Source:http://linkedlifedata.com/resource/pubmed/id/10987828
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2000-10-5
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| pubmed:abstractText |
Previous studies have indicated that recombinant cellular prion protein (PrP(C)), as well as a synthetic peptide of PrP(C), affects intracellular calcium homeostasis. To analyze whether calcium homeostasis in neurons is also affected by a loss of PrP(C), we performed microfluorometric calcium measurements on cultured cerebellar granule cells derived from prion protein-deficient (Prnp(0/0)) mice. The resting concentration of intracellular free calcium [Ca(2+)](i) was found to be slightly, but significantly, reduced in Prnp(0/0) mouse granule cell neurites. Moreover, we observed a highly significant reduction in the [Ca(2+)](i) increase after high potassium depolarization. Pharmacological studies further revealed that the L-type specific blocker nifedipine, which reduces the depolarization-induced [Ca(2+)](i) increase by 66% in wild-type granule cell somas, has no effect on [Ca(2+)](i) in Prnp(0/0) mouse granule cells. Patch-clamp measurements, however, did not reveal a reduced calcium influx through voltage-gated calcium channels in Prnp(0/0) mice. These data clearly indicate that loss of PrP(C) alters the intracellular calcium homeostasis of cultured cerebellar granule cells. There is no evidence, though, that this change is due to a direct alteration of voltage-gated calcium channels.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Caffeine,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, L-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium,
http://linkedlifedata.com/resource/pubmed/chemical/PrPC Proteins
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| pubmed:status |
MEDLINE
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| pubmed:month |
Oct
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| pubmed:issn |
0022-3042
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
75
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1487-92
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:10987828-Animals,
pubmed-meshheading:10987828-Caffeine,
pubmed-meshheading:10987828-Calcium,
pubmed-meshheading:10987828-Calcium Channel Blockers,
pubmed-meshheading:10987828-Calcium Channels, L-Type,
pubmed-meshheading:10987828-Cell Differentiation,
pubmed-meshheading:10987828-Cells, Cultured,
pubmed-meshheading:10987828-Cerebellum,
pubmed-meshheading:10987828-Crosses, Genetic,
pubmed-meshheading:10987828-Homeostasis,
pubmed-meshheading:10987828-Intracellular Fluid,
pubmed-meshheading:10987828-Membrane Potentials,
pubmed-meshheading:10987828-Mice,
pubmed-meshheading:10987828-Mice, Knockout,
pubmed-meshheading:10987828-Neurites,
pubmed-meshheading:10987828-Patch-Clamp Techniques,
pubmed-meshheading:10987828-Potassium,
pubmed-meshheading:10987828-PrPC Proteins
|
| pubmed:year |
2000
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| pubmed:articleTitle |
Altered intracellular calcium homeostasis in cerebellar granule cells of prion protein-deficient mice.
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| pubmed:affiliation |
Department of Neuropathology, Georg-August Universität Göttingen, Göttingen, Germany.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|