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

Voitenko, Nana; Kostyuk, E. P.; Kruglikov, Illya; Kostyuk, P. G.

doi:10.1016/s0306-4522(99)00330-9

Cited by 41 publications

(41 citation statements)

References 15 publications

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“…As has been shown [6], the same parameters in the spinal dorsal horn (DH) neurons revealed similar changes in residual [Ca 2+ ] i measured 60 s after termination of membrane depolarization: 2.8 0.5 % (n = 23) in control and 14.1 1.2 % (n = 19) in the case of STZ-induced diabetes, p < 0.001 (Fig. 1).…”

Section: Resultssupporting

confidence: 57%

“…Similar findings were obtained for small-sized DRG neurons of rats. In contrast, in all tested rat dorsal horn neurons, transient increases in cytosolic Ca 2+ could be evoked by the application of caffeine; superfusion of slices with Ca 2+ -free solu- tion did not affect the transients, showing that they are produced by Ca 2+ release from intracellular stores [6]. Thus, Ca 2+ uptake by endoplasmic reticulum in these neurons can be an important component in the mechanisms which are shaping the time course of depolarization-induced calcium transients.…”

Section: Discussionmentioning

confidence: 82%

“…A detailed comparison of changes in intracellular signalling in primary and secondary nociceptive neurons of diabetic mice and rats would be quite important for evaluation of their true importance, taking into account the differences in incidence and time course of this pathology in different types of experimental animals. Preliminary experimental results of experiments on rat spinal dorsal horn neurons have actually shown substantial changes in Ca 2+ signalling during STZ-induced diabetes [4,6].…”

Section: : 1302±1309]mentioning

confidence: 99%

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

Kostyuk¹,

Voitenko

Kruglikov

et al. 2001

Diabetologia

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Understanding the origin of and discovering a treatment for neurological complications in diabetes mellitus is one of the most important challenges facing both experimental investigation and clinical practice because of their severity and the large numbers of patients affected. Nevertheless, the mechanisms of the development of distal diabetic neuropathy, in particular the incidence of hyperalgesia and allodynia, pain syndromes or, the opposite, loss of sensitivity are not well understood. In particular, data about the changes of intracellular metabolism in nociceptive neurons under diabetic conditions are scarce, especially about changes in intracellular calcium signalling which could be quite important for Diabetologia (2001) 44: 1302±1309 Diabetes-induced changes in calcium homeostasis and the effects of calcium channel blockers in rat and mice nociceptive neurons

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Section: Resultssupporting

confidence: 57%

Section: Discussionmentioning

confidence: 82%

Section: : 1302±1309]mentioning

confidence: 99%

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

Kostyuk¹,

Voitenko

Kruglikov

et al. 2001

Diabetologia

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“…[7±10] and dorsal horn [6,11] neurones. These experiments, however, used a single fluorescence detector, which did not allow signals from neurones and non-neuronal (satellite) cells to be distinguished.…”

mentioning

confidence: 99%

“…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) …”

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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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From Dendrites to Networks: Optically Probing the Living Brain Slice and Using Principal Component Analysis to Characterize Neuronal Morphology

Goldberg

Hamzei-Sichani

MacLean

et al.

Neuroanatomical Tract-Tracing 3

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

Cited by 41 publications

References 15 publications

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

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

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

From Dendrites to Networks: Optically Probing the Living Brain Slice and Using Principal Component Analysis to Characterize Neuronal Morphology

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