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Activation of P2-purino-, alpha 1-adreno and H1-histamine receptors triggers cytoplasmic calcium signalling in cerebellar Purkinje neurons.

https://arctichealth.org/en/permalink/ahliterature11198
Source
Neuroscience. 1996 Aug;73(3):643-7
Publication Type
Article
Date
Aug-1996
Author
S. Kirischuk
V. Matiash
A. Kulik
N. Voitenko
P. Kostyuk
A. Verkhratsky
Author Affiliation
Bogomoletz Institute of Physiology, Kiev, Ukraine.
Source
Neuroscience. 1996 Aug;73(3):643-7
Date
Aug-1996
Language
English
Publication Type
Article
Keywords
Adenosine Triphosphate - pharmacology
Animals
Calcium - metabolism
Cerebellum - drug effects
Dose-Response Relationship, Drug
Epinephrine - pharmacology
Histamine - pharmacology
Mice
Mice, Inbred Strains
Purkinje Cells - drug effects
Receptors, Adrenergic, alpha-1 - drug effects
Receptors, Histamine - drug effects
Receptors, Purinergic - drug effects
Research Support, Non-U.S. Gov't
Abstract
The cytoplasmic calcium concentration ([Ca2+]i) was measured from Purkinje neurons in acutely prepared cerebellar slices. Neurons were loaded with calcium indicator Fura-2 by 40-min slice incubation in Tyrode solution containing 5 microM Fura-2/AM and 0.02% pluronic-F127. Bath applications of ATP (100 microM), epinephrine (10 microM) and histamine (100 microM) triggered a transient increase of [Ca2+]i in Purkinje neurons. ATP-induced [Ca2+]i elevation in Purkinje neurons was mimicked by ADP, but not AMP or adenosine pointing to the involvement of P2Y metabotropic purinoreceptors. Epinephrine-triggered [Ca2+]i responses were blocked by the selective alpha 1-antagonist prazosin and were mimicked by the alpha 1-adrenoreceptor agonist phenylephrine, and were not affected by beta- and alpha 2-adrenoreceptor agonists (isoproterenol and clonidine) and antagonists (propranolol and yohimbine). Histamine-induced [Ca2+]i responses demonstrated specific sensitivity to selective H1 antagonist chlorpheniramine, and were not sensitive to H2 and H3 histamine receptors modulators. The [Ca2+]i responses to all three agonists persisted in Ca(2+)-free extracellular media and were blocked by slice preincubation with thapsigargin (500 nM). We conclude that cerebellar Purkinje neurons are endowed with metabotropic P2 gamma purinoreceptors, alpha 1-adrenoreceptors and H1 histamine receptors which mediate the generation of intracellular [Ca2+]i signals via activation of Ca2+ release from inositol-1,4,5-trisphosphate-sensitive intracellular stores.
PubMed ID
8809785 View in PubMed
Less detail

ATP induces Ca2+ release from IP3-sensitive Ca2+ stores exclusively in large DRG neurones.

https://arctichealth.org/en/permalink/ahliterature11053
Source
Neuroreport. 1997 May 6;8(7):1555-9
Publication Type
Article
Date
May-6-1997
Author
N. Svichar
A. Shmigol
A. Verkhratsky
P. Kostyuk
Author Affiliation
Bogomoletz Institute of Physiology, Kiev, Ukraine.
Source
Neuroreport. 1997 May 6;8(7):1555-9
Date
May-6-1997
Language
English
Publication Type
Article
Keywords
Adenosine Triphosphate - pharmacology
Animals
Calcium - metabolism
Ganglia, Spinal - cytology - drug effects - metabolism
In Vitro
Inositol 1,4,5-Trisphosphate - pharmacology
Mice
Neurons - drug effects
Receptors, Purinergic P2 - metabolism
Research Support, Non-U.S. Gov't
Abstract
PURINORECEPTOR-MEDIATED intracellular Ca2+ release was studied in freshly isolated adult mouse dorsal root ganglia (DRG) neurones. The cytoplasmic Ca2+ concentration ([Ca2+]i) was measured using indo-1-based microfluorimetry. The application of 100 microM ATP in Ca(2+)-free solution triggered an increase in [Ca2+]i in 93% of large DRG neurones but in no small ones. The ATP-induced [Ca2+]i transients in large neurones were inhibited by cells incubation with thapsigargin or by intracellular dialysis with heparin-containing solution. The ATP-triggered increase in [Ca2+]i was not mimicked by adenosine and was blocked by suramin, suggesting the involvement of metabotropic (PZY) purinoreceptors. We conclude that large (proprioceptive) DRG neurones express PZY purinoreceptors linked to the inositol 1,4,5-triphosphate-Ca2+ intracellular signal transduction cascade, whereas small (nociceptive) DRG neurones are devoid of such a mechanism.
PubMed ID
9189891 View in PubMed
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Calcium currents in aged rat dorsal root ganglion neurones.

