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P H Kostiuk

Publications and source records attributed to P H Kostiuk.

11 recordsLinked to original sources
PubMed2006

[Characteristics of inositoltrisphosphate-sensitive Ca2+ stores in the acinar cells of rat submandibular salivary gland].

In the acinar cells of rat submandibular salivary gland activation of cholinoreceptors leads to the release of Ca2+ from endoplasmic reticulum (ER). This Ca2+ release from ER is mainly mediated by InsP3-receptors. In the present work we used Arsenazo III dye and mag-fura 2/AM to measure total cellular calcium content and Ca2+ concentration in the ER ([Ca2+]ER), respectively. We have found that application of InsP3 to the permeabilized acinar cells evoked decrease [Ca2+]ER in dose-dependent manner with EC50 1.3 +/- 0.21 mM. This InsP3-induced Ca2+ release from the ER was potentiated by Ca2+ in the physiological ranges (100-400 nM), modulated by caffeine and ATP. Low concentrations of ATP in (< 1 mM) enhanced the InsP3-induced decrease [Ca2+]ER while high concentrations of ATP markedly suppressed Ca2+ release. Caffeine (2 mM) decreased InsP3-induced Ca2+ release in the presence of Ca2+ however it has no inhibitory effect in the absence of Ca2+. This inhibitory effect of caffeine on InsP3-induced Ca2+ release is overcame by high concentration of InsP3 (20 mM) and ATP (1 mM) indicating that caffeine functionally competes with InsP3 receptor domains. We suggested that the ATP regulation of InsP3-induced Ca2+ release might also play a role in oscillations of intracellular Ca2+ and the maintenance of the cell survival during energy attenuation periods.

Animals↗
PubMed2005

[Dynamic interaction between plasma membrane structures and intracellular calcium stores in neurons of the spinal cord ganglia].

We studied the dynamic contribution of endoplasmic reticulum and mitochondria to depolarization-induced Ca2+ transients in small (18-24 microm) DRG neurons of rats. We have used the application of 10 microM of mitochondrial protonophore CCCP for switching off the calcium uptake by mitochondrial uniporter. For depletion of the store of endoplasmic reticulum we applied 1 microM of thapsigargin. Depolarization-induced transients 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 endoplasmic 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. Inhibition of the mitochondrial uniporter results in reduction of amplitude of repetitive caffeine application compared with control conditions. We have compared the kinetics of mitochondrial 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.

Animals↗
PubMed2004

[70th anniversary of the O.O. Bogomolets Institute of Physiology of the National Academy of Science of Ukraine].

The brief history of creation and basic stages of development of the largest centre of science of the country and global physiological science--A.A. Bogomolets Institute of physiology of National Academy of Sciences of Ukraine is stated. The basic achievements of scientific divisions of Institute for the 70-year's period in area of the most urgent problems of molecular physiology, neurophysiology, physiology of visceral systems are marked. Is covered many-sided and versatile scientific and publishing activity of the employees of Institute, the role of the outstanding scientists--physiologists and biophysicists of Institute in formation of national scientific schools is shown.

Academies and Institutes↗
PubMed2004

[Chronic treatment with GABA A receptor blockers increases efficacy of GABAergic synaptic transmission in rat hippocampal neuron cultures].

