ArticleDiabetes2011
Diabetic visceral hypersensitivity is associated with activation of mitogen-activated kinase in rat dorsal root ganglia.
Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Voltage-Gated Ion Channels in Neuropathic Pain Signaling.Life (Basel, Switzerland) · 2025Review
- Diabetes-induced electrophysiological alterations on neurosomes in ganglia of peripheral nervous system.Biophysical reviews · 2023Review
- KAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Effects of bradykinin on voltage-gated KThe Journal of physiology · 2021Article
- Peripheral Voltage-Gated Cation Channels in Neuropathic Pain and Their Potential as Therapeutic Targets.Frontiers in pain research (Lausanne, Switzerland) · 2021Review
- KFrontiers in cellular neuroscience · 2020Review
- Altered R-spondin 1/CART neurocircuit in the hypothalamus contributes to hyperphagia in diabetes.Journal of neurophysiology · 2019Article
- A-Type KFrontiers in molecular neuroscience · 2018Review
- Alpha-lipoic Acid suppresses P2X receptor activities and visceral hypersensitivity to colorectal distention in diabetic rats.Scientific reports · 2017Article
- Diabetes-induced mechanophysiological changes in the small intestine and colon.World journal of diabetes · 2017Review
- α-lipoic acid suppresses neuronal excitability and attenuates colonic hypersensitivity to colorectal distention in diabetic rats.Journal of pain research · 2017Article
- Roles of Voltage-Gated Tetrodotoxin-Sensitive Sodium Channels NaV1.3 and NaV1.7 in Diabetes and Painful Diabetic Neuropathy.International journal of molecular sciences · 2016Review
- Colonic Hypersensitivity and Sensitization of Voltage-gated Sodium Channels in Primary Sensory Neurons in Rats with Diabetes.Journal of neurogastroenterology and motility · 2016Article
- Obesity Takes Its Toll on Visceral Pain: High-Fat Diet Induces Toll-Like Receptor 4-Dependent Visceral Hypersensitivity.PloS one · 2016Article
- Impairments of the primary afferent nerves in a rat model of diabetic visceral hyposensitivity.Molecular pain · 2015Article
- Visceral Hypersensitivity and Altered Colonic Motility in Type 2 Diabetic Rat.Journal of neurogastroenterology and motility · 2015Article
- Exercise-mediated improvements in painful neuropathy associated with prediabetes in mice.Pain · 2013Article
- Article
- Promoted interaction of nuclear factor-κB with demethylated cystathionine-β-synthetase gene contributes to gastric hypersensitivity in diabetic rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveDiabetic patients often experience visceral hypersensitivity and anorectal dysfunction. We hypothesize that the enhanced excitability of colon projecting dorsal root ganglia (DRG) neurons observed in diabetes is caused by a decrease in the amplitude of the transient A-type K(+) (I(A)) currents resulting from increased phosphorylation of mitogen-activated protein kinases (MAPK) and reduced opening of K(v)4.2 channels. RESEARCH DESIGN AND
methodsWe performed patch-clamp recordings of colon projecting DRG neurons from control and streptozotocin-induced diabetic (STZ-D) rats. Western blot analyses and immunocytochemistry studies were used to elucidate the intracellular signaling pathways that modulate the I(A) current. In vivo studies were performed to demonstrate that abnormal MAPK signaling is responsible for the enhanced visceromotor response to colorectal distention in STZ-D rats.
resultsPatch-clamp studies demonstrated that I(A) current was diminished in the colon projecting DRG neurons of STZ-D rats. Western blot analysis of STZ-D DRG neurons revealed increases in phosphorylated MAPK and K(V)4.2. In diabetic DRG neurons, increased intracellular Ca(2+) ([Ca(2+)](i)), protein kinase C (PKC), and MAPK were involved in the regulation of I(A) current through modulation of K(v)4.2. Hypersensitive visceromotor responses to colorectal distention in STZ-D rats were normalized by administration of MAPK inhibitor U0126.
conclusionsWe demonstrated that reduction of the I(A) current in STZ-D DRG neurons is triggered by impaired [Ca(2+)](i) ion homeostasis, and this in turn activates the PKC-MAPK pathways, resulting in decreased opening of the K(v)4.2 channels. Hence, the PKC-MAPK-K(v)4.2 pathways represent a potential therapeutic target for treating visceral hypersensitivity in diabetes.
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