https://arctichealth.org/en/permalink/ahliterature46588
Source
J Physiol. 1993 Feb;461:467-83
Publication Type
Article
Date
Feb-1993
Author
P. Kostyuk
N. Pronchuk
A. Savchenko
A. Verkhratsky
Author Affiliation
Department of General Physiology of the Nervous System, A.A. Bogomoletz Institute of Physiology, Kiev, Ukraine.
Source
J Physiol. 1993 Feb;461:467-83
Date
Feb-1993
Language
English
Publication Type
Article
Keywords
Aging - metabolism
Animals
Calcium - metabolism
Calcium Channels - physiology
Cells, Cultured
Ganglia, Spinal - metabolism
Membrane Potentials - physiology
Neurons, Afferent - cytology - metabolism
Rats
Research Support, Non-U.S. Gov't
Abstract
1. The whole-cell voltage clamp technique was used to record calcium currents in the somatic membrane of rat cultured dorsal root ganglion neurones. 2. Neurones were enzymatically isolated from animals of three age groups (neonatal, 2-7 days; adult, 7 months; and old, 30 months) and maintained in primary culture 3-14 days. 3. The neurones isolated from neonatal and old rats showed two distinct types of Ca2+ currents, a low-threshold transient current and a high-threshold sustained current, whereas neurones from old rats showed only a high-threshold calcium current. 4. The density of the high-threshold calcium current was 28.4 +/- 6.3 pA/pF (mean +/- S.E.M., n = 54) in neonatal, 39.1 +/- 7.2 pA/pF (n = 62) in adult and 11.0 +/- 4.6 pA/pF (n = 64) in old dorsal root ganglion neurones. 5. We found no difference in elementary high-threshold Ca2+ current characteristics in neurones from different age groups. The single-channel conductance was (with 60 mM Ca2+ in the recording pipette) 16.0 +/- 2.7 pS (mean +/- S.E.M., n = 9) in neonatal, 16.2 +/- 1.7 pS (n = 11) in adult and 16.4 +/- 1.2 pS (n = 12) in old neurones. 6. Current-voltage relations and kinetics of high-threshold calcium currents showed no detectable age-dependent difference. 7. The run-down of high-threshold calcium currents in dorsal root ganglion neurones from old rats was practically insensitive to intracellular administration of cyclic AMP and ATP. The same intervention caused a significant deceleration of Ca2+ current run-down in the majority of neonatal and in some adult cells. 8. We suggest that the disappearance of the low-threshold calcium current and reduction of high-threshold calcium current with ageing is due to a depression of calcium channel expression during late ontogenesis. The decrease of sensitivity of high-threshold calcium channels to phosphorylation by cyclic AMP-dependent protein kinase in aged neurones could also be a reason for altered turnover between silent and functional pools of calcium channels, which may underlie the age-dependent decline in the density of high-threshold calcium channels.
PubMed ID
8394426 View in PubMed
Less detail
Source
Neuroscience. 1994 Nov;63(2):381-404
Publication Type
Article
Date
Nov-1994

Changes in calcium signalling in dorsal horn neurons in rats with streptozotocin-induced diabetes.

