INFLUENCE OF β-AMYLOID PEPTIDE ON PLASMALEMMAL CALCIUM CHANNELS OF HIPPOCAMPAL CELL CULTURE
T.Yu. Korol, E.P. Kostyuk, P.G. Kostyuk
O.O.Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv, Ukraine
DOI: https://doi.org/10.15407/fz55.04.010
Abstract
Anomalous accumulation of b-amyloid peptide in cerebral neurons plays central role in pathogenesis of Alzheimer’s disease (AD). One of the essential pathogenetic factors at AD is disturbance of calcium homeostasis in neurons of central nervous system. It was determined in this work that 24-hour incubation of hippocampal cell culture with b-amyloid peptide caused more than twofold elevation of basal calcium concentration relatively to control value (153,4±11,5 and 71,7±5,4 nM respectively; P < 0,05, n=7). Using whole cell patch-clamp technique it was detected that calcium current density in b-amyloid-treated cells was 70 % higher (P<0.05, n=12) than in control ones. Obtained data broaden our comprehension of disturbance of molecular mechanisms of calcium homeostasis in neurons in AD, particularly mechanisms of elevation of basal calcium concentration by means of enhancement of calcium influx through plasmalemmal voltage-gated calcium channels.
Keywords:
β-amyloid, Alzheimers disease, hippocampal cell culture, voltage-gated calcium channels, calcium homeostasis.
References
- Kostyuk P.G., Zima V.L., Magura I.S. ta іn. Bіofіzika. K.: Oberegi, 2001. 544 s.
- Alzheimer's disease: advances in etiology, pathogenesis and therapeutics / Edited by K. Iqbal, S.S. Sisodia, B. Winblad. Chichester: John Wiley & Sons Ltd, 2001. 841 p.
CrossRef
- Arispe N., Rojas E., Pollard H.B. Alzheimer disease amyloid v protein forms calcium channels in bilayer membranes: blockade by tromethamine and aluminium . Proc. Natl Acad. Sci. USA. 1993. 90. P. 567-571.
CrossRef
PubMed PubMedCentral
- Cowburn R.F., Wiehager B., Sundstrom E. P-Amyloid peptides enhance binding of the calium mobilising second messengers, inisutol(1,4,5)trisphosphate and inositol-(1,3,4,5)tetrakisphosphate to their receptor sites in rat cortical membranes . Neurosci. Lett. 1995. 191. P. 31-34.
CrossRef
- Davidson R.M., Shajenko L., Donta T.S. Amyloid P-peptide potentiates a nimodipine-sensitive L-type barium conductance in N1E-115 neuroblastoma cells . Brain Res. -1994. 643. P. 324-327.
CrossRef
- Furukawa K., Abe Y., Akaike N. Amyloid v protein-induced irreversible current in rat cortical neurons . Neuroreport. 1994. 5. P. 2016-2018.
CrossRef
PubMed
- Grynkiewicz G., Poenie M., Tsien R.Y. A new generation of Ca2+ indicators with greatly improved fluorescence properties . J. Biol. Chem. 1985. 260. -P. 3440-3450.
- Hardy J., Selkoe D.J. The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics . Science. 2002. 297. P. 353-356.
CrossRef
PubMed
- Hardy L. A hundred years of Alzheimer's disease research . Neuron. 2006. 52. P. 3-13.
CrossRef
PubMed
- He L.M., Chen L.Y., Lou X.L. et al. Evaluation of v-amyloid peptide 25-35 on calcium homeostasis in cultured rat dorsal root ganglion neurons . Brain Res. 2002. 939. P. 65-75.
CrossRef
- Kawahara M., Kuroda Y Molecular mechanism ofneurodegeneration induced by Alzheimer's beta-amyloid protein: channel formation and disruption of calcium homeostasis . Brain Res. Bull. 2000. 53, N 4. P. 389-397.
CrossRef
- LaFerla F.M. Calcium dyshomeostasis and intracellular signalling in Alzheimer's disease . Nature. 2002. 3. P. 861-872.
CrossRef
- Leissring M.A., Paul B.A., Parker I. et al. Alzheimer's presenilin-1 mutation potentiates inositol 1,4,5-trisphosphate-mediated calcium signaling in Xenopus oocytes . J. Neurochem. 1999. 72, N. 3. P. 1061-1068.
CrossRef
PubMed
- Li W.Y., Butler J.P., Hale J.E et al. Suppression of an amyloid b peptide-mediated calcium channels response by a secreted b-amyloid precursor protein . Neuro-science. 2000. 95. P. 1-4.
CrossRef
- Mattson M. Cellular actions of b-amyloid precursor protein and its soluble and fibrillogenic derivatives . Physiol. Rev. 1997. 77. P. 1081 1132.
CrossRef
PubMed
- Pierrot N., Ghisdal P., Caumont A., Octave J. Intraneu-ronal amyloid-P1-42 production triggered by sustained increase of cytosolic calcium concentration induces neuronal death . J. Neurochem. 2003. 88. P. 1140-1150.
CrossRef
- Ramsden M., Henderson Z., Peasrson H.A. Modulation of Ca2+ channel currents in primary cultures of rat cortical neurons by amyloid b protein (1-40) is dependent on solubility status. Brain Res. 2002. 956. P. 254-261.
CrossRef
- Resende R., Pereira C., Agostinho P. et al. Susceptibility of hippocampal neurons to Ab peptide toxicity is associates with perturbation of Ca2+ homeostasis . Ibid. 2007. 1143. P. 11-12.
- Rossini P.M., Del Percio C., Pasqualetti P. et al. Conversion from mild cognitive impairment to Alzheimer's disease is predicted by sources and coherence of brain electroencephalography rhythms . Neuroscience. 2006. 147. P. 793-803.
CrossRef
PubMed
- Webster S., Bradt B., Rogers J., Cooper N. Aggregation state-dependent activation of the classical complement pathway by the amyloid b peptide . J. Neurochem. 1997. 69 P. 388-398.
CrossRef
PubMed
- Zerovnik E. Amyloid-fibril formation: proposed mechanisms and relevance to conformational disease . Eur. J. Biochem. 2002. 269. P. 3362-3371.
CrossRef
PubMed
|