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  • 1
    Electronic Resource
    Electronic Resource
    Influence of Selective Inhibition of Monoamine Oxidase A or B on Striatal Metabolism of l-DOPA in Hemiparkinsonian Rats (1995)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 65 (1995), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effect of selective inhibition of monoamine oxidase (MAO) subtypes A and B on striatal metabolism of DOPA to dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), and 4-hydroxy-3-methoxyphenylacetic acid (homovanillic acid; HVA) was studied in halothane-anesthetized rats 3 weeks after unilateral 6-hydroxydopamine lesion of the substantia nigra. Implantation of bilateral microdialysis probes allowed simultaneous quantitation of metabolite production on lesioned and control sides. The DOPA was administered as a 15-min bolus of 1 mM solution in the striatal microdialysate. Rats were pretreated with the selective MAO-A inhibitor clorgyline, or the selective MAO-B inhibitors deprenyl or TVP-101 [2,3-dihydro-N-2-propynyl-1H-inden-1-amine-(1R)-hydrochloride]. Intrastriatal infusion of DOPA caused an increased efflux of DA, DOPAC, and HVA, which was greater on the intact side. Clorgyline, but not deprenyl or TVP-101, increased post-DOPA DA efflux on both intact and lesioned sides. Clorgyline also caused a marked suppression of post-DOPA DOPAC and HVA effluxes, whereas only mild effects were produced by the MAO-B inhibitors. There was no evidence for a differential effect of MAO-B inhibition on efflux of DA or metabolites in the lesioned as compared with the control striatum. The results indicate a major role for MAO-A in DA metabolism both intra- and extraneuronally in the rat striatum.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1995.65031213.x
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  • 2
    Electronic Resource
    Electronic Resource
    The Iron Chelator Desferrioxamine (Desferal) Retards 6-Hydroxydopamine-Induced Degeneration of Nigrostriatal Dopamine Neurons (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 56 (1991), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: A selective increase in content of iron in the pars compacta of the substantia nigra has been implicated in the biochemical pathology of Parkinson's disease. Iron is thought to induce oxidative stress by liberation of oxygen free radicals from H2O2. Because 6-hydroxydopamine (6-OHDA) is thought to induce nigrostriatal dopaminergic neuronal lesions via metal-catalyzed free radical formation, the effect of the iron chelator desferrioxamine was investigated on 6-OHDA-induced dopaminergic neuron degeneration in the rat. Intracerebroventricular injection of 6-OHDA (250 μg) caused a 88, 79, and 70% reduction in striatal tissue content of dopamine (DA), 3,4-dihydroxyphenylacetic acid, and homovanillic acid (HVA), respectively, and a 2.5-fold increase in DA release as indicated by the HVA/DA ratio. Prior injection of desferrioxamine (130 ng i.c.v.) resulted in a significant protection (〈60%) against the 6-OHDA-induced reduction in striatal DA content and a normalization of DA release. Dopaminergic-reiated behavioral responses, such as spontaneous movements in a novel environment and rearing, were significantly impaired in the 6-OHDA-treated group. By contrast, the desferrioxamine-pretreated rats exhibited almost normal behavioral responses. The ability of iron chelators to retard dopaminergic neurodegeneration in the substantia nigra may indicate a new therapeutic strategy in the treatment of Parkinson's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1991.tb11444.x
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  • 3
    Electronic Resource
    Electronic Resource
    Selective Alteration in Blood-Brain Barrier and Insulin Transport in Iron-Deficient Rats (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 50 (1988), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Nutritional iron deficiency induced in rats causes a significant reduction in level of brain nonheme iron and is accompanied by selective reduction of dopamine D2 receptor Bmax. Our previous studies have clearly demonstrated that these alterations can be restored to normal by supplementation with ferrous sulfate; however, neither brain nonheme iron level nor dopamine D2 receptor Bmax can be increased beyond control values even after long-term iron therapy. The possibility that iron deficiency can induce the breakdown of the blood-brain barrier (BBB) was examined. A 70 and 100% increase in brain uptake index (BUI) for l-glucose and insulin, respectively, were noted in iron-deficient rats. However, the BUI for valine was decreased by 40%, and those for l-norepinephine and glycine were unchanged. In addition, it was demonstrated that in normal rats insulin is transported into the brain. The data show that iron deficiency selectively affects the integrity of the BBB for insulin, glucose, and valine transport. Whether the effect of iron deficiency on the BBB is at the level of the capillary endothelial cell tight junction is not yet known. However, this study has shown that an important nutritional disorder (iron-deficiency anemia) has a profound effect on the BBB and brain function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1988.tb03027.x
