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  • 1
    Electronic Resource
    Electronic Resource
    Cluster headache: clinical efficacy of lithium salts in a haemodialysis treated patient (1985)
    USA/Oxford, UK : Blackwell Science Ltd
    Cephalalgia 5 (1985), S. 0 
    Details
    ISSN: 1468-2982
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Over the last ten years the efficacy of lithium salts in cluster headache has been well demonstrated. Our patient, who had been suffering from cluster headache for approximately 30 years, had been in haemodialysis treatment for the last ten years for chronic renal failure. Moreover, he was affected by heart failure and peptic ulcer. The patient was currently under therapy with Digitalis, Isorbide dinitrate, and ranitidine and was dialyzed three times a week for a total of five hours each time. Neither prophylactic headache therapy nor high doses of analgesic drugs had proved effective. Although this patient was in haemodialysis, lithium treatment was indicated. The administration of lithium carbonate 300 mg during dialysis days and 150 mg during non-dialysis days improved the attacks. Complete recovery from the attacks was obtained when the serum levels of lithium reached the therapeutic range. No side effects were noted.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1468-2982.1985.0502095.x
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  • 2
    Electronic Resource
    Electronic Resource
    Differential Interaction of 1-Methyl-4-Phenylpyridinium Ion with the Putatively Vesicular Binding Site of [3H]Tyramine in Dopaminergic and Nondopaminergic Brain Regions (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 60 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The neurotoxin 1-methyl-4-phenylpyridinium ion (MPP+) in the brain striatum has recently been shown to bind at a putatively vesicular site labeled by [3H]tyramine ([3H]TY). Whereas in the rat and mouse striatum MPP+ antagonized TY binding competitively, in the cerebellum there was a mixed-type antagonism, which suggests the simultaneous occupancy of two different sites. Ki values from displacement curves revealed a fourfold difference in the affinity of MPP+ for TY sites in the two brain regions. The degeneration of central noradrenergic terminals induced by an intraperitoneal injection of the toxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine in rats decreased by 80% the maximal number of cerebellar TY binding sites, while not affecting striatal binding. Furthermore, guanethidine, a marker for noradrenaline (NA) vesicles, potently inhibited TY binding in NA-innervated regions, such as the cerebellum and the parietal cortex, and poorly in the striatum. It is concluded (a) that both MPP+ and TY may also label NA vesicles and (b) that the vesicular carriers for dopamine and NA have different characteristics, which may underlie a regional specificity in the rate of endovesicular sequestration of MPP+, with either neurodegenerative or neuroprotective consequences, depending on the brain area involved.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb03212.x
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  • 3
    Electronic Resource
    Electronic Resource
    [3H]1-Methyl-4-Phenyl-2,3-Dihydropyridinium Ion Binding Sites in Mouse Brain: Pharmacological and Biological Characterization (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 54 (1990), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Because 1-methyl-4-phenyl-2,3-dihydropyridinium ion (MPP+) appears to damage the dopaminergic neuron and cause neuronal death, we characterized [3H]MPP+ binding sites in mouse brain membranes. Among several compounds tested, debrisoquin [3,4-dihydro-2(1 H)-isoquinolinecarboxamidine] and some analogues were able to antagonize [3H]MPP+ binding. Debrisoquin is able to block adrenergic transmission and inhibit the activity of monoamine oxidase A (MAO-A). We found a certain correlation between the ability of these agents to displace [3H]MPP+ from its binding sites and their capacity to inhibit MAO-A activity. These data and the finding of a higher number of [3H]MPP+ binding sites in human placenta compared to mouse brain suggest that these sites may correspond to MAO-A enzymes. Recently it has been demonstrated in human brain that neurons in regions rich in catecholamines are positive for MAO-A. Accordingly, we suggest MAO-A as a possible accumulation site of MPP+ within the dopaminergic neuron. We also indicate the chemical structural requirement associated with the best binding of debrisoquin analogues with [3H]MPP+ sites. It would be reasonable to test the effects of debrisoquinlike drugs able to pass the blood-brain barrier on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine toxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb04889.x
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  • 4
    Electronic Resource
    Electronic Resource
