We've seen that ion channels are deeply implicated in pain states and that genetic polymorphisms affecting them probably play a role in ME/CFS. This realization has come about as the tools for describing and understanding ion channels have appeared. A recent study indicates that calcium ion channels play the same role in sleep. Interestingly the activity of these channels increases during sleep.
The description of these mice sounds very much like ME/CFS - fragmented sleep and a failure to attain deep sleep. Other studies indicate that fragmented sleep makes it more difficult to feel positive or hopeful (eg. to access the reward centers of the brain.)
Several studies suggest problems with deep sleep are present in ME/CFS and they appear to mirror the findings here - so far as I can tell.
This
sounds very much like the Zinn's findings that ME/CFS patients were asleep when they were awake....
The description of these mice sounds very much like ME/CFS - fragmented sleep and a failure to attain deep sleep. Other studies indicate that fragmented sleep makes it more difficult to feel positive or hopeful (eg. to access the reward centers of the brain.)
Several studies suggest problems with deep sleep are present in ME/CFS and they appear to mirror the findings here - so far as I can tell.
This calcium channel turns out to be a key player in normal sleep. The mice without working Cav3.1 calcium channels took longer to fall asleep than normal mice, and stayed asleep for much shorter periods. "They basically took cat naps," says Llinás. Their brain activity was also abnormal, more like normal wakefulness than sleep. Most importantly, these mice never reached deep, slow-wave sleep. "This means that we have discovered that Cav3.1 is the channel that ultimately supports deep sleep," Llinás says.
Because these mice completely lack the ability to sleep deeply, they eventually express a syndrome similar to psychiatric disorders in humans. Llinás believes that studying how the brain functions during unconsciousness is key to understanding normal consciousness, as well as abnormal brain activity. This paper begins to uncover one of the key mechanisms of normal sleep, as well as the role for one important calcium channel in overall brain function.
This
Moreover, quite unexpectedly, during unconsciousness, high-frequency oscillations (known as characteristic EEG spectral bands in the aroused state) were increased in mice lacking CaV3.1 channels, compared with control mice.
sounds very much like the Zinn's findings that ME/CFS patients were asleep when they were awake....