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of Iron Chelators on Dopamine D2 Receptors (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 45 (1985), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Nutritional iron deficiency induced in rats causes a selective reduction of [3H]spiperone binding in caudate nucleus. This effect can be reversed by iron supplementation in vivo. The possibility that iron may be involved in the dopamine D2 receptor was investigated by examining the effect of various iron and noniron chelators on the binding of [3H]spiperone in rat caudate nucleus. Iron chelators 1, 10-phenanthroline, 2,4,6-tripyridyl-s-triazine, α,α′-dipyridyl, and desferrioxamine mesylate inhibited the binding of [3H]spiperone. The inhibition by 1,10-phenanthroline was noncompetitive and reversible. In the presence of FeCl2 or FeCl3, the inhibitory effect of 1,10-phenanthroline was potentiated. Iron salts or chelators were without effect on the binding of [3H]dihydroalprenolol to β-adrenoreceptors in caudate nucleus; thus the action of iron chelators on the dopamine D2 receptor tends to be selective. Incubation of caudate nucleus membrane prepared from iron-deficient rats with FeCl2 or FeCl3 did not reverse the diminished binding of [3H]spiperone. The present study indicates that if iron is involved in the physiological regulation of dopamine D2 agonist-antagonist binding sites, it is more complex than hitherto considered.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1985.tb05514.x
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  • 5
    Electronic Resource
    Electronic Resource
    A New Rapid and Sensitive Bioluminescence Assay for Monoamine Oxidase Activity (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 44 (1985), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The in vivo luminescence of an aldehyde-requiring mutant of the luminous bacteria Vibrio harveyi (M42) increases dramatically upon the addition of longchain aliphatic aldehydes (C8–C16). The intensity of this luminescence is linearly related to aldehyde concentration. This property was utilized for the determination of monoamine oxidase activity using n-octylamine and n-decylamine as substrates, which are converted by monoamine oxidase to n-octylaldehyde and n-decylaldehyde, respectively. The addition of the amine to a suspension containing rat liver mitochondria and M42 cells initiated a luminescence that was directly proportional to monoamine oxidase activity according to two parameters: (1) the rate of the initial increase in luminescence and (2) the final “steady-state”level of luminescence. The new assay has advantages of high sensitivity, rapidity, the possibility to perform discontinuous as well as continuous monitoring of monoamine oxidase activity, and applicability to turbid preparations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1985.tb08773.x
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  • 6
    Electronic Resource
    Electronic Resource
    Deamination of Aliphatic Amines by Monoamine Oxidase A and B Studied Using a Bioluminescence Technique (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 44 (1985), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Deamination of n-octylamine and n-decylamine has been studied in various tissues using a new bioluminescence technique. Selectivity of n-octylamine and n-decylamine as substrates for monoamine oxidase (MAO) A or B has been determined using both clorgyline and (–)-deprenyl inhibition curves and kinetic parameters. Homogenates of rat brain, liver and heart containing predominantly MAO-A or -B were prepared by preincubation for 60 min with (–)-deprenyl or clorgyline (30 nM), respectively. Human placenta (MAO-A) and platelet (MAO-B) were used as reference tissues containing only one MAO form. In tissues (rat liver, brain) containing both MAO forms in equal proportion, inhibition curve studies showed a preference of both substrates for the B form of the enzyme; however, where MAO-A was the major form (rat heart, human placenta), clorgyline was the more effective inhibitor. In the beef brain cortex n-octylamine showed marked preference for MAO-B, whereas n-decylamine was selective toward MAO-A. Kinetic studies in general supported the picture of greater selectivity of the aliphatic amine substrates for deamination by MAO-B, as reflected by lower Km values for this enzyme type. However, n-octylamine was more selective for MAO-B than n-decylamine in both kinetic and inhibition curve studies. The deamination of these aliphatic amine substrates cannot be explained only by reference to the binary classification of MAO into types A and B.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1985.tb08772.x
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  • 7
    Electronic Resource
    Electronic Resource
    DEVELOPMENT OF A SPECIFIC RADIOIMMUNOASSAY FOR ACETYLCHOLINE (1978)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 30 (1978), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— The synthesis of an acetylcholine-like immunogen and its use in production of antibodies specific to ACh is described. Cross-reactivity of anti-ACh antibody to choline was only 0.1% that to ACh. Insignificant cross reaction to acetate and phosphorylcholine occurred, enabling use of these antibodies in a radioimmunoassay for determination of endogenous ACh levels. Significant cross-reactivity of the antibody to succinylcholine. decamethonium, dimethylphenylpiperazinium, carbachol and butyr-ylcholine was observed. The correlation coefficient for determination of endogenous ACh by bioassay and radioimmunoassay was 0.994. ACh levels by radioimmunoassay in brain areas of rats killed by microwave irradiation were: striatum, 77.8; cortex, 28.8; hippocampus, 25.4; midbrain. 47; and hypothalamus, 25 nmol/g.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1978.tb10772.x