https://arctichealth.org/en/permalink/ahliterature47921
Source
Neuroscience. 1999;94(3):887-90
Publication Type
Article
Date
1999
Author
N V Voitenko
E P Kostyuk
I A Kruglikov
P G Kostyuk
Author Affiliation
Department of General Physiology of the Nervous System, Bogomoletz Institute of Physiology, Kiev, Ukraine. nana@serv.biph.kiev.ua
Source
Neuroscience. 1999;94(3):887-90
Date
1999
Language
English
Publication Type
Article
Keywords
Animals
Caffeine - pharmacology
Calcium - physiology
Cytoplasm - metabolism
Diabetes Mellitus, Experimental - physiopathology
Fluorescent Dyes
Fura-2 - analogs & derivatives
In Vitro
Male
Membrane Potentials - drug effects
Posterior Horn Cells - drug effects - physiology
Potassium Chloride - pharmacology
Rats
Rats, Wistar
Reference Values
Research Support, Non-U.S. Gov't
Signal Transduction - physiology
Spinal Cord - physiology - physiopathology
Abstract
Intracellular calcium signalling was studied in the dorsal horn from neurons of rats with streptozotocin-induced diabetes versus control animals. The cytoplasmic Ca2+ concentration ([Ca2+]i) was measured in Fura-2 acetoxymethyl ester-loaded dorsal horn neurons from acutely isolated spinal cord slices using a fluorescence technique. The recovery of depolarization-induced [Ca2+]i increase was delayed in diabetic neurons compared with normal animals. In normal neurons, [Ca2+]i after the end of KCl depolarization recovered to the basal level monoexponentially with a time constant of 8.0+/-0.5 s (n = 23), while diabetic neurons showed two exponentials in the [Ca2+]i recovery. The time constants of these exponentials were 7.2+/-0.5 and 23.0+/-0.6 s (n = 19), respectively. The amplitude of calcium release from caffeine-sensitive endoplasmic reticulum calcium stores became significantly smaller in diabetic neurons. The amplitudes of [Ca2+]i transients evoked by 30 mM caffeine were 268+/-29 nM (n = 13) and 31+/-9 nM (n = 17) in control and diabetic neurons, respectively. We conclude that streptozotocin-induced diabetes is associated with prominent changes in the mechanisms responsible for [Ca2+]i regulation, which presumably include a slowdown of Ca2+ elimination from the cytoplasm by the endoplasmic reticulum.
PubMed ID
10579579 View in PubMed
Less detail

Common mechanisms in the damaging effects of hypoxia and hyperglycemia on neuronal function.

https://arctichealth.org/en/permalink/ahliterature47561
Source
Fiziol Zh. 2002;48(1):102-11
Publication Type
Article
Date
2002
Author
E P Kostyuk
P G Kostyuk
Author Affiliation
A.A. Bogomoletz Institute of Physiology, National Academy of Science of Ukraine, Kiev.
Source
Fiziol Zh. 2002;48(1):102-11
Date
2002
Language
English
Publication Type
Article
Keywords
Animals
Brain - cytology
Cell Hypoxia
Diabetic Neuropathies - physiopathology
Humans
Hyperglycemia - physiopathology
Neurons - pathology - physiology
Research Support, Non-U.S. Gov't
PubMed ID
11928624 View in PubMed
Less detail

Diabetes-induced abnormalities in ER calcium mobilization in primary and secondary nociceptive neurons.

