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  • 1
    Electronic Resource
    Electronic Resource
    Increase in Kynurenic Acid in Huntington's Disease Motor Cortex (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Huntington's disease is a neurological disorder characterised by a progressive chorea and dementia. Recent evidence has suggested that dysfunction involving endogenous excitatory amino acids may be important in the pathogenesis of this disease. Following the recent demonstration that kynurenic acid is present in the brain, we examined the levels in various areas of brain from patients who died with Huntington's disease and from age/sex-matched controls. Blocks (100–500 mg) of cortex (Brodmann's areas 4 and 10) and caudate nucleus and globus pallidus (lateral and medial parts) were obtained from the Cambridge Brain Bank. The tissue was then processed for the extraction and analysis of kynurenic acid. Whereas no differences in the content of kynurenic acid were observed in the caudate nucleus, lateral or medial globus pallidus, or prefrontal cortex (area 10) between controls' brains and those from patients who died with Huntington's disease, there was a 94% (p 〈 0.01; n = 5) increase in the kynurenic acid content in the motor cortex (area 4) from Huntington's disease brains, relative to those of controls. Some time ago we suggested that a subtle change in the relative concentrations of quinolinic and kynurenic acids might be important in the pathogenesis of neurodegeneration. It is possible that the observation of raised kynurenic acid levels supports this supposition. Further work is now in progress to determine whether the change in kynurenic acid is a primary effect or a compensatory response to an increase in excitatory activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb02552.x
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  • 2
    Electronic Resource
    Electronic Resource
    Presence of Kynurenic Acid in the Mammalian Brain (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 51 (1988), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Kynurenic acid, a tryptophan metabolite able to antagonize the actions of the excitatory amino acids, has been identified and measured for the first time in the brain of mice, rats, guinea pigs, and humans by using an HPLC method. Its content was 5.8 ± 0.9 in mouse brain, 17.8 ± 2.0 in rat brain, 16.2 ± 1.5 in guinea pig brain, 26.8 ± 2.9 in rabbit brain, and 150 ± 30 in human cortex (pmol/g wet wt, mean ± SE). The regional distribution of this molecule was uneven. In rats, guinea pigs, and rabbits, the brainstem was the area richest in this compound. Tryptophan administration (100–300 mg/kg, i.p.) to rats resulted in a significant increase of the brain content of kynurenic acid. Similarly, 1 h after probenecid administration (200 mg/kg, i.p.), the brain content of kynurenate increased by fourfold, thus suggesting that its turnover rate is relatively fast.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1988.tb04852.x
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  • 3
    Electronic Resource
    Electronic Resource
    Increase in the Content of Quinolinic Acid in Cerebrospinal Fluid and Frontal Cortex of Patients with Hepatic Failure (1986)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 47 (1986), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Quinolinic acid (QUIN), an excitotoxic tryptophan metabolite, has been identified and measured in human cerebrospinal fluid (CSF) using a mass-fragmentographic method. Furthermore, its content has been evaluated in frontal cortex obtained at autopsy from the cadavers of patients who died after hepatic coma. During the coma, the concentration of QUIN in the CSF was 152 ± 38 pmol ml-1. In contrast, the concentration in control patients affected by different pathologies was 22 ± 7 pmol ml-1. In the frontal cortex of patients who died after episodes of hepatic encephalopathy, the content of QUIN was three times higher than in controls (2.6 ± 0.6 versus 0.80 ± 0.08 nmol/g wet weight). As a result of these investigations we are now able to extend our previous observations on the increase of QUIN in the brains of rats used as experimental models of hepatic encephalopathy to man. QUIN should therefore be added to the list of compounds possibly involved in the pathogenesis and symptomatology of brain disorders associated with liver failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1986.tb13071.x
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  • 4
    Electronic Resource
    Electronic Resource
    Content of Quinolinic Acid and of Other Tryptophan Metabolites Increases in Brain Regions of Rats Used as Experimental Models of Hepatic Encephalopathy (1986)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 46 (1986), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The content of the tryptophan metabolites quinolinic acid (QUIN), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) was measured in various brain areas of rats bearing a portocaval anastomosis (PCA) for 4 weeks, using mass fragmentography or HPLC. In these animals, the content of the excitotoxic compound QUIN increased by 75% in the cortex and 125% in the cerebellum. The content of 5-HT increased by 27% in the brainstem. No changes occurred in other brain areas. On the other hand, the content of 5-HIAA increased by 66% in the cortex, 65% in the caudate, 64% in the hippocampus, 120% in the diencephalon, and 185% in the brainstem. Probenecid administration caused a larger increase of 5-HIAA accumulation in various brain areas of PCA-bearing rats than in those of sham-operated controls. The cortical content of QUIN and 5-HIAA increased after administration of ammonium acetate (7 mmol/kg), whereas an equimolar amount of sodium acetate was inactive. These results confirm that profound changes in the disposition of tryptophan occur in the brains of experimental animals used as models of hepatic encephalopathy. Furthermore, this study adds the excitotoxic compound QUIN to the list of molecules possibly involved in the pathogenesis of this brain disorder.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1986.tb13052.x
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  • 5
    Electronic Resource
    Electronic Resource
    The DIX domain targets dishevelled to actin stress fibres and vesicular membranes (2002)
    [s.l.] : Macmillian Magazines Ltd.
