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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
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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
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Long-term induction of beta-CGRP mRNA in rat lungs by allergic inflammation.

https://arctichealth.org/en/permalink/ahliterature15123
Source
Life Sci. 2004 Nov 26;76(2):163-77
Publication Type
Article
Date
Nov-26-2004
Author
Jun Tsukiji
Kazunori Sango
Naoko Udaka
Haruaki Kageyama
Takaaki Ito
Haruhiro Saito
Hidenori Horie
Shuji Inoue
Hitoshi Kitamura
Eri Hagiwara
Hirotada Ikeda
Takao Okubo
Yoshiaki Ishigatsubo
Author Affiliation
Department of Internal Medicine and Clinical Immunology, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan. jtsukiji@yokohama-cu.ac.jp
Source
Life Sci. 2004 Nov 26;76(2):163-77
Date
Nov-26-2004
Language
English
Publication Type
Article
Keywords
Allergens - immunology
Animals
Calcitonin Gene-Related Peptide - biosynthesis
Disease Models, Animal
Ganglia, Spinal - metabolism
Immunohistochemistry
Inflammation - immunology - metabolism
Lung - metabolism
Male
Nodose Ganglion - metabolism
RNA, Messenger - biosynthesis
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Respiratory Hypersensitivity - immunology - metabolism
Reverse Transcriptase Polymerase Chain Reaction
Time Factors
Abstract
Calcitonin gene-related peptide (CGRP) is one of the major neuropeptides released from sensory nerve endings and neuroendocrine cells of the lung. Two CGRP isoforms, alpha-and beta-CGRP, have been identified in rats and humans, but no studies have attempted to reveal direct evidence of differences in action or location of these isoforms in allergic inflammation (AI). We investigated mRNA expressions of alpha-and beta-CGRP in lungs, nodose ganglia (NG), and dorsal root ganglia (DRG) of an animal model for AI of the airways, utilizing a model created by sensitizing Brown Norway (BN) rats with ovalbumin (OVA). By semiquantitative RT-PCR analysis, long-lasting enhanced expression of the beta-CGRP mRNA was shown in the lungs of the AI rats (14.5-fold enhancement at 6 hr, 8.1-fold at 24 hr, and 3.7-fold at 120 hr after OVA-challenge compared to the level in the lungs of phosphate-buffered saline (PBS)-challenged control rats). In contrast, the mRNA expression of the alpha-CGRP in AI lungs showed only a transient increase after OVA-challenge (2.7-fold at 6 hr) followed by a lower level of expression (0.5-fold at 48 hr and 0.6-fold at 120 hr). The mRNA expressions of both isoforms in NG, but not in DRG, were transiently up-regulated at 6 hr after antigen challenge. In situ RT-PCR in combination with immunohistochemical analysis revealed that beta-CGRP was expressed in neuroendocrine cells in clusters (termed neuroepithelial bodies [NEBs]) in AI lungs. These results indicate that the long-term induction of beta-CGRP in NEBs may play an important role in pulmonary AI such as bronchial asthma.
PubMed ID
15519362 View in PubMed
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