL) and then injected with central 6-hydroxydopamin...

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Bibliographic Details
Published in:Physiology & behavior 1999-07, Vol.66 (5), p.785-795
Main Authors: Willis, Gregory L, Armstrong, Stuart Maxwell
Format: Article
Language:English
Subjects:
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Animals
Atenalol
Biological and medical sciences
Biological Availability
Body Weight - drug effects
Body Weight - radiation effects
Bright-light therapy
Catecholamines
Circadian Rhythm - physiology
Disease Models, Animal
Dopamine
Dyskinesia, Drug-Induced - therapy
Free Radical Scavengers - pharmacology
Free Radical Scavengers - radiation effects
Hormones. Endocrine system
Male
Medical sciences
Melatonin
Melatonin - pharmacology
Melatonin - radiation effects
Melatonin antagonist
Motor Activity - drug effects
Motor Activity - radiation effects
Noradrenaline
Oxidopamine
Parkinson Disease - therapy
Pharmacology. Drug treatments
Photoperiod
Phototherapy
Pineal gland
Pineal Gland - surgery
Pinealectomy
Rats
Rats, Sprague-Dawley
Schizophrenia
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Summary:To determine the effects of endogenous and exogenous melatonin on experimental models of Parkinson’s disease (PD), Sprague–Dawley rats were exposed to intracerebroventricular implants of slow release melatonin, pinealectomy (PX), or constant light (LL) and then injected with central 6-hydroxydopamine (6-OHDA) or i.p. 1-methyl-4-phenyl,1-1,2,3,6-tetrahydropyridine (MPTP). The resulting impairment of motor function and related behavioural impairment were exacerbated by melatonin implantation, while PX and exposure to LL significantly reduced the severity of experimental PD. These results are consistent with previous work highlighting the importance of aberrant amine production in neurological disease and demonstrate that treatments that reduce endogenous melatonin bioavailability can ameliorate experimental PD. Furthermore, these findings illustrate that melatonin is not the universal remedy that it is currently claimed to be, and may pose considerable problems in neurological diseases characterised by dopamine degeneration.
ISSN:0031-9384
1873-507X
DOI:10.1016/S0031-9384(99)00023-2