https://arctichealth.org/en/permalink/ahliterature9510
Source
Pflugers Arch. 2004 Jul;448(4):395-401
Publication Type
Article
Date
Jul-2004
Author
I. Kruglikov
O. Gryshchenko
L. Shutov
E. Kostyuk
P. Kostyuk
N. Voitenko
Author Affiliation
Bogomoletz Institute of Physiology, 4 Bogomoletz St., 01024, Kiev, Ukraine.
Source
Pflugers Arch. 2004 Jul;448(4):395-401
Date
Jul-2004
Language
English
Publication Type
Article
Keywords
Animals
Caffeine - pharmacology
Calcium - metabolism
Diabetes Mellitus, Experimental - metabolism
Diabetic Neuropathies - metabolism
Endoplasmic Reticulum - metabolism
Ganglia, Spinal - cytology - metabolism
Homeostasis - physiology
Inositol 1,4,5-Trisphosphate - metabolism
Ionomycin - pharmacology
Ionophores - pharmacology
Male
Neurons, Afferent - drug effects - metabolism
Nociceptors - drug effects - metabolism
Phosphodiesterase Inhibitors - pharmacology
Rats
Rats, Wistar
Research Support, Non-U.S. Gov't
Ryanodine Receptor Calcium Release Channel - metabolism
Abstract
Development of diabetic sensory polyneuropathy is associated with alterations in intracellular calcium homeostasis in primary and secondary nociceptive neurons. We have shown previously that in a model of streptozotocin (STZ)-induced diabetes, the calcium signal is prolonged and calcium release from ryanodine-sensitive calcium stores down-regulated in neurons of the nociceptive system. The aim of the present study was a more detailed characterization of calcium homeostasis in primary (dorsal root ganglia, DRG) and secondary (dorsal horn, DH) nociceptive neurons in STZ-induced diabetes. Fluorescence video-imaging was used to measure free cytosolic [Ca2+] ([Ca2+]i) in lumbar nociceptive neurons of control and streptozotocin-diabetic rats. Resting [Ca2+]i rose progressively in these neurons with the duration of diabetes and calcium mobilization from the endoplasmic reticulum (ER) decreased during diabetes. The amplitude of calcium release from both ryanodine- and IP3-sensitive calcium stores induced by caffeine, ionomycin, ATP or glutamate was significantly (P
PubMed ID
15048576 View in PubMed
Less detail

Diabetes-induced changes in calcium homeostasis and the effects of calcium channel blockers in rat and mice nociceptive neurons.

https://arctichealth.org/en/permalink/ahliterature47648
Source
Diabetologia. 2001 Oct;44(10):1302-9
Publication Type
Article
Date
Oct-2001
Author
E. Kostyuk
N. Voitenko
I. Kruglikov
A. Shmigol
V. Shishkin
A. Efimov
P. Kostyuk
Author Affiliation
Institute of Endocrinology, Kiev, Ukraine.
Source
Diabetologia. 2001 Oct;44(10):1302-9
Date
Oct-2001
Language
English
Publication Type
Article
Keywords
Animals
Caffeine - pharmacology
Calcium - metabolism
Calcium Channel Blockers - pharmacology
Diabetes Mellitus, Experimental - metabolism
Ganglia, Spinal - metabolism
Homeostasis
Male
Membrane Potentials
Mice
Mice, Inbred C57BL
Neurons - drug effects - metabolism
Nifedipine - pharmacology
Nociceptors - drug effects - metabolism
Rats
Rats, Wistar
Research Support, Non-U.S. Gov't
Signal Transduction
Substantia Gelatinosa - metabolism
Abstract
AIMS/HYPOTHESIS: Distal neuropathy is the most common complication of diabetes mellitus, making it important to reveal the cellular mechanisms leading to its development, one of which might be the alteration in intracellular calcium homeostasis in primary and secondary nociceptive neurons. We aimed to investigate these possible changes. METHODS: Control and streptozotocin-treated diabetic rats and mice were used. Changes in intracellular free calcium concentrations ([Ca(2+)]i) were measured fluorometrically in primary nociceptive neurons from dorsal root ganglia and in secondary nociceptive neurons from substantia gelatinosa of spinal dorsal horn slices. RESULTS: Measurements of [Ca(2+)]i increases induced in dorsal root ganglion and dorsal horn neurons by membrane depolarization did not show any substantial difference in their peak amplitudes in control and diabetic animals. However, a definite prolongation of the decay phase of the transients was observed under diabetic conditions. Caffeine application to dorsal root ganglion and dorsal horn neurons induced a transient elevation of [Ca(2+)]i which was less prominent in cells from diabetic animals. Short-term application of a calcium channel blocker nifedipine showed a substantial amplification of its action in diabetic neurons. However, chronic administration of nimodipine induced a clear increase in the peak values of transients in dorsal root ganglion neurons of diabetic animals compared with those of untreated animals. CONCLUSION/INTERPRETATION: The described changes of calcium signalling in nociceptive neurons could be the reason for the development of distal polyneuropathy and its symptoms in the early stages of diabetes mellitus.
PubMed ID
11692179 View in PubMed
Less detail

Effect of streptozotocin-induced diabetes on the activity of calcium channels in rat dorsal horn neurons.

