Ues (Pardal and Lopez-Barneo, 2002b). In this in vitro system, rat CB glomus cells secrete neurotransmitter when exposed to a glucose-free option (Figures 1A,B) (Garcia-Fernandez et al., 2007). This secretory activity is reversible, depending on external Ca2+ influx (Figure 1C), and is proportional to the degree of glucopenia. Responses to hypoglycemia, including neurotransmitter PAK list release and sensory fiber discharge, have also been observed in other in vitro studies working with rat CB slices (Garcia-Fernandez et al., 2007; Zhang et al., 2007), rat CB/petrosal ganglion co-culture (Zhang et al., 2007), and cat CB (Fitzgerald et al., 2009). Not too long ago, the hypoglycemia-mediated secretory response has also been detected in human glomus cells dispersed from post mortemThe molecular mechanisms underlying CB glomus cell activation by PDE11 Storage & Stability hypoglycemia have already been investigated in both reduced mammals and human CB tissue samples (Pardal and Lopez-Barneo, 2002b; Garcia-Fernandez et al., 2007; Zhang et al., 2007; Fitzgerald et al., 2009; Ortega-Saenz et al., 2013). In our initial study we reported that, like O2 sensing by the CB, macroscopic voltage-gated outward K+ currents are inhibited in patch-clamped rat glomus cells exposed to glucose-free options (Pardal and Lopez-Barneo, 2002b). Having said that, we soon realized that besides this phenomenon, low glucose elicits a membrane depolarization of eight mV (Figures 1D,E) (Garcia-Fernandez et al., 2007), that is the key method leading to extracellular Ca2+ influx into glomus cells, as demonstrated by microfluorimetry experiments applying Fura-2AM labeled cells (Figure 1F) (Pardal and Lopez-Barneo, 2002b; Garcia-Fernandez et al., 2007; Ortega-Saenz et al., 2013). The raise in intracellular Ca2+ , which is demonstrated by the inhibition of your secretory activity by Cd2+ , a blocker of voltagegated Ca2+ channels (Pardal and Lopez-Barneo, 2002b; GarciaFernandez et al., 2007), benefits in exocytotic neurotransmitter release (Pardal and Lopez-Barneo, 2002b; Garcia-Fernandez et al., 2007; Zhang et al., 2007; Ortega-Saenz et al., 2013). This neurotransmitter release triggers afferent discharge and activation of counter-regulatory autonomic pathways to improve the blood glucose level (Zhang et al., 2007; Fitzgerald et al., 2009). The depolarizing receptor possible triggered by low glucose includes a reversal potential above 0 mV and is as a result of boost of a standing inward cationic current (carried preferentially by Na+ ions) present in glomus cells (Figures 1G,H) (Garcia-Fernandez et al., 2007). Certainly, in contrast with hypoxia, low glucose decreases the membrane resistance of glomus cells recorded with all the perforated patch configuration of the patch clamp approach to 50 of control (Gonz ez-Rodr uez and L ez-Barneo, unpublished benefits). As reported by other folks (Carpenter and Peers, 2001), the background Na+ current plays a significant role in chemotransduction by glomus cells since it sets the membrane potential to fairly depolarized levels, close to the threshold for the opening of Ca2+ channels.Frontiers in Physiology | Integrative PhysiologyOctober 2014 | Volume 5 | Write-up 398 |Gao et al.Carotid body glucose sensing and diseaseFIGURE 1 | Counter-regulatory response to hypoglycemia in rat carotid body (CB) slices and isolated glomus cells. A representative secretory response (A) and typical secretion price (B) induced by glucopenia in glomus cells from CB slices (n = 3). (C) Abolition on the secretory response to hypoglycemia by 100 M.
