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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. 1999; 45(4): 48-54

Changes in calcium signaling in mammalian nociceptive neurons in diabetes mellitus

Voĭtenko NV, Kostiuk OP, Kruhlykov IA, Svichar NV, Shymkin VO

    A. A. Bogomoletz Institute of Physiology, National Academy of Science of the Ukraine, Kiev


The changes in neuronal Ca2+ homeostasis were studied on dorsal horn neurons from spinal cord rat slices and freshly isolated dorsal root ganglion neurons of mice in control condition and under streptozotocin (STZ)-induced diabetes. The cytoplasmic free Ca2+ concentration ([Ca2+]i) was measured using fura-2 and indo-1 based microfluorimetry. The recovery of depolarization-induced [Ca2+]i increase was delayed in diabetic neurons compared with normal animals. The amplitude of calcium release from caffeine-sensitive endoplasmic reticulum calcium stores became significantly smaller in diabetic neurons. The participation of mitochondria in [Ca2+]i homeostasis was determined by investigation of changes which occurred after addition of mitochondrial protonophore (CCCP) to the extracellular solution. In control cells 10 (M CCCP applied before membrane depolarization induced an increase of the amplitude of depolarization-induced [Ca2+]i transients and disappearance of their delayed recovery, indicating the participation of mitochondria in fast uptake of Ca2+ ions from the cytosol during the peak of the transient and subsequent slow release them back during its decay. In neurons from diabetic animals the increase of the peak transient amplitude under the action of CCCP became diminished, and the delayed elevation of [Ca2+]i disappeared in small size neurons. We conclude that streptozotocin-induced diabetes is associated with prominent changes in the mechanisms responsible for [Ca2+]i regulation in neurones of the nociceptive system, which presumably include a slow down of Ca2+ elimination from the cytoplasm by endoplasmic reticulum and mitochondria.


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