s6v3d, on 13 January 2012 - 06:35 AM, said:
Out of curiosity, might I ask for a link to your references? I think we're a few pages off from being homeostatic with eachother as Atonia is symptom commonly called full body paralysis and is an effect of the body transitioning into a REM state (
http://www.medterms....articlekey=9811 ). A state that as I said before was an essential factor of dreaming the dreams that restore and reiterate us and our experiences (
http://sleep.health....leep/REM-sleep/ ). Orixen-A itself is dually a sleep cycle control hormone or an energy booster of sorts when in lack there of (
http://www.scienceda...80102093936.htm ).
I've made a personal study of dreams and the dreaming brain for over three decades and have written a couple of books on the subject. In that time, I've notice how little some researchers understand about their own research. Focusing on a specific idea or area of study without a proper foundation has likely limited their ability to fully comprehend what their findings actually suggests. The proper foundation for understanding the components of sleep or any component of brain function begins with brain evolution and where in that evolution did those components first likely appear. If we can prove that atonia evolved independent of REM and that REM can arise independent of atonia, then it is highly likely that atonia did not evolve to serve the REM state.
First, atonia defines the loss or lack of muscle tone or elasticity rather than muscle paralysis, as is the standard medical definition, which is indeed a condition opposite the ready and responsive state of muscle tonal posture. Therefore, atonia also describes a loss or lack of muscle readiness. Atonia is mediated by the
peri-locus ceruleus, which is located in that part of our central nervous system that does not generate the low-amplitude, high-frequency EEG waves associated with REM (
http://sleep.health....leep/REM-sleep/). The
locus ceruleus is situated in the metencephalic segment of
brainstem, which envelopes neural functions considered less recent in our contemporary brain development than those brain structures (
neocortex) where dream generation is thought to occur. Therefore, the neural components of sleep that generate atonia likely developed or evolved in what would become our neurostructure before that structure was capable of generating dreams. This suggest that atonia evolved for some reason other than the inhibition of movement amid dreaming. Animal studies have shown that "...subceruleus lesions created REM sleep without atonia." Therefore, atonia is not essential to the production of REM. The position of the structure believed to mediate atonia in the pimitive segment of brainstem coupled with the creation of REM sleep without atonia suggest that atonia likely did not evolve to serve the REM state.
Regarding
http://www.scienceda...80102093936.htm, if you'll read the article,
orexin-A is indeed described as a
peptide that
is produced by a "small mumber of neurons".The article goes on to say that orexin-A effectiveness is cognitive related rather than energy boosting. The article states that this peptide "has no effect on performance if the animals where not sleep deprived." Rather than fueling or boosting the energy level of test animals, this article suggest that the orexin peptide merely establishes normal acuity or cognitive efficiency in brain function, which is unlike the boosting effects of energizers such as glucose or anphetimines.