Accessibility navigation


Modulation of hTREK-1 by carbon monoxide

Dallas, M. L., Scragg, J. L. and Peers, C. (2008) Modulation of hTREK-1 by carbon monoxide. Neuroreport, 19 (3). pp. 345-348. ISSN 1473-558X

Full text not archived in this repository.

It is advisable to refer to the publisher's version if you intend to cite from this work. See Guidance on citing.

To link to this item DOI: 10.1097/WNR.0b013e3282f51045

Abstract/Summary

TREK-1 is a background K channel important in the regulation of neuronal excitability. Here, we demonstrate that recombinant human TREK-1 is activated by low concentrations of carbon monoxide (CO) and nitric oxide (NO), applied via their respective donor molecules. Related channels hTASK-1 and hTASK-3 were unaffected by CO. Effects of both CO and NO were prevented by preincubation of cells with the protein kinase G inhibitor, Rp-8-Br-PET-cGMPS. The effects of CO were independent of NO formation. At higher concentrations, both NO and CO were inhibitory. As both NO and CO are important neuronal gasotransmitters and TREK is crucial in regulating neuronal excitability, our results provide a novel means by which these gases may modulate neuronal activity.

Item Type:Article
Refereed:Yes
Divisions:Faculty of Life Sciences > School of Chemistry, Food and Pharmacy > School of Pharmacy
No Reading authors. Back catalogue items
ID Code:30355
Publisher:Lippincott Williams & Wilkins

University Staff: Request a correction | Centaur Editors: Update this record

Page navigation