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  • 1990-1994  (8)
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  • 1
    Electronic Resource
    Electronic Resource
    Enhancement by Cytidine of Membrane Phospholipid Synthesis (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Cytidine, as cytidine 5′-diphosphate choline, is a major precursor in the synthesis of phosphatidylcholine in cell membranes. In the present study, we examined the relationships between extracellular levels of cytidine, the conversion of [14C]choline to [14C]phosphatidylcholine, and the net syntheses of phosphatidylcholine and phosphatidyleth-anolamine by PC12 cells. The rate at which cytidine (as [3H]cytidine) was incorporated into the PC12 cells followed normal Michaelis-Menten kinetics (Km= 5 μM; Vmax= 12 × 10−3 mmol/mg of protein/min) when the cytidine concentrations in the medium were below 50 μM; at higher concentrations, intracellular [3H]cytidine nucleotide levels increased linearly. Once inside the cell, cytidine was converted mainly into cytidine triphosphate. In pulse-chase experiments, addition of cytidine to the medium caused a time- and dose-dependent increase (by up to 30%) in the incorporation of [14C]choline into membrane [14C]-phosphatidylcholine. When the PC12 cells were supplemented with both cytidine and choline for 14 h, small but significant elevations (p 〉 0.05) were observed in their absolute contents of membrane phosphatidylcholine, phospha-tidylethanolamine, and phosphatidylserine, all increasing by 10–15% relative to their levels in cells incubated with choline alone. Exogenous cytidine, acting via cytidine triphosphate, can thus affect the synthesis and levels of cell membrane phospholipids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08909.x
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of Catechol-O-Methyltransferase Inhibitors and L-3,4-Dihydroxyphenylalanine With or Without Carbidopa on Extracellular Dopamine in Rat Striatum (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 effects of two new catechol-O-methyltransferase (COMT) inhibitors, OR-611 and Ro 40-7592, in combination with L-3,4-dihydroxyphenylalanine (L-dopa) with or without carbidopa on extracellular levels of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 3-O-methyldopa (3-OMD), and 5-hydroxyindoleacetic acid in rat striatum were studied. A dose of 10 mg/kg i.p. of Ro 40-7592 alone, in contrast to the same dose of OR-611, decreased the dialysate level of HVA and increased that of DOPAC; this dose was thus used to differentiate between the effects of central and peripheral COMT inhibition. L-Dopa (50 mg/kg i.p.) alone slightly increased extracellular levels of DA, DOPAC, and HVA. The effects of L-dopa were potentiated by carbidopa (50 mg/kg i.p.), and even 3-OMD levels in dialysate samples became detectable. Both OR-611 and Ro 40-7592 significantly further increased the DA and DOPAC efflux from striatum produced by L-dopa. This increase was more pronounced when carbidopa was added to the treatment. OR-611 did not modify the effect of L-dopa or carbidopa/L-dopa on dialysate HVA levels, whereas Ro 40-7592 markedly reduced those levels. Both OR-611 and Ro 40-7592 very clearly suppressed dialysate 3-OMD levels produced by carbidopa/L-dopa. Ro 40-7592 was more effective than OR-611 in potentiating the effects of L-dopa or carbidopa/L-dopa. These in vivo data show that the new COMT inhibitors markedly inhibit the O-methylation of L-dopa and increase its availability to brain, which is reflected as increased DA formation. A significant effect can be achieved even by inhibiting only the peripheral COMT activity. The data suggest that COMT inhibitors may be of clinical importance as adjuncts in the treatment of Parkinson's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb05831.x
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  • 3
    Electronic Resource
    Electronic Resource
    4-Aminopyridine Increases Acetylcholine Release Without Diminishing Membrane Phosphatidylcholine (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: 4-Aminopyridine (10-4–10-5M) increased severalfold the release of acetylcholine from rat striatal slices superfused with an eserine-containing, choline-free medium, and caused stoichiometric decreases in the release of choline. It had no effect on tissue acetylcholine and choline levels. Electrical stimulation of the striatal slices increased acetylcholine release without affecting that of choline. Superfusion of the stimulated slices with 4-aminopyridine decreased choline release and increased the ratio of acetylcholine to choline in superfusates. As shown previously, electrical stimulation of the striatal slices decreased their contents of phospholipids, principally phosphatidylcholine; 4-aminopyridine fully protected against these membrane changes. In synaptosomal preparations, 4-aminopyridine was found to enhance the high-affinity uptake of [14C]choline and its conversion to [14C]acetylcholine. This effect on choline uptake may underlie 4-aminopyridine's ability to enhance acetylcholine release in the absence of supplemental choline while suppressing the “autocannibalism” of membrane phospholipids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb01963.x
