[Intracellular calcium homeostasis in sensory neurons during hypoxia].
Hypoxia is the main reason leading to neuronal death during different forms of brain diseases. The main phenomenon observed at hypoxia is excessive growth of intraneuronal Ca2+ concentration leading to irreversible cell damage. Despite extensive studies of this process, the intracellular mechanisms responsible for disturbance in Ca2+ are still unclear. The aim of present investigations was to explore these mechanisms. Ca2+ was measured by spatial screening of isolated dorsal root ganglion (sensory) neurons loaded with fluorescent dye Fura-2AM after exposing them hypoxic solution. Hypoxia resulted in a reversible elevation of Ca2+, which could be partly prevented by several pharmacological agents. We concluded that in sensory neurons hypoxia-induced elevation of cytosolic Ca2+ is induced by primary changes in ionic channels and secondary in function of mitochondria.
Kostiuk
P H
PH
A.A. Bogomoletz Institute of Physiology, International Center for Molecular Physiology, Kiev, Ukraine.
Stanika
R I
RI
Koval'
L M
LM
Luk'ianets
O O
OO
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000378:metabolism; D015687:Cell Hypoxia; D002462:Cell Membrane / Q000378:metabolism / Q000648:ultrastructure; D004721:Endoplasmic Reticulum / Q000378:metabolism / Q000648:ultrastructure; D016257:Fura-2 / Q000494:pharmacology; D005727:Ganglia, Spinal / Q000166:cytology; D008854:Microscopy, Electron; D008928:Mitochondria / Q000378:metabolism / Q000648:ultrastructure; D009475:Neurons, Afferent / Q000378:metabolism*; D009543:Nifedipine / Q000494:pharmacology; D051381:Rats; D019831:Sodium-Calcium Exchanger / Q000378:metabolism
D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D019831:Sodium-Calcium Exchanger; D009543:Nifedipine; D002118:Calcium; D016257:Fura-2