Tandem-pore K+ channels mediate inhibition of orexin neurons by glucose.

Abstract:

:Glucose-inhibited neurons orchestrate behavior and metabolism according to body energy levels, but how glucose inhibits these cells is unknown. We studied glucose inhibition of orexin/hypocretin neurons, which promote wakefulness (their loss causes narcolepsy) and also regulate metabolism and reward. Here we demonstrate that their inhibition by glucose is mediated by ion channels not previously implicated in central or peripheral glucose sensing: tandem-pore K(+) (K(2P)) channels. Importantly, we show that this electrical mechanism is sufficiently sensitive to encode variations in glucose levels reflecting those occurring physiologically between normal meals. Moreover, we provide evidence that glucose acts at an extracellular site on orexin neurons, and this information is transmitted to the channels by an intracellular intermediary that is not ATP, Ca(2+), or glucose itself. These results reveal an unexpected energy-sensing pathway in neurons that regulate states of consciousness and energy balance.

journal_name

Neuron

journal_title

Neuron

authors

Burdakov D,Jensen LT,Alexopoulos H,Williams RH,Fearon IM,O'Kelly I,Gerasimenko O,Fugger L,Verkhratsky A

doi

10.1016/j.neuron.2006.04.032

subject

Has Abstract

pub_date

2006-06-01 00:00:00

pages

711-22

issue

5

eissn

0896-6273

issn

1097-4199

pii

S0896-6273(06)00369-2

journal_volume

50

pub_type

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