    Nature 419 (2002), S. 726-729 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Colorectal cancer results from mutations in components of the Wnt pathway that regulate β-catenin levels. Dishevelled (Dvl or Dsh) signals downstream of Wnt receptors and stabilizes β-catenin during cell proliferation and embryonic axis formation. Moreover, Dvl contributes to ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nature01056
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  • 6
    Electronic Resource
    Electronic Resource
    Identification and measurement of kynurenic acid in the rat brain and other organs
    Amsterdam : Elsevier
    Analytical Biochemistry 169 (1988), S. 89-94 
    Details
    ISSN: 0003-2697
    Keywords: HPLC techniques ; gas chromatography-mass spectrometry ; glutamate antagonists ; neurochemistry ; tryptophan
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0003-2697(88)90258-8
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  • 7
    Electronic Resource
    Electronic Resource
    Homotaurine and muscimol mimic taurine and gaba effects on muscle tone and temperature regulation (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 305 (1978), S. 155-158 
    Details
    ISSN: 1432-1912
    Keywords: Taurine ; Homotaurine ; GABA ; Muscimol ; Intraventricular administration ; Muscle tone ; Temperature regulation ; Electrocorticogram
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Taurine, homotaurine, GABA and muscimol, given intraventricularly to the conscious, unrestrained rabbit cause hypothermia and a reduction in skeletal muscle tone. Taurine and homotaurine desynchronize areas of the motor and limbic cortices, while GABA and muscimol synchronize both tracings and markedly depress the arousal reaction following external stimuli.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508286
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  • 8
    Electronic Resource
    Electronic Resource
    Muscle relaxation induced in the rabbit by intracerebroventricular taurine injection (1976)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 295 (1976), S. 95-97 
    Details
    ISSN: 1432-1912
    Keywords: Taurine ; Intracerebroventricular administration ; Muscle tone ; Temperature regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Taurine, given intracerebroventricularly to the conscious unrestrained rabbit, causes hypothermia and a reduction in skeletal muscle tone. Evidence has been produced that the latter effect is of a central, supraspinal origin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00509779
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  • 9
    Electronic Resource
    Electronic Resource
    Ammonium acetate inhibits ionotropic receptors and differentially affects metabotropic receptors for glutamate (1994)
    Springer
    Journal of neural transmission 97 (1994), S. 187-196 
    Details
    ISSN: 1435-1463
    Keywords: Ammonia toxicity ; glutamate receptors ; 1S,3R-ACPD ; cyclic AMP ; inositol phosphates ; hepatic encephalopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of ammonium salts in concentration similar to those found in plasma in course of hepatic encephalopathy (2–4 mM) were studied in brain slices in order to clarify how glutamate synapses are affected by this pathological situation. Electrophysiological (mice cortical wedge preparations) and biochemical techniques (inositol phosphates and cyclic AMP measurements) were used so that the function of both the ionotropic and metabotropic glutamate receptors was evaluated. Ammonium acetate (2–4 mM), but not sodium acetate reduced the degree of depolarization of cortical wedges induced by different concentrations of N-methyl-D-aspartic acid (NMDA) or (S)-alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). This reduction was non-competitive in nature and did not reverse during the experimental period (90 min). In a similar manner, ammonium acetate reduced the formation of inositol phosphates induced by (1S,3R)-1-amynocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) (100μM), the prototype agonist of metabotropic glutamate receptors. When the metabotropic glutamate receptors negatively linked to the forskolin-stimulated cyclic AMP formation were evaluated, ammonium acetate significantly hampered forskolin effects and its actions were additive with those of the metabotropic glutamate receptor agonist 1S,3R-ACPD. In conclusion, our results suggest that toxic concentrations of ammonium impair the function of glutamate receptors of NMDA and AMPA type and of the metabotropic glutamate receptors linked to inositol phosphate formation while they functionally potentiate the action of glutamate agonists on the receptors negatively linked to adenylyl cyclase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02336140
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