ITWire

U.S. neuroscientist Leslie C. Griffith, from the department of Biology and the National Center for Behavioral Genomics, Brandeis University (Waltham, Massachusetts), led a team of scientists on research with the two-winged fruit fly Drosophila melanogaster.

The researchers included Jose Agosto, James C. Choi, Katherine M. Parisky, Michael Rosbash, all from Brandeis University; and Geoffrey Stilwell, from Cambria Biosciences (Woburn, Massachusetts).

The researchers were the first scientists to discover that a receptor for the chemical gamma-aminobutyric acid (GABA), an important inhibitory neurotransmitter that controls sleep cycles in humans, is also found in the fruit fly (D. melanogaster). They found that GABA did not control the amount of sleep but did control when sleep occurs in the fruit flies.

They also discovered that a mutation in GABA, something having to do an alteration in the receptor gene called Rdl, can cause fruit flies to fall asleep faster than normal fruit flies.

On the other end of sleep, the researchers found that the anti-convulsant and mood stablizing drug called carbamazepine (CBZ), if given to fruit flies, keeps them awake.

The research performed by the Griffith team may one day help people sleep better.

Their research, entitled “Modulation of GABA_A receptor desensitization uncouples sleep onset and maintenance in Drosophila,” was written up in the February 1, 2008 issue of the journal Nature Neuroscience.

Their abstract to the paper reads, “Many lines of evidence indicate that GABA and GABA_A receptors make important contributions to human sleep regulation. Pharmacological manipulation of these receptors has differential effects on sleep onset and sleep maintenance insomnia.”

“Here we show that sleep is regulated by GABA in Drosophila and that a mutant GABA_A receptor, RdlA^302S, specifically decreases sleep latency.”

“The drug carbamazepine (CBZ) has the opposite effect on sleep; it increases sleep latency as well as decreasing sleep. Behavioral and physiological experiments indicated that RdlA^302S mutant flies are resistant to the effects of CBZ on sleep latency and that mutant RDLA^302S channels are resistant to the effects of CBZ on desensitization, respectively.”

“These results suggest that this biophysical property of the channel, specifically channel desensitization, underlies the regulation of sleep latency in flies. These experiments uncouple the regulation of sleep latency from that of sleep duration and suggest that the kinetics of GABA_A receptor signaling dictate sleep latency.”