Results 91 to 100 of about 308 (125)
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Effects of 6-Hydroxydopamine on Sleep in the Rat
Nature, 1971THERE is evidence that biogenic amines are involved in the mechanisms of sleep1,2. Although the exact relationship is not clear, recent results suggest that decreases in the concen-tration of catecholamines (noradrenaline or dopamine) in the brain cause increased desynchronized sleep (D) (sleep with rapid desynchronized cortical activity, also known as
E, Hartmann +3 more
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Central cardiovascular effects of 6-hydroxydopamine
European Journal of Pharmacology, 1972Abstract Effects of 6-hydroxydopamine (6-OHDA) on the vasomotor loci of medulla oblongata, hypothalamus and spinal cord have been investigated in anaesthetized (chloralosed) cats. Intracerebroventricular (i.c.v.) and intrathecal (i.t.) administration of 6-OHDA, 0.5–2.0 mg, inhibited reflex, as well as direct, excitability of vasomotor loci. The blood
P P, Gupta, R C, Srimal, B N, Dhawan
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Mechanism of 6-hydroxydopamine neurotoxicity
1997The catecholaminergic neurotoxin 6-hydroxydopamine (6-OHDA) has recently been found to be formed endogenously in patients suffering from Parkinson's disease. In this article, we highlight the latest findings on the biochemical mechanism of 6-OHDA toxicity.
Y, Glinka, M, Gassen, M B, Youdim
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6-Hydroxydopamine, a new oxidation mechanism
European Journal of Pharmacology, 1972Abstract Electrochemical and chemical studies, supported by EPR, NMR and UV evidence, show that 6-hydroxydopamine does not oxidize in vitro at physiological pH to the cyclized indoline (aminochrome) as previously believed. The implications of these results to the chemical sympathectomy actions of 6-hydroxydopamine are discussed.
R N, Adams +4 more
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2000
Abstract 6-Hydroxydopamine (6-OH-DA) was originally synthesized in 1959 (38,39); the authors suggested that 6-OH-DA might be a naturally occurring oxidation product/metabolite of its congener dopamine. Systemic administration of 6-OH-DA caused a long-lasting depletion of noradrenaline from sympathetically innervated organs (28,32,42).
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Abstract 6-Hydroxydopamine (6-OH-DA) was originally synthesized in 1959 (38,39); the authors suggested that 6-OH-DA might be a naturally occurring oxidation product/metabolite of its congener dopamine. Systemic administration of 6-OH-DA caused a long-lasting depletion of noradrenaline from sympathetically innervated organs (28,32,42).
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Oxidation of 6-hydroxydopamine catalyzed by tyrosinase
International Journal of Biochemistry, 19931. The oxidation of 3,4-dihydroxyphenylethylamine (dopamine) by O2 catalyzed by tyrosinase yields 4-(2-aminoethyl)-1,2-benzoquinone, with its amino group protonated (o-dopaminequinone-H+), which evolves non-enzymatically through two branches or sequences of reactions, whose respective operations are determined by the pH of the medium. 2.
J N, Rodriguez-López +2 more
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Perinatal 6-Hydroxydopamine Modeling of ADHD
2015The neonatally 6-hydroxydopamine (n6-OHDA)-lesioned rat has been the standard for 40 years, as an animal model of attention-deficit hyperactivity disorder (ADHD). Rats so lesioned during postnatal ontogeny are characterized by ~99 % destruction of dopaminergic nerves in pars compacta substantia nigra, with comparable destruction of the nigrostriatal ...
Kostrzewa, John P. +4 more
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A New Synthesis of 6-Hydroxydopamine
Canadian Journal of Chemistry, 1972An efficient synthesis of 6-hydroxydopamine is described. The key step involves oxidation of an N-protected 3-hydroxy-4-methoxyphenethylamine to the corresponding p-quinone by means of Fremy's salt.
Pius A. Wehrli, F. Pigott, V. Chu
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6-Hydroxydopamine: a far from simple neurotoxin
Journal of Neural Transmission, 20206-Hydroxydopamine (6-OHDA), which is a neurotoxin that selectively destroys catecholaminergic nerves in sympathetically innervated tissues, has been used to provide a model of Parkinson's disease in experimental animals. It is rapidly autoxidised to yield potentially toxic products and reactive oxygen species. Its ability to release Fe(II) from protein
Damir Varešlija +3 more
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Turnover of 5-hydroxydopamine in adrenergic nerves
Experientia, 1977In adrenergic nerve endings of the guinea-pig vas deferens the population of small granular vesicles increases from 19% in control animals to 80-90% 1-3 h after the administration of 5-hydroxydopamine, and gradually declines to control values in 10 days. Large granular vsicles were also loaded but the loss of enhanced granulation was more rapid than in
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