Sleep v.s. potassium channel

Look over the topics on flies sleeping through the years: First peole found flies do sleep! Then people found the controlling location related to the mushroom body. (It's not surprising because people say the mushroom body in the fly is like the hippocampus in mammals. It's a little surprising is that an "iso-hippocampus" can have the role of controlling sleep.) Later on people found a signal pathway seem to be playing a very important role: EGFR/ERK, Rho signaling.

But what's interest me more here is, potasium channels, esp. Kv4.2 is involved!!

"What are the identities of the downstream targets for EGFR-ERG signaling in the TriC region of the fly brain? ERK directly phosphorylates the potassium channel Kv4.2 (ref. 12). Phosphorylated ERK seems to be expressed in the processes, but not in the soma of the TriC neurons. Thus, the final target of this signaling pathway may well be changes in electrical activity or synaptic transmission in these neurons. This suggestion fits nicely with work in Drosophila indicating that a mutation in the potassium channel Kv1.4 also produces abnormalities in sleep maintenance."

"Shaker, which encodes a voltage-dependent potassium channel controlling membrane repolarization and transmitter release, may thus regulate sleep need or efficiency."

"It is possible that the mns mutation, by affecting an ion channel that controls membrane repolarization, may be close to the core cellular mechanisms of sleep. In mammals, potassium channels are involved in the generation of sleep rhythms. It is not known whether human extreme short sleepers have mutations in depolarization or voltage-dependent potassium channels. However, in Morvan's syndrome, a rare autoimmune disorder with central nervous system symptoms, marked sleeplessness has been associated with autoantibodies against voltage-dependent potassium channels that may have crossed the blood−brain barrier. The finding that a point mutation in a voltage-dependent potassium channel produces an extreme short-sleeping phenotype with preserved performance is relevant..."

Another 2 papers:

Increased motor drive and sleep loss in mice lacking Kv3-type potassium channels. (2004 Genes Brain Behav)

Sleep EEG in mice that are deficient in the potassium channel subunit K.v.3.2. ( 2002 Brain Research)