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International Journal of Physiology and Pathophysiology
SJR: 0.106

ISSN Imprimer: 2155-014X
ISSN En ligne: 2155-0158

Archives: Volume 1, 2010 to Volume 9, 2018

International Journal of Physiology and Pathophysiology

DOI: 10.1615/IntJPhysPathophys.v5.i4.80
pages 355-362

Changes in Kinetics of Calcium Signals in Response to Prolonged High Frequency Stimulation of Cultured Hippocampal Neurons

Anastasiya A. Moskaluk
Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, Russia
Sergiy. Voytenko
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Svetlana A. Fedulova
O. O. Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Mycola S. Veselovsky
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine

RÉSUMÉ

Dynamic changes in the intracellular free Ca2+ concentration ([ Ca2+ ] i) were studied in hippocampal cultured neurons using fluorescent Ca2+ -indicator dye Indo-1 and somatic whole-cell recordings. During the tetanus stimulation, Ca2+ -transients increased their amplitude up to a steady-state level during repetitive stimulation. We identified two groups of neurons based on calcium signal dynamics after the end of stimulation: in the first group (n = 24), the monoexponential [ Ca2+ ] i decay was observed just after the end of the tetanus; in the second group (n = 32), monoexponential [ Ca2+ ] i decay was delayed after the end of the tetanus, and the duration of delay varied from 1 to 27 s, depending on duration and frequency of stimulation. Peak amplitudes of Ca2+ -transients were statistically different between the first (1820 ± 195 nM, n = 24) and the second (2618 ± 165 nM, n = 23) groups. A linear dependence between decay time constant and frequency of stimulation was found for the second group of neurons only. In all cases when the delayed decay was observed, the decay time constant changed reliably after emergence of delayed decay; the average rise made up 41 = 8 %. We suggest that dynamic changes and essential rise in the intracellular free Ca2+ concentration arise from the presence of intracellular low-affinity buffer. This statement is to be further tested using pharmacological approach.


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