Deletion of TASK1 and TASK3 channels disrupts intrinsic excitability but does not abolish glucose or pH responses of orexin/hypocretin neurons.

Journal article

The firing of hypothalamic hypocretin/orexin neurons is vital for normal sleep-wake transitions, but its molecular determinants are not well understood. It was recently proposed that TASK (TWIK-related acid-sensitive potassium) channels [TASK1 (K(2P)3.1) and/or TASK3 (K(2P)9.1)] regulate neuronal firing and may contribute to the specialized responses of orexin neurons to glucose and pH. Here we tested these theories by performing patch-clamp recordings from orexin neurons directly identified ...

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Authors: González, J; Jensen, LT; Doyle, SE; Miranda-Anaya, M; Menaker, M

• Publication status: Published
• Journal: European journal of neuroscience
• Volume: 30
• Issue: 1
• Pages: 57-64
• Publication date: 2009-07-01
• DOI: 10.1111/j.1460-9568.2009.06789.x
• EISSN: 1460-9568
• ISSN: 0953-816X
• Language: English
• Keywords: Nerve Tissue Proteins; Feeding Behavior; Mice; Potassium Channels, Tandem Pore Domain; Mice, Transgenic; Animals; Mice, Knockout; Action Potentials; Green Fluorescent Proteins; Intracellular Signaling Peptides and Proteins; Membrane Potentials; Patch-Clamp Techniques; Glucose; Hydrogen-Ion Concentration; Neurons; Potassium Channels; Brain; Motor Activity; Neuropeptides