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  • 1
    Electronic Resource
    Electronic Resource
    Evidence for a G Protein-Coupled γ-Hydroxybutyric Acid Receptor (2000)
    Oxford UK : Blackwell Science Ltd.
    Journal of neurochemistry 75 (2000), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract:γ-Hydroxybutyric acid (GHB) is a naturally occurring metabolite of GABA that has been postulated to exert ubiquitous neuropharmacological effects through GABAB receptor (GABABR)-mediated mechanisms. The alternative hypothesis that GHB acts via a GHB-specific, G protein-coupled presynaptic receptor that is different from the GABABR was tested. The effect of GHB on regional and subcellular brain adenylyl cyclase in adult and developing rats was determined and compared with that of the GABABR agonist (-)-baclofen. Also, using guanosine 5′-O-(3-[35S]thiotriphosphate) ([35S]GTPγS) binding and low-Km GTPase activity as markers the effects of GHB and (-)-baclofen on G protein activity in the brain were determined. Neither GHB nor baclofen had an effect on basal cyclic AMP (cAMP) levels. GHB significantly decreased forskolin-stimulated cAMP levels by 40-50% in cortex and hippocampus but not thalamus or cerebellum, whereas (-)-baclofen had an effect throughout the brain. The effect of GHB on adenylyl cyclase was observed in presynaptic and not postsynaptic subcellular tissue preparations, but the effect of baclofen was observed in both subcellular preparations. The GHB-induced alteration in forskolin-induced cAMP formation was blocked by a specific GHB antagonist but not a specific GABABR antagonist. The (-)-baclofen-induced alteration in forskolin-induced cAMP formation was blocked by a specific GABABR antagonist but not a specific GHB antagonist. The negative coupling of GHB to adenylyl cyclase appeared at postnatal day 21, a developmental time point that is concordant with the developmental appearance of [3H]GHB binding in cerebral cortex, but the effects of (-)-baclofen were present by postnatal day 14. GHB and baclofen both stimulated [35S]GTPγS binding and low-Km GTPase activity by 40-50%. The GHB-induced effect was blocked by GHB antagonists but not by GABABR antagonists and was seen only in cortex and hippocampus. The (-)-baclofen-induced effect was blocked by GABABR antagonists but not by GHB antagonists and was observed throughout the brain. These data support the hypothesis that GHB induces a G protein-mediated decrease in adenylyl cyclase via a GHB-specific G protein-coupled presynaptic receptor that is different from the GABABR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2000.0751986.x
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  • 2
    Electronic Resource
    Electronic Resource
    Mutations in a gene encoding a novel protein tyrosine phosphatase cause progressive myoclonus epilepsy (1998)
    [s.l.] : Nature America Inc.
    Nature genetics 20 (1998), S. 171-174 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Lafora's disease (LD; OMIM 254780) is an autosomal recessive form of progressive myoclonus epilepsy characterized by seizures and cumulative neurological deterioration. Onset occurs during late childhood and usually results in death within ten years of the first symptoms1,2. With few exceptions, ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/2470
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  • 3
    Electronic Resource
    Electronic Resource
    Pharmacologic rescue of lethal seizures in mice deficient in succinate semialdehyde dehydrogenase (2001)
    [s.l.] : Nature Publishing Group
    Nature genetics 29 (2001), S. 212-216 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Succinate semialdehyde dehydrogenase (ALDH5A1, encoding SSADH deficiency is a defect of 4-aminobutyric acid (GABA) degradation that manifests in humans as 4-hydroxybutyric (gamma-hydroxybutyric, GHB) aciduria. It is characterized by a non-specific neurological disorder including psychomotor ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/ng727
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  • 4
    Electronic Resource
    Electronic Resource
    Electroencephalographic and behavioral correlates in rats during repeated ethanol withdrawal syndromes (1984)
    Springer
    Psychopharmacology 83 (1984), S. 140-146 
    Details
    ISSN: 1432-2072
    Keywords: Ethanol ; Physical dependence ; Ethanol withdrawal syndrome ; EEG withdrawal signs ; Blood ethanol levels ; Readdiction ; Repeated ethanol withdrawals ; Ethanol potentiation hypothesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rats chronically implanted with electrodes in the amygdala, thalamus, hippocampus, and cortex were addicted twice, separated by an interval of 2 weeks, with 18 days of ethanol liquid diet. The diet consumption and the blood ethanol levels (BELs) were carefully controlled twice a day during both addictive phases. After ethanol removal the behavioral and electroencephalographic (EEG) changes were continuously monitored for 24 h. During each withdrawal the behavioral and EEG changes appeared at the same time, the EEG changes being of shorter duration Behavioral and EEG changes (primarily in hippocampus) were more severe and of earlier onset during the second withdrawal. In spite of an ethanol liquid diet intake comparable to that of the first addiction, during the ethanol readdiction the BELs were found to fluctuate. The results support the hypothesis of an ethanol withdrawal potentiation through a mechanism of kindling of different brain areas related to the observed BEL fluctuations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00429722
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