ArticleGastroenterology2016
Increased Activation of the TRESK K
Article in Gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Progressive impairment in gastric and duodenal slow waves and autonomic function during progression of type 2 diabetes in rats.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Diabetes-induced electrophysiological alterations on neurosomes in ganglia of peripheral nervous system.Biophysical reviews · 2023Review
- Diabetes mellitus differently affects electrical membrane properties of vagal afferent neurons of rats.Physiological reports · 2023Article
- Contribution of Neuronal and Glial Two-Pore-Domain Potassium Channels in Health and Neurological Disorders.Neural plasticity · 2021Review
- High-fat diet-induced vagal afferent dysfunction via upregulation of 2-pore domain potassium TRESK channel.JCI insight · 2019Article
- Effect of Hyperglycemia on Purinergic and Nitrergic Inhibitory Neuromuscular Transmission in the Antrum of the Stomach: Implications for Fast Gastric Emptying.Frontiers in medicine · 2018Article
- Plasticity of vagal afferent signaling in the gut.Medicina (Kaunas, Lithuania) · 2017Review
Corrections and comments
- Retraction · 2024-01-10Falsification/Fabrication of Data · Investigation by Company/Institution · · See also: https://pubpeer.com/publications/1430BA2AD44B27F2D7EC4A23CEDBED
- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND &
aimsPatients with diabetes have defects in the vagal afferent pathway that result in abnormal gastrointestinal function. We investigated whether selective increased activation of the 2-pore domain potassium channel TRESK (2-pore-domain weak inward-rectifying potassium channel-related spinal cord potassium channel) contributes to nodose ganglia (NG) malfunction, disrupting gastrointestinal function in diabetic rats.
methodsWe conducted whole-cell current-clamp and single-unit recordings in NG neurons from diabetes-prone BioBreeding/Worcester rats and streptozotocin-induced diabetic (STZ-D) rats and compared them with control rats. NG neurons in rats or cultured NG neurons were exposed to pharmacologic antagonists and/or transfected with short hairpin or small interfering RNAs that reduced expression of TRESK. We then made electrophysiologic recordings and studied gastrointestinal functions.
resultsWe observed reduced input resistance, hyperpolarized membrane potential, and increased current threshold to elicit action potentiation in NG neurons of STZ-D rats compared with controls. NG neuron excitability was similarly altered in diabetes-prone rats. In vivo single-unit NG neuronal discharges in response to 30 and 60 pmol cholecystokinin octapeptide were significantly lower in STZ-D rats compared with controls. Reducing expression of the TRESK K
conclusionsIn 2 rate models of diabetes, we found that activation of the TRESK K
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