    1 -Methyl-4-Phenyl- 1,2,3,6-Tetrahydropyridine: Correspondence of Its Binding Sites to Monoamine Oxidase in Rat Brain, and Inhibition of Dopamine Oxidative Deamination In Vivo and In Vitro (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: A saturable, specific, high-affinity binding site for [3H] 1 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine was found in rat brain homogenates. The CNS regional distribution, the subcellular fractionation, and the displacement by pargyline, clorgyline, and deprenyl suggest that this binding site may correspond to monoamine oxidase. I -Methyl-4-phenyl-1,2,3,6-tetrahydropyridine inhibited the oxidative deamination of dopamine, both in vivo and in vitro. Striatal levels of 3,4-dihydroxyphenylacetic acid were significantly reduced shortly after intravenous administration, and returned to normal values after a few hours. The in vitro formation of 3,4-dihydroxyphenylacetic acid from dopamine was inhibited by concentrations of 1-methyl-4-phenyl- 1,2,3,6-tetrahydropyridine comparable to those of pargyline.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1985.tb04045.x
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  • 5
    Electronic Resource
    Electronic Resource
    Localization of MPP+ binding sites in the brain of various mammalian species (1992)
    Springer
    Journal of neural transmission 4 (1992), S. 181-190 
    Details
    ISSN: 1435-1463
    Keywords: MPP+ ; binding sites ; autoradiography mammalian brain ; dopamine ; neurotoxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The distribution and density of3H-MPP+ binding sites were studied by in vitro quantitative autoradiography in the brain of the mouse, rat and monkey. The highest levels of3H-MPP+ specific binding were observed in rat brain. The substantia nigra in rat and monkey, and the anterior caudate-putamen formation in mouse and monkey showed the lowest density of autoradiographic grains. The presence of a relatively high density of MPP+ sites in the hippocampus of all species studied could be of interest to explain some effects of MPTP administration on convulsions caused by chemoconvulsants. The finding of a 60–70% reduction of3H-MPP+ binding sites in the rat caudate-putamen, on the side of quinolinic acid infusion and no changes after 6-hydroxydopamine lesion of dopaminergic nigrostriatal neurons suggests the presence of these sites mainly on striatal cells. The results suggest that the distribution of MPP+ binding sites in brain would not seem to be related to MPTP toxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02260902
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  • 6
    Electronic Resource
    Electronic Resource
    Parkinsonism by haloperidol and piribedil (1978)
    Springer
    Psychopharmacology 59 (1978), S. 139-141 
    Details
    ISSN: 1432-2072
    Keywords: Piribedil ; Haloperidol ; Parkinsonism ; Self-inhibitory dopamine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Three groups of schizophrenic patients were treated with haloperidol, with a low dose of piribedil (a dopamine agonist), and with a combination of the two treatments, respectively. After a few days, all 7 patients treated with the drug combination showed marked rigidity and akinesia, while patients treated with haloperidol alone (4) and piribedil alone (4) showed either mild or no symptoms of parkinsonism. The drug combination induced mainly an akinetic-hypertonic syndrome, while tremors were absent or mild. The results suggest that low doses of the DA-agonist potentiate the extrapyramidal side effects of haloperidol by acting on self-inhibitory DA receptors, thereby blocking the compensatory increase in dopaminergic firing elicited by the neuroleptic agent.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00427747
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  • 7
    Electronic Resource
    Electronic Resource
    Therapeutical efficacy of a combination of apomorphine with sulpiride or metoclopramide in parkinsonism (1976)
    Springer
    Psychopharmacology 47 (1976), S. 169-173 
    Details
    ISSN: 1432-2072
    Keywords: Apomorphine ; Sulpiride ; Metoclopramide ; Haloperidol ; Parkinson's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In healthy volunteers the emetic effect of apomorphine (5–10 mg, i.m.) was prevented by haloperidol (2 mg), metoclopramide (10 mg) and sulpiride (100 mg), injected intramuscularly. In parkinsonian patients, apomorphine (1 mg) given alone ameliorated the neurological symptoms (30% improvement in the disability score), but the improvement was accompanied by nausea, vomiting, sedation or sleepiness. Haloperidol (2 mg) prevented not only the emetic effect of apomorphine (10 mg), but also its therapeutic efficacy in parkinsonism. Indeed, the disability score was worsened by the drug combination in some patients. Moreover, after haloperidol, apomorphine produced deep sedation and sleep. By contrast, in parkinsonian patients pretreated with metoclopramide (10 mg) or sulpiride (100 mg), apomorphine (10 mg) markedly diminished tremor and rigidity and failed to produce nausea, vomiting and sleepiness.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00735817
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