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  • 4
    Electronic Resource
    Electronic Resource
    Phospholipid and Phospholipid Metabolites in Rat Frontal Cortex Are Decreased following Nucleus Basalis Lesions (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 695 (1993), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: Membrane phospholipid metabolism is abnormal in Alzheimer's disease (AD) brain. Phosphatidylcholine and phosphatidylethanolamine levels are decreased as are choline and ethanolamine, while glycerophosphocholine (GPC) and glycerophosphoethanolamine are increased.1 To develop a rat model for these changes, we examined the effects of unilateral lesion of the cholinergic nucleus basalis (nBM) with ibotenic acid (10 mg/ml in PBS, 0.5 μl) and sham lesion on frontocortical phospholipid, choline and GPC. After one week, choline acetyltransferase activity in frontal cortex was decreased (26%, p 〈 0.005, n = 14) on the nBM ibotenate-lesion side relative to the contralateral side, while there were no differences following the nBM sham-lesion. Levels of membrane phospholipids (nmol/mg protein) in adjacent frontal cortex sections exhibited concomitant decreases (13%, p 〈 0.05, n = 14) on the nBM ibotenate-lesion side, while there were no differences following the nBM sham-lesion. Tissue nBM ibotenate-lesion frontocortical choline and GPC levels were also decreased relative to those in control tissues (choline: 21%, p 〈 0.05, n = 14; GPC: 10%,p 〈 0.05, n = 14), while nBM sham-lesion showed no effect. Muscarinic receptor sensitivity in frontal cortex following nBM ibotenate-lesion was increased, as measured by carbachol-sdmulated inositol phosphate production (p 〈 0.001, n = 12), indicating that increased receptor mediated phospholipid hydrolysis in cortex may occur following nBM ibotenate-lesion. These data suggest that impaired cholinergic transmission alters phospholipid metabolism in cholinergic target regions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb23060.x
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  • 5
    Electronic Resource
    Electronic Resource
    Preface (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 695 (1993), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: This volume contains the papers and poster abstracts compiled for the seventh meeting of the International Study Group on the Pharmacology of Memory Disorders Associated with Aging (ISG), that took place in Zürich, Switzerland, on February 12–14, 1993. The ISG was founded 14 years ago in the belief that the development of effective treatments for Alzheimer's disease (AD) and other dementias would be accelerated by periodic meetings of scientists and physicians from around the world who are actively working on issues related to dementia. There have been six previous “Zurich Meetings”—in 1979, 1981, 1984, 1987, 1989, and 1991. The proceedings of the second ISB meeting were published by Raven Press in 1982 (Alzheimer's Disease: A Report of Progress in Research; Corkin, Davis, Growdon, Usdin, and Wurtman, editors); the proceedings of the fourth ISG meeting were published by Springer-Verlag in 1988 as Supplement 24 of the Journal of Neural Transmission (Topics in the Basic and Clinical Science of Dementia; Wurtman, Corkin, and Growdon, editors); the proceedings of the fifth ISB meeting were published by Raven Press in 1990 (Alzheimer's Disease, Advances in Neurology, Volume 51; Wurtman, Corkin, Growdon, and fitter-Walker, editors); and the proceedings of the sixth ISG meeting were published by the New York Academy of Sciences in 1992 (Aging and Alzheimer's Disease, Volume 640; Growdon, Corkin, fitter-Walker, and Wurtman, editors).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb23017.x
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  • 6
    Electronic Resource
    Electronic Resource
