Specific calcium channel vital for healthy sleep identified. Results showed Cav3.1 played integral role in normal sleep. Mice lacking calcium channel took longer time to fall asleep and had reduced hours of total sleep time as well

A recent paper by Choi, Yu, Lee and Rodolfo Llinás, Professor of Neuroscience at New York University School of Medicine and a Whitman Center Investigator at the Marine Biological Laboratory (MBL) in Woods Hole claimed to have identified a particular calcium channel that is critically involved in healthy sleeping patterns. This could be the first step towards understanding how brain functions differ in abnormal and normal waking, and how a single specific calcium channel could be involved in its regulation.

Question At Hand

Sleep is a simple concept – a state of resting and revitalization required by almost all vertebrates to function normally and survive. Surprisingly, the brain responds differently to stimuli when a person is awake as opposed to when he is resting, and this phenomenon is not clearly understood. This raises a very important and intriguing question – since it is the same brain with the same nerve cells requiring the same specifics such as oxygen etc, why is does this difference in responses exist?

Finding The Answer

Llinás and his team tackled the question by focusing on one important structure in mice – calcium channels. These selective ion gates are present in various places within the body, including the walls of the nerve cells where they play a crucial role in controlling neuron firing and keeping all parts of the brain connected with each other via neural signaling.

It is known that during sleep the activity of these calcium channels is increased, forming slower rhythms as compared to those during wakefulness. Based on this knowledge, the team removed a specific type of calcium channel – Cav3.1 – and observed how its absence affected brain function in mice.
Interesting findings

Results demonstrated that Cav3.1 played an integral role in normal sleep. Mice lacking the calcium channel took a longer time to fall asleep and had reduced hours of total sleep time as well. Brain activity was also seen to be abnormal, resembling that of wakefulness rather than sleep.

Most significantly, these mice never reached the stage of a deep, slow-wave sleep. “They basically took cat naps,” explained Llinás. “These findings show that we have discovered that Cav3.1 is the channel that ultimately supports deep sleep.”

Due to their lack of ever attaining a deep sleep, the mice eventually start exhibiting a syndrome quite similar to human psychiatric disorders. Llinás highlighted that understanding brain functioning mechanisms during unconsciousness is the key to understanding conscious behavior and brain abnormalities.