The study also gives us a clue to understanding both normal and abnormal waking brain functions.
“It is the same brain, same neurons and similar requirements for oxygen and so on. So what is the difference between these two states?” asked Rodolfo Llinas, a professor of neuroscience at New York University School of Medicine and a Whitman Center Investigator at the Marine Biological Laboratory (MBL) in Woods Hole.
To tackle the broad question of sleep, Llinas and his colleagues focused on one crucial part of the puzzle in mice, Marine Biological Laboratory.
Calcium channels, selective gates in neuron walls, are integral in neuron firing, ensuring that all parts of the brain keep talking to one other. But during sleep, calcium channel activity is increased, keeping a slow rhythm that is different from patterns found during wakefulness.
Based on this clue, the scientists removed one type of calcium channel, Cav3.1, and looked at how the absence of that channel’s activity affected mouse brain function.
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.
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,” Llinas said.
Because these mice completely lack the ability to sleep deeply, they eventually express a syndrome similar to psychiatric disorders in humans.
The findings appeared in the Proceedings of the National Academy of Sciences.
2015 Kashmir Despatch