    Regulation of Amyloid Precursor Protein Release By Protein Kinase C in Swiss 3T3 Fibroblasts (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 695 (1993), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: Release of the amyloid precursor protein (APP) of Alzheimer's disease from Swiss 3T3 fibroblasts was stimulated in a concentration-dependent manner by phorbol 12-myristate 13-acetate. In fibroblasts overexpressing protein kinase Co (PKCα), the EC50 for this response was 7 nM, while in control cells the EC50 was 63 nM. The effect of PMA was inhibited by the PKC antagonist H-7 in control cells, but not in cells that overexpressed PKCα. Basal release of APP was higher in cells that overexpressed PKCα, and was not affected by the phosphatase inhibitor okadaic acid, although this compound doubled APP release from control cells. The results suggest that PKCα regulates APP processing in mammalian cells. Alterations in the activity of PKC have been reported to occur in Alzheimer's disease and might potentially contribute to abnormalities of APP metabolism characteristic of this disorder.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb23040.x
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  • 7
    Electronic Resource
    Electronic Resource
    Receptor-coupled Amyloid Precursor Protein Processing (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 695 (1993), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: The family of β-amyloid protein precursors (APP) can be processed via several alternative proteolytic pathways. Some generate potentially amyloidogenic AFP derivatives, whereas others preclude the formation of such fragments. The cellular mechanisms regulating the relative activities of these pathways are thus important in determining the factors contributing to the formation of amyloidogenic APP derivatives. In order to investigate whether cell-surface receptor activity can regulate APP processing, HEK 293 cell lines stably expressing human muscarinic acetylcholine receptors (mAChR; subtypes m1, m2, m3, m4) were stimulated with the muscarinic agonist carbachol, and the release of APP derivatives was measured. Carbachol increased the release of large amino-terminal APP-fragments 4-to 6-fold in cell lines expressing the m1 or m3 receptors but not in those expressing m2 or m4 subtypes. This increase was blocked by various protein kinase inhibitors and mimicked by phorbol esters, indicating that it is mediated by protein kinase activation, presumably by protein kinase C (PKC). To determine whether additional cell-surface receptor types linked to this signal transduction pathway could also regulate APP processing, we stimulated differentiated PC-12 cells with bradykinin and found that this neuropeptide also increased the secretion of amino-terminal APP derivatives. We next investigated the possibility that neuronal depolarization might affect APP processing in mammalian brain. Electrically stimulated rat hippocampal slices released two times more amino-terminal APP derivatives than unstimulated control slices. This release increased with increasing stimulation frequencies in the physiological firing range of hippocampal pyramidal cells, and was blocked by tetrodotoxin. These results suggest that, in brain, APP processing is regulated by neuronal activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb23039.x
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  • 8
    Electronic Resource
    Electronic Resource
    Effect of pharmacological daytime doses of melatonin on human mood and performance (1993)
    Springer
    Psychopharmacology 112 (1993), S. 490-496 
    Details
    ISSN: 1432-2072
    Keywords: Human ; Melatonin ; Mood ; Performance ; Reaction time ; Vigilance ; Fatigue ; Circadian ; Sleep ; Alertness
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Melatonin (10, 20, 40, or 80 mg, PO) or placebo was administered at 1145 hours on five separate occasions to 20 healthy male volunteers and the effects on serum melatonin levels, mood, performance, and oral temperature were monitored. Subjects were studied between 0930 and 1700 hours. A battery of interactive computer tasks designed to assess performance and mood was completed, oral temperature was measured, and blood samples were taken for serum melatonin radioimmunoassay. The areas under the time-melatonin concentration curve (AUC) varied significantly in proportion to the various melatonin doses. Compared with placebo treatment, all melatonin doses significantly decreased oral temperature, number of correct responses in auditory vigilance, response latency in reaction time, and self-reported vigor. Melatonin also increased self-reported fatigue, confusion, and sleepiness.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02244899
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