Українська Русский English

ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)

Fiziologichnyi Zhurnal

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2009; 55(4): 10-16


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


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, Alzheimer’s disease, hippocampal cell culture, voltage-gated calcium channels, calcium homeostasis.


  1. Kostyuk P.G., Zima V.L., Magura I.S. ta іn. Bіofіzika. K.: Oberegi, 2001. 544 s.
  2. 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  
  3. 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
  5. 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  
  6. 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  
  7. Furukawa K., Abe Y., Akaike N. Amyloid v protein-induced irreversible current in rat cortical neurons . Neuroreport. 1994. 5. P. 2016-2018. CrossRef PubMed
  9. 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.
  11. 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
  13. Hardy L. A hundred years of Alzheimer's disease research . Neuron. 2006. 52. P. 3-13. CrossRef PubMed
  15. 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  
  16. 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  
  17. LaFerla F.M. Calcium dyshomeostasis and intracellu­lar signalling in Alzheimer's disease . Nature. 2002. 3. P. 861-872. CrossRef  
  18. 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
  20. 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  
  21. Mattson M. Cellular actions of b-amyloid precursor protein and its soluble and fibrillogenic derivatives . Physiol. Rev. 1997. 77. P. 1081 1132. CrossRef PubMed
  23. 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  
  24. 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  
  25. 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.
  27. 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
  29. 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
  31. Zerovnik E. Amyloid-fibril formation: proposed mechanisms and relevance to conformational disease . Eur. J. Biochem. 2002. 269. P. 3362-3371. CrossRef PubMed

© National Academy of Sciences of Ukraine, Bogomoletz Institute of Physiology, 2014-2019.