title: Orexin neurons and the TASK of glucosensing.
abstract: Relatively little is known about the mechanisms that link changing levels of glucose and neuronal activity. A paper in the current issue of Neuron by Burdakov et al. demonstrates that orexin/hypocretin neurons are inhibited by rising glucose in part due to membrane potential effects mediated by tandem-pore K(+) (K(2P)) channels. The findings may shed light on the mechanisms that link hypoglycemia and coordinated arousal and autonomic responses.
authors.affiliation: Center for Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, 75390, USA.
authors.forename: Michael M
authors.initials: MM
authors.lastname: Scott
authors.forename: Jacob N
authors.initials: JN
authors.lastname: Marcus
authors.forename: Joel K
authors.initials: JK
authors.lastname: Elmquist
mesh_terms: D000818:Animals; D005947:Glucose / Q000378:metabolism*; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism*; D009419:Nerve Tissue Proteins; D009474:Neurons / Q000502:physiology*; D009479:Neuropeptides / Q000378:metabolism*; D000068797:Orexins; D024683:Potassium Channels, Tandem Pore Domain / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D009419:Nerve Tissue Proteins; D009479:Neuropeptides; D000068797:Orexins; D024683:Potassium Channels, Tandem Pore Domain; C420132:potassium channel subfamily K member 3; D005947:Glucose