| First Author | Guyon A | Year | 2009 |
| Journal | J Neurosci | Volume | 29 |
| Issue | 8 | Pages | 2528-33 |
| PubMed ID | 19244527 | Mgi Jnum | J:145944 |
| Mgi Id | MGI:3836352 | Doi | 10.1523/JNEUROSCI.5764-08.2009 |
| Citation | Guyon A, et al. (2009) Glucose inhibition persists in hypothalamic neurons lacking tandem-pore K+ channels. J Neurosci 29(8):2528-33 |
| abstractText | Glucose sensing by hypothalamic neurons triggers adaptive metabolic and behavioral responses. In orexin neurons, extracellular glucose activates a leak K(+) current promoting electrical activity inhibition. Sensitivity to external acidification and halothane, and resistance to ruthenium red designated the tandem-pore K(+) (K(2P)) channel subunit TASK3 as part of the glucose-induced channel. Here, we show that glucose inhibition and its pH sensitivity persist in mice lacking TASK3 or TASK1, or both subunits. We also tested the implication of another class of K(2P) channels activated by halothane. In the corresponding TREK1/2/TRAAK triple knock-out mice, glucose inhibition persisted in hypothalamic neurons ruling out a major contribution of these subunits to the glucose-activated K(+) conductance. Finally, block of this glucose-induced hyperpolarizing current by low Ba(2+) concentrations was consistent with the conclusion that K(2P) channels are not required for glucosensing in hypothalamic neurons. |
