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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 65 (1995), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The protein kinase C (PKC) family is composed of at least four conventional (α, βI, βII, and γ) and several related novel (δ, ε, η, and ζ) isoforms with different distribution and sensitivity to Ca2+ and phorbol esters. The enzyme is known to be present in cerebral endothelial cells. We have investigated the occurrence of seven isoforms (α, β, γ, δ, ε, η, and ζ) by using reverse transcriptase-polymerase chain reaction in rat brain, in a freshly isolated brain microvessel fraction, in primary cultures of rat brain endothelial cells, in an immortalized rat brain endothelial cell line, and in aortic endothelial cell cultures. Brain tissue contained all seven investigated isoforms. A similar expression pattern was seen in freshly purified microvessels, but the PKC-γ isoform could not be detected. Primary cultures of endothelial cells expressed PKC-α, -β, -δ, -η, and -ε isoenzymes, whereas the immortalized cell line expressed PKC-α, -δ, -ε, and -η. The rat aortic endothelium contained only PKC-α and -δ isoforms. The variety of expression patterns of PKC family members in endothelial cells of different type may reflect differences in the functional responsiveness to environmental stimuli. Because PKC has been shown to be involved in the regulation of the blood-brain barrier permeability, the presence of different isoforms may confer a sophisticated intracellular regulatory mechanism to the brain endothelial cells.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Key words Glutamate neurotoxicity ; Mitochondria ; Calcium accumulation ; Neuronal cultures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of serum proteins on glutamate-induced mitochondrial calcium accumulation was studied in primary cortical and hippocampal cultures using oxalate-pyroantimonate staining with electron microscopy. Cultures were prepared from rat embryos on gestational day 17–19 and cultivated for 8 days in minimal essential medium (MEM) containing 5% native horse serum. At this time cultures were exposed for 5 min to 100 μM or 1.0 mM glutamate, followed by recovery in either serum-free or serum-containing culture medium. Mitochondrial calcium accumulation was assessed before glutamate treatment, at the end of glutamate exposure, and after 5 min, 30 min, 6 h and 24 h of recovery. Under control conditions and at the end of glutamate exposure, mitochondria contained only a few calcium deposits. If cultures were placed in serum-free medium after glutamate treatment, mitochondria were progressively loaded with calcium. At 5 min after glutamate exposure mitochondrial calcium deposits were prominent in both cortical and hippocampal cultures, followed by a further steady increase and neuronal death within 24 h. When cultures were allowed to recover after glutamate treatment in serum-containing MEM, calcium sequestration and ultrastructural changes of mitochondria were essentially absent, and neurons survived. No differences between cortical and hippocampal cultures were observed. The data demonstrate that prevention of glutamate neurotoxicity by serum proteins is associated with prevention of post-glutamate mitochondrial calcium accumulation.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 92 (1996), S. 428-429 
    ISSN: 1432-0533
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 132 (1995), S. 87-91 
    ISSN: 0942-0940
    Keywords: Subarachnoid haemorrhage ; SAH ; natriuretic peptide ; ANP ; brain oedema
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of centrally administered atrial natriuretic peptide (ANP) on the brain water and electrolyte contents were investigated in a rodent subarachnoid haemorrhage (SAH) model. SAH caused statistically significant increases in the brain sodium and water contents, while the potassium content did not change significantly, indicating that the brain oedema could be classified as having a primarily vasogenic component. Two μg or 5 μg of rat ANP administered into the lateral ventricle at the time of SAH induction statistically significantly decreased the water and sodium accumulation measured 90 minutes following SAH. The same treatment did not inhibit development of brain oedema measured 3 hours following SAH. However, when 5 μg of ANP was administered intraventricularly at the time of SAH induction and also 90 minutes later, the brain oedema 3 hours following SAH was again reduced statistically significantly. These effects of ANP were found not to be mediated by primary changes in serum osmolality and electrolyte concentrations. The present results confirm that centrally administered ANP may act directly on the central nervous system to inhibit brain water and sodium accumulation in SAH-induced brain oedema. The potentials of influencing the central neuro-endocrine system as a novel way of the treatment of brain oedema are discussed.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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