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  • 1
    Electronic Resource
    Electronic Resource
    Positron emission tomographical studies of 1-11C-acetoacetate, 2-18F-fluoro-deoxy-D-glucose, and L-1-11C-tyrosine uptake by cat brain with an experimental lesion (1989)
    Springer
    Acta neurochirurgica 99 (1989), S. 166-172 
    Details
    ISSN: 0942-0940
    Keywords: Positron emission tomography ; 18F-fluorodeoxyglucose ; ketone bodies ; 11C-tyrosine ; brain oedema ; blood-brain barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In cat brain with a freezing injury, the uptake of 1-11C-acetoacetate (11C-ACAC), 2-18F-fluorodeoxy-D-glucose (18FDG), and L-1-11C-tyrosine (11C-TYR) was monitored by positron emission tomography following intravenous administration of the tracers, at 1 day and 1–3 weeks after the injury. The development and further course of the cold-induced oedema was monitored by magnetic resonance imaging. In the fresh (1 day old) lesion there was increased uptake of11C-ACAC, probably due to release of the restrictive influence of the blood-brain barrier upon passage of the substance into brain. The uptake of18FDG, which normally occurs by carrier-mediated transport at the barrier, was decreased in the fresh lesion, probably as a result of damage of the carrier mechanism. In the 3 week old lesion18FDG uptake was still reduced, and11C-ACAC uptake was still increased, although barrier function to Evans blue had recovered. It is suggested, that the increased11C-ACAC uptake in the chronic lesion bears upon the proliferation of macrophages and reactive glial cells in the lesion. This is supported by the increased uptake of11C-TYR in the 2 weeks old lesion, while in the fresh lesion11C-TYR uptake was unchanged.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01402328
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  • 2
    Electronic Resource
    Electronic Resource
    β-Amyloid neurotoxicity is mediated by a glutamate-triggered excitotoxic cascade in rat nucleus basalis (2000)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 12 (2000), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Whereas a cardinal role for β-amyloid protein (Aβ) has been postulated as a major trigger of neuronal injury in Alzheimer's disease, the pathogenic mechanism by which Aβ deranges nerve cells remains largely elusive. Here we report correlative in vitro and in vivo evidence that an excitotoxic cascade mediates Aβ neurotoxicity in the rat magnocellular nucleus basalis (MBN). In vitro application of Aβ to astrocytes elicits rapid depolarization of astroglial membranes with a concomitant inhibition of glutamate uptake. In vivo Aβ infusion by way of microdialysis in the MBN revealed peak extracellular concentrations of excitatory amino acid neurotransmitters within 20–30 min. Aβ-triggered extracellular elevation of excitatory amino acids coincided with a significantly enhanced intracellular accumulation of Ca2+ in the Aβ injection area, as was demonstrated by 45Ca2+ autoradiography. In consequence of these acute processes delayed cell death in the MBN and persistent loss of cholinergic fibre projections to the neocortex appear as early as 3 days following the Aβ-induced toxic insult. Such a sequence of Aβ toxicity was effectively antagonized by the N-methyl- d-aspartate (NMDA) receptor ligand dizocilpine maleate (MK-801). Moreover, Aβ toxicity in the MBN decreases with advancing age that may be associated with the age-related loss of NMDA receptor expression in rats. In summary, the present results indicate that Aβ compromises neurons of the rat MBN via an excitotoxic pathway including astroglial depolarization, extracellular glutamate accumulation, NMDA receptor activation and an intracellular Ca2+ overload leading to cell death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2000.00164.x
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  • 3
    Electronic Resource
    Electronic Resource
    In vivo labelling and axonal transport of monoamine oxidase in the rat basal ganglia using radioactive pargyline (1986)
    Springer
    Journal of neural transmission 66 (1986), S. 21-36 
    Details
    ISSN: 1435-1463
    Keywords: Axonal transport ; monoamine oxidase ; pargyline ; striatum ; substantia nigra
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The enzyme monoamine oxidase was labelled in the rat striatum or substantia nigra with locally injected radioactive pargyline. The binding was prevented by a pretreatment with non-radioactive pargyline, or with a combination of clorgyline and deprenyl. Most of the MAO labelled with3H-pargyline was of the B-type, but also some MAO-A was labelled, as shown in rats pretreated with clorgyline or deprenyl separately. Seven days after the injection of (3H)-pargyline into the striatum a significant labelling was observed in the substantia nigra. This labelling was clorgyline sensitive, indicating type A MAO, and was not present when striatal neurons were destroyed with kainic acid. Labelling of the striatum following3H-pargyline injection into the substantia nigra was also less in kainate intoxicated striata. Damage of nigral dopamine neurons with 6-hydroxydopamine did not influence the distribution of the label. Thus by using3H-pargyline, specific labelling and axonal transport of type A MAO in striatal neurons projecting to the substantia nigra was demonstrated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01262955
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  • 4
    Electronic Resource
    Electronic Resource
    Central levels of noradrenaline, 3-methoxy-4-hydroxyphenylethyleneglycol and cyclic AMP in the rat after activation of Locus coeruleus neurons: Influence of single and repeated neuroleptic treatment (1980)
    Springer
    Psychopharmacology 70 (1980), S. 239-245 
    Details
    ISSN: 1432-2072
    Keywords: Noradrenaline ; 3-Methoxy-4-Hydroxy-phenylethyleneglycol ; Cyclic AMP ; Locus coeruleus ; Neuroleptic treatment ; Clozapine ; Haloperidol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The influence of single and repeated neuroleptic treatment on noradrenaline (NA) metabolism in two areas of the central nervous system with different neuronal organizations (forebrain and spinal cord) was studied. The doses of the neuroleptics studied were chosen because of their maximum effects on turnover of dopamine in various brain areas. The endogenous levels of 3-methoxy-4-hydroxy-phenylethyleneglycol (MOPEG) in the forebrain and spinal cord of the rat were markedly increased by single intraperitoneal doses of clozapine (15 mg/kg), haloperidol (1.0 mg/kg) or chlorpromazine (2.0 mg/kg). The levels of noradrenaline (NA) in the hippocampus were decreased by a single dose of clozapine and haloperidol. Fluphenazine (0.1 mg/kg) and sulpiride (40 mg/kg) caused only slight increases of MOPEG in the forebrain and none in the spinal cord. Following repeated treatment with either clozapine or haloperidol tolerance to the stimulatory effects on NA turnover developed more rapidly in the spinal cord than in the forebrain (within 4 and 15 days respectively). After 4 days of repeated treatment the initial decrease in hippocampal NA levels had disappeared. Unilateral electrical stimulation of the locus coeruleus (LC) after a single dose of either clozapine or haloperidol induced smaller reductions of hippocampal NA (ipsilateral versus contralateral) than in saline treated control animals. In subchronically clozapine or haloperidol treated rats, LC-stimulation induced an ipsilateral decrease of NA similar to that in controls. The levels of MOPEG after LC-stimulation were elevated compared to untreated stimulated rats both in the ipsilateral and contralateral forebrain. Neither single nor repeated treatment with clozapine or haloperidol altered basal cyclic AMP levels or inhibited the cyclic AMP response to LC-stimulation. This study is evidence: (1) that neuroleptics decrease NA by release of the amine from a rapidly releasable pool (2) that even when the influence of subchronic neuroleptic treatment on cerebral NA metabolism has ceased, such treatment has a lasting influence on NA-neurons (3) that in vivo the formation of cyclic AMP is not influenced by neuroleptic treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00427880
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