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  • 8
    Electronic Resource
    Electronic Resource
    CARDIOVASCULAR RESPONSIVENESS TO VASOACTIVE AGENTS IN RATS WITH OBSTRUCTIVE JAUNDICE (1982)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 9 (1982), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Pressor responses to tyramine, β-phenylethylamine and angiotensin II were normal in urethane-anaesthetized rats 7 days after division of the common bile duct. The pressor response to noradrenaline was enhanced at the highest dose level used.2. The hypotensive response to haemorrhage was exaggerated in bile duct divided rats. The exaggerated haemorrhagic hypotension of bile duct divided rats is unlikely to be the result of impaired vascular response to noradrenaline or angiotensin II, or of accumulation of false neurotransmitters by sympathetic nerves.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1982.tb00835.x
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  • 9
    Electronic Resource
    Electronic Resource
    Peripheral noradrenergic function during chronic lithium treatment in the rat (1992)
    Springer
    Journal of neural transmission 87 (1992), S. 77-83 
    Details
    ISSN: 1435-1463
    Keywords: Lithium ; 3 H-noradrenaline release ; vas deferens ; α1adrenoceptor ; α2-adrenoceptor ; neuronal uptake
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Noradrenergic function was evaluated in the rat vas deferens following chronic treatment with lithium (30 mM in the diet for 2 weeks followed by 50 mM for 1 week). No alteration could be detected in: a)3 H-noradrenaline release evoked by electrical field stimulation, b) α1adrenoceptor function as assessed by contractile response to noradrenaline, c) active neuronal uptake of3 H-noradrenaline, d) α2-adrenoceptor activity, as assessed by yohimbine-enhancement of evoked release of3 H-noradrenaline. The data argue against a primary action of lithium on the noradrenergic nerve. On the other hand, these findings do not rule out the possibility that the function of CNS noradrenergic neurons could be altered as a result of the known effects of lithium on the phosphatidyl-inositol system, and the greater sensitivity of CNS neurons to depletion of the neuronal membrane inositol pool.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01253112
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  • 10
    Electronic Resource
    Electronic Resource
    Chronic clorgyline treatment enhances release of norepinephrine following sympathetic stimulation in the rat (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 332 (1986), S. 236-242 
    Details
    ISSN: 1432-1912
    Keywords: Clorgyline ; Norepinephrine ; Epinephrine ; α-adrenoceptors ; Down-regulation of adrenoceptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Plasma catecholamine levels were determined in pithed rats during electrical stimulation of the entire sympathetic nervous system. In animals treated chronically with clorgyline (1 mg/kg daily for 21 days) the increment in plasma norepinephrine concentration during stimulation was greather than in control animals, whereas a single dose of clorgyline (2 mg/kg 2 h before pithing), which produced the same degree of inhibition of arterial MAO type A and a similar increase in arterial norepinephrine content, had no effect on the plasma norepinephrine response to stimulation. Injection of yohimbine (1 mg/kg) produced the same degree of enhancement of plasma norepinephrine response to stimulation in chronically treated and control animals, showing that the overall gain of the α2-adrenoceptor inhibitory loop in vascular sympathetic nerves was not affected. Plasma epinephrine concentration during electrical stimulation was also increased by chronic but not by acute clorgyline treatment. Chronic clorgyline treatment did not significantly affect the total systemic metabolic clearance rate of infused norepinephrine, thus the increased plasma norepinephrine response to stimulation reflects an increased release rate from sympathetic neurons. In rats treated chronically with clorgyline, the pressor response to norepinephrine in the presence of yohimbine (0.3 mg/kg) was significantly reduced, whereas the pressor response to guanabenz was unchanged. There was also no change in the guanabenz-induced inhibition of the tachycardic response to electrical stimulation. These results show that the enhanced norepinephrine release produced by chronic clorgyline treatment leads to down-regulation of post-synaptic α1-adrenoreceptors with no change in post-synaptic α2-adrenoceptors or in cardiac presynaptic α2-adrenoreceptors, and are in agreement with an intrasynaptic location of α1-adrenoceptors and an extra-synaptic location of α2-adrenoceptors in the rat vasculature.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00504860
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