Journal ArticleDOI
Neurochemical and Histochemical Characterization of Neurotoxic Effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine on Brain Catecholamine Neurones in the Mouse
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TLDR
Systemic administration of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine caused a rapid and long‐lasting reduction of both 3‐dihydroxyphenylalanine (dopamine, DA) and noradrenaline (NA) in mouse brain, as observed histo‐ and neurochemically.Abstract:
Systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) caused a rapid and long-lasting reduction of both 3,4-dihydroxyphenylalanine (dopamine, DA) and noradrenaline (NA) in mouse brain, as observed histo- and neurochemically. The depleting effects were more pronounced after repeated MPTP administration and the most marked reductions were observed after 2 X 50 mg MPTP/kg s.c., when DA in striatum and NA in frontal cortex were reduced by greater than 90% 1 week after MPTP. Mice with such catecholamine depletions were markedly sedated and almost completely immobilized. The behavioural syndrome after MPTP resembled that seen after reserpine, a monoamine-depleting drug. MPTP also caused a long-lasting reduction of catecholamine uptake in striatal DA and cortical NA nerve terminals and reduced tyrosine hydroxylase activity in these regions. There was no evidence that MPTP caused any marked DA and NA cell body death. MPTP given acutely transiently elevated serotonin levels. The results are compatible with a neurotoxic action of MPTP on both DA and NA nerve terminals. The nigro-striatal DA and the locus coeruleus NA neurone systems appeared to be most susceptible. Synthesis and utilization of residual striatal DA and cortical NA were increased, as often observed in partially denervated monoamine-innervated brain regions. Both DA and NA showed a gradual recovery, which took months to become complete and may have been related to a regrowth of catecholamine nerve terminals.read more
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Journal ArticleDOI
Non-motor features of Parkinson disease.
TL;DR: Recent advances that have helped to establish the presence, severity and effect on the quality of life of non-motor symptoms in PD are discussed, and the neuroanatomical and neuropharmacological mechanisms involved are discussed.
Journal ArticleDOI
Animal models of Parkinson's disease: a source of novel treatments and clues to the cause of the disease
Susan Duty,Peter Jenner +1 more
TL;DR: The MPTP‐treated primate model of PD, which closely mimics the clinical features of PD and in which all currently used anti‐parkinsonian medications have been shown to be effective, is undoubtedly the most clinically‐relevant of all available models.
Journal ArticleDOI
Time course and morphology of dopaminergic neuronal death caused by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
TL;DR: This study demonstrates that the MPTP mouse model replicates several key features of neurodegeneration of DA neurons in PD and provides no in vivo evidence that, using this specific paradigm of injection, MPTP kills DA neurons by apoptosis.
Journal ArticleDOI
Adrenal medulla grafts enhance recovery of striatal dopaminergic fibers
TL;DR: Observations in mice suggest that, in mice, adrenal medullary grafts exert a neurotrophic action in the host brain to enhance recovery of dopaminergic neurons, which may be relevant to the symptomatic recovery in Parkinson's disease patients who have received adrenal MedullARY grafts.
Journal ArticleDOI
Midbrain dopaminergic cell loss in Parkinson's disease: computer visualization.
TL;DR: It is suggested that Parkinson's disease preferentially destroys midbrain dopaminergic neurons in nuclei A8, A9, and A10, which project to the striatum, as opposed to cortical and limbic sites in animal neuroanatomical tracing experiments.
References
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Journal ArticleDOI
Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis
TL;DR: It is proposed that this chemical selectively damages cells in the substantia nigra in patients who developed marked parkinsonism after using an illicit drug intravenously.
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Fluorescence of Catechol Amines and Related Compounds Condensed With Formaldehyde
TL;DR: In this article, the reaction between formaldehyde and phenylalanine and phenylethylamine derivatives has been studied under mild conditions and it has been shown that the amines primarily condense with formaldehyde to 1,2,3,4-tetrahydroisoquinolines which are involved in a secondary reaction to become highly fluorescent and at the same time insoluble.
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A primate model of parkinsonism: selective destruction of dopaminergic neurons in the pars compacta of the substantia nigra by N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
TL;DR: The N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated monkey provides a model that can be used to examine mechanisms and explore therapies of parkinsonism and the pathological and biochemical changes produced by NMPTP are similar to the well-established changes in patients with parkinsonistan.
Journal ArticleDOI
Chronic Parkinsonism secondary to intravenous injection of meperidine analogues.
Glenn C. Davis,Adrian C. Williams,Sanford P. Markey,Michael H. Ebert,Eric D. Caine,Cheryl M. Reichert,Irwin J. Kopin +6 more
TL;DR: Biogenic amines and metabolites in the cerebrospinal fluid and microscopic evaluation of the brain at necropsy were consistent with damage to aminergic neurons in the substantia nigra.
Journal ArticleDOI
Central Catecholamine Neuron Systems: Anatomy and Physiology of the Norepinephrine and Epinephrine Systems
R Y Moore,Floyd E. Bloom +1 more
TL;DR: The intensity of research on the central catecholaminergic neuron systems has continued unabated since last year's review of the dopaminergic systems, and the richness of important details deserving of inclusion resulted in a richness of information exceeding the pages available.