Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Editor

Personal info

View

About

Terms

Javascript disabled

Please enable Javascript support in your browser to use this application.

Instructions on how to enable JavaScript on different browsers can be found here: http://www.google.com/support/bin/answer.py?answer=23852.

[edit this page]

Pirisino, R. et al.

Pirisino, Ghelardini, Pacini, Galeotti, Raimondi,

Methylamine, but not ammonia, is hypophagic in mouse by interaction with brain Kv1.6 channel subtype.

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.[1]

References

Methylamine, but not ammonia, is hypophagic in mouse by interaction with brain Kv1.6 channel subtype. Pirisino, R., Ghelardini, C., Pacini, A., Galeotti, N., Raimondi, L. Br. J. Pharmacol. (2004) [Pubmed]

Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenes Open Access Licence Privacy Policy Terms of Use apsburg

The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.