ArticleThe Journal of physiology1995
Voltage-dependent calcium currents are enhanced in dorsal root ganglion neurones from the Bio Bred/Worchester diabetic rat.
Article in The Journal of physiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Diabetes-induced electrophysiological alterations on neurosomes in ganglia of peripheral nervous system.Biophysical reviews · 2023Review
- Painful diabetic neuropathy leads to functional CaExperimental neurology · 2021Article
- Targeting T-type/CaV3.2 channels for chronic pain.Translational research : the journal of laboratory and clinical medicine · 2021Review
- Article
- Painful Diabetic Neuropathy: Prevention or Suppression?International review of neurobiology · 2016Review
- Molecular Basis of Regulating High Voltage-Activated Calcium Channels by S-Nitrosylation.The Journal of biological chemistry · 2015Article
- High-Fat Diet-Induced Retinal Dysfunction.Investigative ophthalmology & visual science · 2015Article
- CaV1.2 and CaV1.3 channel hyperactivation in mouse islet β cells exposed to type 1 diabetic serum.Cellular and molecular life sciences : CMLS · 2015Article
- Antioxidant strategies in the management of diabetic neuropathy.BioMed research international · 2015Review
- Targeting of CaV3.2 T-type calcium channels in peripheral sensory neurons for the treatment of painful diabetic neuropathy.Pflugers Archiv : European journal of physiology · 2014Review
- Nociceptive neurons differentially express fast and slow T-type Ca²⁺ currents in different types of diabetic neuropathy.Neural plasticity · 2014Article
- Reversal of neuropathic pain in diabetes by targeting glycosylation of Ca(V)3.2 T-type calcium channels.Diabetes · 2013Article
- Neuropathic pain: role for presynaptic T-type channels in nociceptive signaling.Pflugers Archiv : European journal of physiology · 2013Review
- Interplay of sorbitol pathway of glucose metabolism, 12/15-lipoxygenase, and mitogen-activated protein kinases in the pathogenesis of diabetic peripheral neuropathy.Biochemical pharmacology · 2012Article
- Sensory neurons derived from diabetic rats have diminished internal Ca2+ stores linked to impaired re-uptake by the endoplasmic reticulum.ASN neuro · 2012Article
- Effect of insulin and an erythropoietin-derived peptide (ARA290) on established neuritic dystrophy and neuronopathy in Akita (Ins2 Akita) diabetic mouse sympathetic ganglia.Experimental neurology · 2011Article
- Diabetic neuropathy enhances voltage-activated Ca2+ channel activity and its control by M4 muscarinic receptors in primary sensory neurons.Journal of neurochemistry · 2011Article
- Nutrient excess and altered mitochondrial proteome and function contribute to neurodegeneration in diabetes.Mitochondrion · 2011Review
- Diabetic visceral hypersensitivity is associated with activation of mitogen-activated kinase in rat dorsal root ganglia.Diabetes · 2011Article
- T-type voltage-gated calcium channels as targets for the development of novel pain therapies.British journal of pharmacology · 2011Review
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3 authors.
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Abstract
1. Whole-cell, high-threshold, voltage-dependent calcium currents (ICa) were enhanced in acutely dissociated, capsaicin-sensitive dorsal root ganglion neurones from diabetic Bio Bred/Worchester (BB/W) rats, compared with those from age-matched, non-diabetic controls. The magnitude of the enhancement increased with the duration of diabetes, and reached significance at diabetic durations of 6 months (diabetic: 6.3 +/- 0.4 nA; current density (CD), 157 +/- 12 pA pF-1; means +/- S.E.M., n = 9, P < 0.01; control: 3.9 +/- 0.6 nA; CD, 116 +/- 11 pA pF-1; n = 18) and 8 months (diabetic: 7.6 +/- 0.4 nA; CD, 177 +/- 25 pA pF-1; n = 11, P < 0.005; control: 5.1 +/- 0.5 nA; CD, 111 +/- 26 pA pF-1; n = 15). Low-threshold, voltage-dependent ICa were also enhanced in neurones from animals diabetic for 8 months (diabetic: 2.5 +/- 0.7 nA, n = 4, P < 0.05; control: 0.7 +/- 0.5 nA, n = 6). 2. The ICa enhancement was prevented by long-term treatment of diabetic animals with an aldose reductase inhibitor (ARI; peak ICa at 6 months: 4.41 +/- 0.48 nA, n = 2; at 8 months: 4.32 +/- 0.60 nA, n = 9). 3. The ICa enhancement was not due to a shift in the voltage dependence of either the current-voltage relationship or steady-state inactivation. 4. The L channel antagonist nifedipine and preferential N channel antagonist omega-conotoxin GVIA (omega-CgTX) caused a greater inhibition of high-threshold ICa in diabetic neurones compared with controls (nifedipine: control: 25 +/- 3%, n = 26; diabetic: 36 +/- 7%, n = 11; omega-CgTX: control: 40 +/- 4%, n = 21; diabetic: 50 +/- 7%, n = 7). Diabetic neurones also demonstrated a significantly greater residual current (2.44 +/- 0.34 nA, n = 7) in the presence of both antagonists vs. controls (1.28 +/- 0.30 nA, n = 8, P < 0.05), suggesting that N-, L- and additional non-N-, non-L-type high-threshold ICa were enhanced.
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