Caffeine-induced calcium release from internal stores in cultured rat sensory neurons

Usachev, Yuriy M.; Shmigol, A.; Pronchuk, Nina; Kostyuk, P. G.; Verkhratsky, Alexei

doi:10.1016/0306-4522(93)90029-f

Cited by 152 publications

(118 citation statements)

References 59 publications

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“…1, B and C). The responses resembled those seen in bullfrog and rat sympathetic neurons and also in rodent central neurons (6,7,31). The caffeine responses were blocked by ryanodine (5-10 M), an antagonist of the ryanodine receptor at these concentrations (see legend to Fig.…”

supporting

confidence: 61%

Cyclic ADP-ribose Enhances Coupling between Voltage-gated Ca2+ Entry and Intracellular Ca2+ Release

Empson

Galione

1997

Journal of Biological Chemistry

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supporting

confidence: 61%

Cyclic ADP-ribose Enhances Coupling between Voltage-gated Ca2+ Entry and Intracellular Ca2+ Release

Empson

Galione

1997

Journal of Biological Chemistry

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“…The imaging data were acquired and analysed using MetaFluor/MetaMorph software (Universal Imaging, Downingtown, USA). The fura-2 signal was calibrated using an ionomycin-based in situ procedure [16]; the parameters R min , R max and K* were 0.2, 1.0 and 451 nmol/l respectively. All reagents were purchased from Sigma (Dorset, UK), and fura-2/AM was obtained from Molecular Probes (Eugene, Ore., USA).…”

Section: Methodsmentioning

confidence: 99%

“…4). The latter is known to activate Ca 2+ -gated Ca 2+ release channels (ryanodine receptors) resident in the endoplasmic reticulum membrane [16,23]. In L4-L6 DRG neurones, the percentage of cells responding to caffeine (when the amplitude of the [Ca 2+ ] i increase was triggered by drug application exceeded 50 nmol/l) decreased from 80 % in the control groups to 50 % after 14 weeks of diabetes and NT-3 treatment was effective in normalising the cell number responding to caffeine (data not shown). ]…”

Section: +mentioning

confidence: 99%

Diabetes-induced alterations in calcium homeostasis in sensory neurones of streptozotocin-diabetic rats are restricted to lumbar ganglia and are prevented by neurotrophin-3

et al. 2002

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A variety of hyperglycaemia-induced secondary metabolic defects have been identified as possible causal factors in the aetiology of the symmetrical sensory polyneuropathy observed in diabetes mellitus. These include polyol pathway flux [1], protein glycosylation [2], oxidative stress [3] and impaired neurotrophic support [4]. Alteration of cytoplasmic calcium homeostasis and calcium signalling might also be responsible for neurodegenerative diabetic complications [5,6]. Studies have shown altered Ca 2+ signalling in response to cell depolarisation in sensory Diabetologia (2002) AbstractAims/hypothesis. In diabetic sensory polyneuropathy the earliest and most severe pathophysiology occurs in neurones with the longest axons. The aim of this study was to characterise a diabetes-induced neurodegenerative marker that was selective for sensory neurones with the longest axons. We studied alterations in calcium homeostasis since this occurs in other neurodegenerative diseases. Methods. Sensory neurones were cultured from control and streptozotocin-diabetic rats, treated with or without human recombinant neurotrophin-3 (hrNT-3), and neurones from L4-L6 dorsal root ganglia (DRG) which exhibit the longest axons in vivo were compared with those from C5-L3 DRG. Fluorescent video-imaging was used to measure cytoplasmic calcium dynamics. Results. Streptozotocin diabetes of 8 to 14 weeks, induced an increase in resting internal Ca 2+ concentration ([Ca 2+ ] i ), from 67 7 nmol/l in small neurones and 79 9 nmol/l in big neurones obtained from control animals to 214 19 nmol/l in small neurones and 273 30 nmol/l in big neurones after 14 weeks of diabetes (p < 0.05) in L4-L6 DRG cultures. Neurones from C5-L3 ganglia and non-neuronal cells were not affected. Treatment of 14-week streptozotocin-diabetic rats with subcutaneous injection of 5 mg/kg NT-3 normalised the increase in resting [Ca 2+ ] i . The amplitudes induced by depolarisation, caffeine and ATP [Ca 2+ ] i responses were reduced in small ( < 30mm diameter) but not big ( > 35mm diameter) neurones of L4-L6 DRG from streptozotocin-diabetic animals; the C5-L3 DRG were not similarly affected and the changes in the L4-L6 DRG were corrected by NT-3 treatment. Conclusions/interpretation. Altered calcium homeostasis could be an early molecular marker linked to the onset of diabetic sensory neuropathy. This neurodegenerative index can be corrected by NT-3 therapy and should encourage further work aimed at understanding the mechanistic basis of these observations. [Diabetologia (2002) 45:560±570]

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“…22,23 To measure the contribution of CICR to the Ca 2+ transient after K + depolarization, we treated 17 neurons (3 large, 14 small, with comparable results) with ryanodine (10 μM; fig. 6A).…”

Section: Regulation Of Transient By Intracellular Ca 2+ Storesmentioning

confidence: 99%

Painful Nerve Injury Shortens the Intracellular Ca2+ Signal in Axotomized Sensory Neurons of Rats

2007

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Caffeine-induced calcium release from internal stores in cultured rat sensory neurons

Cited by 152 publications

References 59 publications

Cyclic ADP-ribose Enhances Coupling between Voltage-gated Ca2+ Entry and Intracellular Ca2+ Release

Cyclic ADP-ribose Enhances Coupling between Voltage-gated Ca2+ Entry and Intracellular Ca2+ Release

Diabetes-induced alterations in calcium homeostasis in sensory neurones of streptozotocin-diabetic rats are restricted to lumbar ganglia and are prevented by neurotrophin-3

Painful Nerve Injury Shortens the Intracellular Ca2+ Signal in Axotomized Sensory Neurons of Rats

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