| First Author | Herms JW | Year | 2000 |
| Journal | J Neurochem | Volume | 75 |
| Issue | 4 | Pages | 1487-92 |
| PubMed ID | 10987828 | Mgi Jnum | J:126619 |
| Mgi Id | MGI:3761750 | Doi | 10.1046/j.1471-4159.2000.0751487.x |
| Citation | Herms JW, et al. (2000) Altered intracellular calcium homeostasis in cerebellar granule cells of prion protein-deficient mice. J Neurochem 75(4):1487-92 |
| 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. |
