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  • 1
    Electronic Resource
    Electronic Resource
    EFFECT OF PRETREATMENT UNDER VARIOUS CATIONIC CONDITIONS ON ACETYLCHOLINE CONTENT AND CHOLINE TRANSPORT IN RAT WHOLE BRAIN SYNAPTOSOMES (1978)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 31 (1978), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effects of different ionic environments were measured on the concentration of acetyl-choline (ACh) from synaptosomes and their effect on subsequent high affinity choline (Ch) transport and ACh synthesis after resuspension of the synaptosomes in the normal Krebs medium. KCl (40 mM) was used to induce ACh release and reduce synaptosomal ACh content. The effects of Na+ omission, Ca2+ omission, and high Mg2+ on spontaneous (KC1: 4.75 mM) and potassium induced (KC1: 40 mM) ACh release and other cholinergic parameters are presented. The high affinity transport of Ch was more highly correlated with the reciprocal of the ACh level (r= 0.934, P= 9.7 × 10-4) than with the ACh release rate during preincubation (r= 0.792, P= 3.4 × 10-2). The results are consistent with the view that the consequences of the various ionic conditions on Ch transport and ACh synthesis are dependent on their effects on intrasynaptosomal ACh levels and only secondarily on synaptosomal ACh release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1978.tb00112.x
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  • 2
    Electronic Resource
    Electronic Resource
    REGULATION OF ACETYLCHOLINE SYNTHESIS: CONTROL OF CHOLINE TRANSPORT AND ACETYLATION IN SYNAPTOSOMES (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 high affinity transport of choline (Ch) and the synthesis of acetylcholine (ACh) were measured in synaptosomes by measuring the utilization of [2H4]Ch. The synthesis of ACh was reduced under several conditions which reduce the availability of acetyl coenzyme A (AcCoA) including no glucose added, replacement of glucose with succinate or impairment of glucose utilization by bromopyr-uvate, NaCN, or pentobarbital. These conditions did not reduce the amount of unacetylated [2H4]Ch in the synaptosomes indicating that the high affinity transport of Ch is not directly coupled to the synthesis of ACh.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1978.tb12386.x
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  • 3
    Electronic Resource
    Electronic Resource
    Conditioned avoidance response and acetylcholine and choline levels in rat brain (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
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1978.tb10507.x
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  • 4
    Electronic Resource
    Electronic Resource
    THE REGULATION OF PYRUVATE DEHYDROGENASE IN BRAIN IN VIVO (1976)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 26 (1976), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: —The activity of pyruvate dehydrogenase in the brains of mice frozen in liquid nitrogen was 14·0 nmol/min per mg protein. It rose to 23·8 nmol/min per mg protein after incubation of the brain homogenate with 10mm-MgCl2 to activate (dephosphorylate) the enzyme, indicating that approx 60% of the enzyme was originally in the active form. Treatment with amobarbital or pentobarbital halved the proportion of pyruvate dehydrogenase in the active form. The proportion of pyruvate dehydrogenase in the active form increased during ischemia, activation being complete within one min. Anesthesia with amobarbital slowed the activation during ischemia but did not alter the total amount of pyruvate dehydrogenase activity. The concentration of ATP, the ATP/ADP ratio and the adenylate energy charge increased as the proportion of pyruvate dehydrogenase in the active form decreased during barbiturate anesthesia, and they decreased as the proportion of pyruvate dehydrogenase in the active form increased during ischemia. After treatment with insulin, the proportion of pyruvate dehydrogenase in the active form increased by 30%. but the energy charge did not change. Treatment of mice with ether, morphine, ethanol, or diazepam did not change the proportion of pyruvate dehydrogenase in the active form although these treatments have been reported to alter pyruvate oxidation in brain in vivo. Treatments which altered pyruvate oxidation in the brain did not consistently alter the proportion of pyruvate dehydrogenase in the active form, unless they also altered energy charge.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1976.tb04440.x-i1
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  • 5
    Electronic Resource
    Electronic Resource
    Formation of triple-stranded bovine DNA in vitro (1975)
    [s.l.] : Nature Publishing Group
