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Showing entries tagged sleepwake cycle.  Show all entries

October 23, 2011

One Prick and you are Out

Isn't it crazy with one prick of anesthetics you can be out and then awaken hours later and have no recollection of what just happened? Sleep is like this too except, you have to close your eyes for a little then all sudden "poof", you awake to a morning sun. Sleep and anesthesia seem to be one in the same, but in reality they are not. Researchers in Canada measured the long field potentiation and coherence of cortical neurons in anesthetize and sleeping cats to investigate the differences.

Slow wave sleep (SWS) or what we call sleep is characterized by sleep slow oscillations, a characteristic of anesthesia. These oscillations form by cortical cells alternating between depolarizing and hyperpolarizing states. Depending on these oscillations neurons can either be active, a state of high synaptic activity or a silent state, low synaptic activity. Both aestheticize cats and sleeping cats were found in silent states but the amount of time aestheticizes cats were in the silent state differed.

Cats in SWS were found to have irregular slow waves or slow oscillations within each of the recorded cortical regions. When the anesthesia Ketamine- xylazine was injected into the cats, these regions showed consistent slow oscillations. These findings concluded that during SWS not all the brain regions are in silent states or inactive, so in sense, the brain still can processes information from the outside world. Opposite of that, aestheticize cats cannot process information because most the brain regions are in an inactive phase. So when a person receives anesthetics for surgery, they are not able to process that surgeons are cutting open their bodies, compared to a person who is able to wake up in the middle of the night because he or she processed that there might be a fire outside.

With the use of three different frequencies, regions of the brain could were investigated whether there are synchronous or non synchronous activities in the brain during the SWS and anesthesia. Aestheticized cats were found to have synchronous frequencies in contrast to nonsynchronous activities in SWS cats. These findings explain why a person can recall some of their dreams when they wake up compared to a person waking up from receiving an anesthetic. Because slow waves start to decrease as a person is about to wake up, there is a point in time where the active state is a little longer than a second, allowing a person to somewhat recall their dreams. While when someone is under anesthesia, the time in silent state is double compared to SWS. Synchronous brain activity allows for not time for regions of the brain to become consciousness during the transition from silent to an active state.

With these finding it hoped that further investigation of consciousness and unconsciousness could be understood. With many patients under comas for many days, months, and years, wouldn't it be a miracle if there was a way to wake them up?

Chauvette, Sylvain, Crochet, Sylvain, Tinofeev, Igor, Volgushev, Maxim. "Properties of Slow Oscillation during Slow- Wave Sleep and Anesthesia in Cats." The Journal of Neuroscience. 31 (2011)
Posted by      Erika L. at 2:33 PM MDT
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October 22, 2011

Sleep and spines modulate your mind...and your brain?

"The mind is the brain doing its job." - Simon LeVay, 1994

We know that sleep is good for us: it's a daily, regularly- or irregularly-scheduled body and brain maintenance check. The sleep/wake cycle maintenance staff in particular is profoundly important in synaptic renormalization (homeostasis) by modulating (decreasing) synaptic size and/or strength in the adult brain. In the adult brain; surprisingly, this doesn't exactly hold for the adolescent brain, where sleep/wake cycle maintenance staff is responsible for more synaptogenesis (synaptic formation) and synaptic pruning (synaptic elimination).

A recent article published in Nature Neuroscience examined the process of cortical development (that involves synaptogenesis and pruning) in adolescent YFP-mice (through two-photon microscopy) as a function of different sleep/wake cycles: W1S2 mice (wake followed by sleep), and S1W2 mice (sleep first followed by wake). Mice were allowed to sleep or kept awake for each behavioral state (sleep/wake) for durations that mimic physiological sleep/wake cycles (6-8 h) and then imaged. Interestingly enough, they found overall decreased spine density in W1S2 mice and increased spine density in S1W2 mice; there was no variation observed in mice in early or late adolescence. Waking results in a net increase in cortical spines, and sleep is associated with net spine loss.
A third experimental group of W1SD2 mice (wake followed by sleep deprivation), to control for decreased spine density as a function of the passage of time showed a net increase in synaptic density.

In summary:
Wake followed by sleep (W1S2) = spine loss
Sleep followed by wake (S1W2) = spine gain
Wake followed by sleep deprivation (W1SD2) = spine gain

Sleep might actually be bad! (...for dendritic spines, that is)

The wake-sleep deprived group presents an interesting case. Sleep-deprivation, akin to pulling an all-nighter, shows a net increase in spine density. Therefore, sleep deprivation is one way to keep your dendritic spine density (that is, until you crash of exhaustion). Sleeping for the recommended 8 hours a night is also a default option. For those of us in adolescence, retaining spine density though sleep-deprivation is still theoretically a viable option. A different experiment conducted by the same researchers imaged the mice after 2-3 hours of sleep (short sleep) or wake (short wake). Both groups showed no net changes after short sleep or short waking. It may be theoretically possible to maintain spine density through a sleep-deprivation following wake with short sleep sleep/wake cycle (power naps anyone?).

This article concludes by suggesting that behavioral state modulates spine turnover in a manner consistent with the need for synaptic homeostasis; in the adult brain this translates into synaptic renormalization, and in the adolescent brain (regardless of exact developmental stage of adolescence) this translates into synaptogenesis and synaptic pruning. Sleep may therefore facilitate spine elimination or spine loss in certain phases of development. Sleep deprivation during adolescence may affect synaptic turnover, as it blocks sleep-related spine pruning; however, it does not result in a further increase in spine density. It is currently unclear to what extent the role of sleep in spine elimination is permissive and/or instructive.

So what does sleep and spine density have to do with anything? In the adult brain, it decreases synaptic size and/or strength; in the adolescent brain, it modulates synaptic pruning during a period of massive synaptic remodeling. Synaptic spine density is a part of how the brain does its job. Spine density therefore affects the mind (the brain doing its job that feeds to the mind). Changes in our minds are therefore a result of the brain doing its job differently, and how the brain does its job differently can involve changes in synaptic spine density. Spine density subsequently affects the different jobs of the brain; spine density affects the mind. Sleep (the sleep/wake cycle), therefore, is especially critical in cortical development during adolescence in modulating synaptic spine density (long-term potentiation anyone?)

I should probably get more sleep myself...

Posted by      Patricia W. at 10:19 PM MDT
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