It has been proposed to consider plasticity in neuronal network as occurring in two forms: use-dependent plasticity which modifies the network properties, and homeostatic plasticity which may counteract use-dependent changes. Chronic block of some of transmitter receptors is often used as a model for studying homeostatic plasticity. We studied whether chronic block of GABAA receptors can affect GABAergic transmission. Using whole-cell voltage clamp recording and local extracellular stimulation we investigated evoked inhibitory postsynaptic currents (IPSCs) in cultured rat hippocampal neurons grown in the presence of GABAA receptor antagonist--bicuculline (20mM) and in control conditions. Cell for both control and pretreated cultures were obtained from same dissection and were grown in parallel. We compared the amplitudes of the evoked IPSC, the reversal potentials of the responses IPSC coefficient of variation and depression evoked by paired stimulation. Chronic bicuculline treatment did not significantly affect the paired-pulse depression (PPD) and IPSC reversal potentials. In contrast we found that amplitude of evoked IPSCs was increased about two times in cultures treated with bicuculline. However, IPSC coefficients of variation were not significantly different. We conclude that chronic block of GABAA receptors enhances efficacy of GABAergic synaptic transmission in rat hippocampal cell cultures and this effect is likely to postsynaptic mechanism(s) because IPSC increase was not accompanied with changes of IPSC coefficient of variation. A possibility that the effect of chronic block of GABAA receptors on GABAergic transmission is mediated by neurotrophin BDNF is discussed.

Animals↗
PubMed2004

[Effect of synaptic transmission blockade and hypoglycemia on neuron impulse activity in cultured rat hippocampal neurons].

Spontaneous neuronal activity was studied in rat hippocampal cell cultures using patch clamp technique in cell-attached or loose-patch configuration. It was found that in spite of relatively low average frequency (1-2 Hz) of neuronal activity in the cell cultures, neurons often fire doublets or triplets of action potentials with interspike interval of 60 ms and less. Interspike interval histograms were substantially better fitted by double exponential decay functions than by single exponential ones. On average, estimated decay time constant for the fits were tau1 approximately 36, ms and tau2 approximately 1000 ms respectively. Spontaneous neuronal firing to a large extent depended on glutamatergic excitation and GABA(A)ergic inhibition: a blocker of AMPA/kainate receptor CNQX (10 microM) either substantially decreased or completely blocked spontaneous action potentials; a blocker of GABA(A) receptors bicuculine (10 microM) increased neuronal firing. Effect of glucose deprivation on action potential frequency was also studied. It was found that glucose deprivation reduces AP frequency to 25% of control. Taken together, these results support an idea that hypoglycaemia alters synaptic transmission in hippocampus.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2003

[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.

Animals↗
PubMed2003

[Permeabilized salivary gland cells as a model to study Ca2+-transporting systems of endoplasmic reticulum membrane].

A method for chemical permeabilization of secretory cells of rat submandibular salivary gland has been elaborated. It was shown that the effects of digitonin on total calcium content in permeabilized acinar cells and protein content in their incubation medium correlated with concentration and duration of the detergent treatment. Digitonin-permeabilized acinar cells perform Ca(2+)-dependent protein secretion, which level depends on the duration of cell incubation in an intracellular buffer solution. The ability of permeabilized acinar cells to perform thapsigargin-sensitive ATP-dependent Ca2+ transport was established by using biochemical approaches and monitoring of the intrareticular calcium concentration with mag-fura 2 dye. Thapsigargin-insensitive Ca2+ store in the permeabilized acinar cells of the salivary gland was shown to be also available. Thus, these data give evidence to conclude that digitonin-permeabilized secretory cells of the submandibular salivary gland are an adequate model to study the mechanisms of Ca(2+)-dependent control of the exocytosis and membrane Ca(2+)-transporting systems of the intracellular calcium stores.

Animals↗
PubMed1999

[Low-threshold potential-controlled calcium channels--their properties and functions].

Low voltage-activated calcium channels discovered 15 year ago are unique molecular structures which play a specific role in the functioning of different types of excitable cells. This conclusion is supported by recent identification of special channel-forming 1- subunits which after expression in artificial cellular systems generate transmembrane currents characteristic for low-voltage-activated calcium channels. At the same time, analysis of recent experimental data indicate the existence of several subtypes of low voltage-activated channels which differ in the characteristics of their permeability, kinetics and pharmacological sensitivity. The expression of different subtypes of low-voltage activated channels is found to be highly coordinated, on one hand, with different phases of the ontogenetic development of excitable cells and, on the other, with their fulfillment of specific functions. Therefore the search for selective modulators of the activity of these channels is an extremely important goal for modern investigations.

Animals↗