Orexin neurons and the TASK of glucosensing.
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.
Scott
Michael M
MM
Center for Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, 75390, USA.
Marcus
Jacob N
JN
Elmquist
Joel K
JK
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*
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