"It has been known for a while that people and animals can become sleepy and less active after a meal, but brain signals responsible for this were poorly understood. We have pinpointed how glucose - the sugar in food - can stop brain cells from producing signals that keep us awake," said Denis Burdakov of the University of Manchester in England.

His team figured out how glucose blocks neurons that make orexins, which are tiny proteins that help us stay conscious. "These cells are critical for responding to the ever-changing body-energy state with finely orchestrated changes in arousal, food seeking, hormone release and metabolic rate to ensure that the brain always has adequate glucose," Burdakov explained.

In their experiments, the researchers engineered mice to produce a fluorescent protein only in orexin neurons. Thus, the researchers could isolate the neurons in brain slices from the mice, and perform precise biochemical and electrophysiological studies to explore how glucose acted on those neurons. In particular, the researchers performed experiments in which they exposed the neurons to the subtle changes in glucose levels known to occur in daily cycles of hunger and eating.

The experiments showed that glucose inhibits orexin neurons by acting on a class of potassium ion channels known as "tandem pore" channels, about which little was known. Such ion channels are porelike proteins in the cell membrane that affect cellular responses by controlling the flow of potassium into the cell. "Together, these results identify an unexpected physiological role for the recently characterized [tandem pore potassium] channels and shed light on the long-elusive mechanism of glucose inhibition, thus providing new insights into cellular pathways regulating vigilance states and energy balance," wrote Burdakov and his colleagues.

Scientists write that this discovery about how slight changes of glucose levels affect firing of orexin "raises the possibility that, besides being important for adaptive responses to starvation, modulation of orexin cells by glucose has a much wider behavioral role, contributing to the continuous daily readjustments in the level of arousal and alertness."

"Now we know how glucose stops orexin neurons 'firing', we have a better understanding of what may occur in disorders of sleep and body weight," said Burdakov. "This may well provide an explanation for after-meal tiredness and why it is difficult to sleep when hungry."

Malfunction of orexin neurons can lead to narcolepsy, where sufferers cannot stay awake, and obesity; there is also evidence that orexin neurons play a role in learning, reward-seeking and addiction.

"This research perhaps sheds light on why our European friends are so fond of their siestas," added Burdakov.