    Nature 254 (1975), S. 86-87 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] We used a magnesium salt of bovine DNA, which was prepared from bovine spleen by substituting MgCl2 for the sodium chloride-sodium citrate medium (SSC) in a standard DNA preparation procedure4. Sodium xylene sulphonate (Naxonate G) was added to precipitate protein. The MgDNA so prepared was ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/254086a0
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  • 6
    Electronic Resource
    Electronic Resource
    Glycogen synthase kinase-3β, β-catenin, and tau in postmortem bipolar brain (1999)
    Springer
    Journal of neural transmission 106 (1999), S. 1217-1222 
    Details
    ISSN: 1435-1463
    Keywords: Keywords: Bipolar disorder, glycogen synthase kinase-3β, β-catenin, tau.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Therapeutic concentrations of the anti-bipolar drug lithium inhibit the activity of glycogen synthase kinase-3β, which raises the possibility that this enzyme and its substrates may be altered in the brain of subjects with bipolar disorder. Therefore, in prefrontal cortical samples from subjects with bipolar disorder and age-matched control subjects, we examined the levels of glycogen synthase kinase 3β and of two proteins modified by it, β-catenin and the microtubule associated protein tau. There were no significant differences between subject groups among these measurements, but there was a tendency for the tau isoform profile to be modified in bipolar tissue. Thus, while there are no differences between bipolars and controls in prefrontal cortical levels of glycogen synthase kinase-3β, β-catenin, or tau, tau isoform levels or phosphorylation states may be modified in bipolar disorder.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007020050235
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  • 7
    Electronic Resource
    Electronic Resource
    Circadian variation in rat brain AP-1 DNA binding activity after cholinergic stimulation: modulation by lithium (1995)
    Springer
    Psychopharmacology 122 (1995), S. 363-368 
    Details
    ISSN: 1432-2072
    Keywords: Lithium ; AP-1 ; Circadian rhythm ; Cholinergic stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The potential influence of a circadian rhythm and its modulation by lithium on the stimulation of AP-1 DNA binding activity by the cholinergic agonist pilocarpine was investigated in rat cerebral cortex. Stimulation of AP-1 binding after pilocarpine (30 mg/kg) was evident within 1 h and was maximally stimulated by 200% at 2 h. Pilocarpine-stimulated AP-1 binding exhibited a circadian rhythm in AP-1 binding measured at 0800, 1200, and 1600 hours, 2 h after pilocarpine. Pilocarpine-stimulated AP-1 binding at 0800 hours was approximately twice the level measured at 1600 hours. After acute lithium treatment, pilocarpine administration induced generalized seizures after about 20 min and stimulated AP-1 binding which increased continuously for 4.5 h, at which time the stimulation was 900% above control. A circadian variation was apparent in AP-1 binding stimulated by acute lithium plus pilocarpine, with stimulation at 0800 hours being 1.5 times that at 1600 hours. After chronic lithium and pilocarpine, which also produced seizures, there was no circadianvariation in pilocarpine-stimulated AP-1 binding. Thus pilocarpine-induced AP-1 binding in rat cerebral cortex was influenced by a circadian rhythm, but this was abolished by chronic lithium administration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02246267
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  • 8
    Electronic Resource
    Electronic Resource
    Alpha-1 adrenergic receptor binding and adrenergic-stimulated cyclic AMP production in rat cerebral cortex after chronic lithium treatment (1990)
    Springer
    Journal of neural transmission 82 (1990), S. 197-204 
    Details
    ISSN: 1435-1463
    Keywords: Lithium ; cyclic AMP ; alpha adrenergic receptor ; chlorethylclonidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Administration to rats of dietary lithium for 30 days was followed by evaluation of alpha-1 adrenergic receptor binding and of adrenergic-stimulated cyclic AMP (cAMP) accumulation in rat cerebral cortex. Chronic lithium treatment did not alter the binding characteristics of [3H]prazosin or the proportion of alpha-1 adrenergic receptor subtypes distinguished by chlorethylclonidine (CEC) pretreatment in rat cerebral cortical membranes. Accumulation of cAMP in cortical slices incubated with adrenergic agonists was unaffected in lithium-treated rats. These results demonstrate that chronic lithium treatment-induced reduction of norepinephrine (NE)-stimulated phosphoinositide (PI) hydrolysis (Casebolt and Jope, 1987) is not due to changes in the alpha-1 adrenergic receptor and is more sensitive to in vivo lithium treatment than is adrenergic-stimulated cAMP accumulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01272762
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