Українська Русский English

ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)
DOI: https://doi.org/10.15407/fz

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. 2005; 51(1): 19-25


Dynamic interaction between plasmamembrane structures and intracellu-lar calcium stores in drg neurons

I.V. Stepanova, P.G. Kostyuk, E.P. Kostyuk

    О.О. Bogomolets Institute of Physiology, National Academyof Sciences of Ukraine, KyivInternational Centre for Molecular Physiology, Kyiv


Abstract

We studied the dynamic contribution of endoplasmic reticulum and mitochondria to depolarization-induced Ca2+ transients in small (18-24 µm) DRG neurons of rats. We have used the application of 10 µM of mitochondrial protonophore CCCP for switching off the calcium uptake by mitochondrial uniporter. For depletion of the store of endoplasmic reticulum we applied 1 µM of thapsigargin. Depolarization-induced tran- sients in control conditions and in conditions when one of the mechanisms (mitochondria or endoplasmic reticulum) does not participate in the forming of the shape of Ca2+ transient have been studied. This allowed us to clarify the kinetics of mitochondrial and endoplasmic reticulum uptake and release of calcium in the process of the neuronal activity. We have determined the main characteristics of functioning of above- named calcium stores in the process of cell excitation, such as time of the beginning of uptake, time and duration of maximum activity etc. We concluded, that mitochondria and endoplas- mic reticulum are acting in opposite directions at least in the phase of the beginning of the transient. Mitochondria are limiting the amplitude of the transient during depolarization, at the same time the endoplasmic reticulum is increasing the amplitude of the transient by CICR (calcium-induced calcium release) mechanism. Mitochondria store calcium released from endoplasmic reticulum by application of 30 mM caffeine. In- hibition of the mitochondrial uniporter results in reduction of amplitude of repetitive caffeine application compared with control conditions. We have compared the kinetics of mito- chondrial participation in the formation of calcium signal when the initial sources of calcium ions were different. Our results allow us to suggest a close functional dynamic interactions between mitochondria and endoplasmic reticulum during calcium signaling in sensory neurons.

References

  1. Berridge M.J. Neuronal calcium signaling / / Neuron. –1998. – №21. – P. 13–26.
  2. Berridge M.J. The endoplasmc reticulum: a multifunc-tional signaling organelle / / Cell Calcium. – 2002. –№5–6. – Р. 235–249.
  3. Carafoli E. Calcium signaling: a tale for all seasons / / Proc.Natl. Acad. Sci. USA. – 2002. – №99. – P. 1115–1122.
  4. Filippin L., Paulo J. Magalhaes L. et.al. Stable interac-tion between mitochondria and endoplasmic reticulumallow rapid accumulation of calcium in a subpopula-tion of mitochondria / / J. Biol. Chem. – 2003. – 278,№40. – P. 39224–39234.
  5. Grynkiewicz G., Poenie M., Tsien R.Y. A new genera-tion of Ca2+ indicators with greatly improved fluores-cence properties / / J. Biol. Chem. – 1985. – №6. –P. 3440–3450.
  6. Guang J. W., Joshua G., Jackson et al. Altered distri-bution of mitochondria impairs calcium homeostasisin rat hippocampal neurons in culture / / J. Neurochem. –2003. – №87. – P. 85–94.
  7. Hajnoczky G. Luminal communication between intracel-lular calcium stores modulated by GTP and cytoskeleton/ / J. Biol. Chem. – 1994. – №269. – P. 10280–10287.
  8. Hajnoczky G., Robb-Gaspers L.D., Seitz M.B. et al.Decoding of cytosolic calcium oscillations in the mito-chondria / / Cell. – 1995. – №82. – P. 415–424.
  9. 9. Montero M., Alonso M.T., Carnicero E. et. al.Chromaffin-cell stimulation triggers fast millimolarmitochondrial Ca2+ transients that modulate secretion // Nat.Cell. Biol. – 2000. – №2. – P. 57–61.
  10. 10. Rizutto R., Bastianutto C., Brini M. et. al. Mitochon-drial Ca2+ homeostasis in intact cells / / Cell Biology. –1994. – №126. – P. 1183–1194.
  11. Rizutto R., Brini M., Murgia M. et. al. Microdomainswith high Ca2+ concentration that are sensed by neigh-boring mitochondria / / Science. – 1993. – №262. –P. 744–747.
  12. Shishkin V., Potapenko E., Kostyuk E. et. al. Role ofmitochondria in intracellular calcium signaling in pri-mary and secondary sensory neurons of rats / / CellCalcium. – 2002. – №32. – P. 121–130.
  13. Svichar N., Kostyuk P., Verkhratsky A. Mitochondriabuffer Ca2+ entry but not intracellular Ca2+ release inmouse DRG neurons / / NeuroReport. – 1997. – № 8. –P. 3929–3932.
  14. Svichar N., Shishkin V., Kostyuk P. Mitochondrialparticipation in the modulation of calcium transientsin DRG neurons / / Ibid. – 1999. – №10. – P. 1257–1261.
  15. Usachev Y., Shmigol A., Pronchuk P. et.al. Caffeine-induced calcium release from internal stores in culturedrat sensory neurons / / Neuroscience. – 1993. – №3. –P. 845–859.
  16. Verkhratsky A. The endoplasmic reticulum and neuronalcalcium signaling / / Cell Calcium. – 2002. – №32. –P. 393–404.

© National Academy of Sciences of Ukraine, Bogomoletz Institute of Physiology, 2014-2018.