https://arctichealth.org/en/permalink/ahliterature47905
Source
Neuroscience. 2000;95(2):519-24
Publication Type
Article
Date
2000
Author
N V Voitenko
I A Kruglikov
E P Kostyuk
P G Kostyuk
Author Affiliation
Department of General Physiology of Nervous System, Bogomoletz Institute of Physiology, Kiev, Ukraine.
Source
Neuroscience. 2000;95(2):519-24
Date
2000
Language
English
Publication Type
Article
Keywords
Animals
Calcium - metabolism
Calcium Channel Blockers - pharmacology
Calcium Channels, L-Type - physiology
Diabetes Mellitus, Experimental - physiopathology
Diabetic Neuropathies - physiopathology
Fluorescent Dyes
Fura-2 - analogs & derivatives
Male
Membrane Potentials - drug effects - physiology
Nickel - pharmacology
Nifedipine - pharmacology
Posterior Horn Cells - chemistry - physiology
Potassium Chloride - pharmacology
Rats
Rats, Wistar
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Stimulation, Chemical
omega-Conotoxins - pharmacology
Abstract
We have previously found that spinal dorsal horn neurons from streptozotocin-diabetic rats, an animal model for diabetes mellitus, show the prominent changes in the mechanisms responsible for [Ca2+]i regulation. The present study aimed to further characterize the effects of streptozotocin-induced diabetes on neuronal calcium homeostasis. The cytoplasmic Ca2+ concentration ([Ca2+]i) was measured in Fura-2AM-loaded dorsal horn neurons from acutely isolated spinal cord slices using fluorescence technique. We studied Ca2+ entry through plasmalemmal Ca2+ channels during potassium (50 mM KCl)-induced depolarization. The K+-induced [Ca2+]i elevation was inhibited to a different extent by nickel ions, nifedipine and omega-conotoxin suggesting the co-expression of different subtypes of plasmalemmal voltage-gated Ca2+ channels. The suppression of [Ca2+]i transients by Ni2+ (50 microM) was the same in control and diabetic neurons. On the other hand, inhibition of [Ca2+]i transients by nifedipine (50 microM) and omega-conotoxin (1 microM) was much greater in diabetic neurons compared with normal animals. These data suggest that under diabetic conditions the activity of N- and L- but not T-type voltage-gated Ca2+ channels substantially increased in dorsal horn neurons.
PubMed ID
10658632 View in PubMed
Less detail

InsP3-induced Ca2+ release in dorsal root ganglion neurones.

https://arctichealth.org/en/permalink/ahliterature11052
Source
Neurosci Lett. 1997 May 16;227(2):107-10
Publication Type
Article
Date
May-16-1997
Author
N. Svichar
A. Shmigol
A. Verkhratsky
P. Kostyuk
Author Affiliation
Bogomoletz Institute of Physiology and International Center of Molecular Physiology, Kiev, Ukraine.
Source
Neurosci Lett. 1997 May 16;227(2):107-10
Date
May-16-1997
Language
English
Publication Type
Article
Keywords
Adenosine Triphosphate - pharmacology
Animals
Calcium - metabolism
Ganglia, Spinal - drug effects - metabolism
Heparin - pharmacology
Inositol 1,4,5-Trisphosphate - pharmacology
Mice
Research Support, Non-U.S. Gov't
Abstract
The intracellular calcium signalling was studied on subpopulation of freshly isolated adult mouse dorsal root ganglia (DRG) neurones with large somatas (30-45 microns in diameter). The cytoplasmic Ca2+ concentration ([Ca2+]i) was measured using indo-1 based microfluorimetry. The extracellular application of ATP (100 microM) triggered both inward current and [Ca2+]i elevation. Removal of extracellular Ca2+ had no effect on both ATP-induced current and [Ca2+]i transient. The ATP-induced Ca2+ elevation was inhibited by intracellular perfusion of DRG neurones with 20 microM heparin, or by cells incubation with thapsigargin or ryanodine. We conclude that mouse proprioceptive sensory neurones are endowed with Ca2+-impermeable ionotropic P2X purinoreceptors and metabotropic P2Y purinoreceptors, which, by means of phospholipase C-driven inositol-trisphosphate (InsP3) production, trigger the InsP3-induced Ca2+ release from intracellular stores.
PubMed ID
9180215 View in PubMed
Less detail

11 records – page 1 of 2.