Mechanism Of Oxygen Sensing By The Glomus [Type 1]Cell In The Cartoid Body
A bulk of evidence suggests that glomus (type I) cells are the initial site of transduction and that they release transmitters in response to hypoxia, which causes depolarization of nearby afferent nerve endings, leading to an increase in sensory discharge. Despite progress in CB cellular physiology, the molecular mechanisms underlying glomus cell O2 sensing, i.e. how the change in O2 tension is translated into decrease of K+ conductance, remain essentially unknown (López- Barneo, 2008: 259-287) . Several possible O2-sensing mechanisms, including the direct interaction of O2 with the ion channels or their indirect modulation through O2-sensing molecules, have been postulated. Since numerous K+ channel types have been reported to be O2 sensitive, it is assumed that there could be several O2 sensors coexisting in the same cell or distributed among the different O2-sensitive cell types, even in closely related animal species. Understanding CB O2 sensing at the molecular level is, however, challenged by the small size of the organ, which precludes elaborated biochemical and molecular biology experiments, and the gaseous nature of the detected molecule, which is easily diffusible across cell membranes and difficult to keep under strict control in the open chambers normally used for in vitro studies (Peers , 2010: 1-9).
Haemoxygenase (HO)-2 is an antioxidant enzyme constitutively expressed in most cells, including CB cells. This enzyme uses O2 to convert haem into biliverdin, iron and carbon monoxide. The possible involvement of HO-2 in CB acute O2 sensing has been suggested because it co-immunoprecipitates with heterologously expressed maxi-K+ channels and its inhibition with small interfering RNA abolishes the O2 modulation of recombinant channels. HO-2 is expressed in rat CB glomus cells and, in addition, ...