ArticleBritish journal of pharmacology2004
Methylamine, but not ammonia, is hypophagic in mouse by interaction with brain Kv1.6 channel subtype.
Article in British journal of pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Utilizing NMR fecal metabolomics as a novel technique for detecting the physiological effects of food shortages in waterfowl.Frontiers in physiology · 2023Article
- Methylamine induced hypophagia is mediated via dopamine D1 and D2 receptors in neonatal meat chicks.Veterinary research communications · 2016Article
- Article
- Relationship of impaired olfactory function in ESRD to malnutrition and retained uremic molecules.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2008Article
- Methylamine-dependent release of nitric oxide and dopamine in the CNS modulates food intake in fasting rats.British journal of pharmacology · 2007Article
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
Ammonia and methylamine (MET) are endogenous compounds increased during liver and renal failure, Alzheimer's disease, vascular dementia and diabetes, where they alter some neurobehavioural functions probably acting as potassium channel blockers. We have already described that potassium channel blockers including tetraethylammonium (TEA), ammonia and MET are hypophagic in mice. Antisense oligonucleotides (aODNs) against Shaker-like Kv1.1 gene abolished the effect of TEA but not of ammonia and MET. The central effects elicited in fasted mice by ammonia and MET were further studied. For MET, an ED(50) value 71.4+/-1.8 nmol mouse(-1) was calculated. The slope of the dose-response curves for these two compounds and the partial hypophagic effect elicited by ammonia indicated a different action mechanism for these amines. The aODNs pretreatments capable of temporarily reducing the expression of all seven known subtypes of Shaker-like gene or to inactivate specifically the Kv1.6 subtype abolished the hypophagic effect of MET but not that of ammonia. Reverse transcription-polymerase chain reaction, Western blot and immunohistochemical results indicate that a full expression in the brain of Kv1.6 is required only for the activity of MET, and confirms the different action mechanism of ammonia and MET.
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