ArticleSubstance abuse : research and treatment2010
Effect of potassium channel modulators on morphine withdrawal in mice.
Article in Substance abuse : research and treatment, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Minoxidil ameliorates myelodysplastic syndrome by targeting Wnt4 while sparing normal hematopoiesis.Cell communication and signaling : CCS · 2025Article
- Xenon gas as a potential treatment for opioid use disorder, alcohol use disorder, and related disorders.Medical gas research · 2025Review
- KThe Journal of pharmacology and experimental therapeutics · 2023Article
- Loss of SUR1 subtype KBehavioural brain research · 2021Article
- Morphine Efficacy, Tolerance, and Hypersensitivity Are Altered After Modulation of SUR1 Subtype KFrontiers in neuroscience · 2019Article
- Minoxidil is a potential neuroprotective drug for paclitaxel-induced peripheral neuropathy.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study was conducted to investigate the effect of potassium channel openers and blockers on morphine withdrawal syndrome. Mice were rendered dependent on morphine by subcutaneous injection of morphine; four hours later, withdrawal was induced by using an opioid antagonist, naloxone. Mice were observed for 30 minutes for the withdrawal signs ie, the characteristic jumping, hyperactivity, urination and diarrhea. ATP-dependent potassium (K(+) (ATP)) channel modulators were injected intraperitoneally (i.p.) 30 minutes before the naloxone. It was found that a K(+) (ATP) channel opener, minoxidil (12.5-50 mg/kg i.p.), suppressed the morphine withdrawal significantly. On the other hand, the K(+) (ATP) channel blocker glibenclamide (12.5-50 mg/kg i.p.) caused a significant facilitation of the withdrawal. Glibenclamide was also found to abolish the minoxidil's inhibitory effect on morphine withdrawal. The study concludes that K(+) (ATP) channels play an important role in the genesis of morphine withdrawal and K(+) (ATP) channel openers could be useful in the management of opioid withdrawal. As morphine opens K(+) (ATP) channels in neurons, the channel openers possibly act by mimicking the effects of morphine on neuronal K(+) currents.
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Registered trials
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