To satisfy my addiction with this blog, I had a few moments before some additional work to post a few things that R and I have been working on for the last few weeks. They are some models that show the cycle from wake to sleep and some hypothesized processes that partake in this cycle.
Model 1 shows the process from wake to disassociation. By disassociation I mean by anything that alters the consciousness into a state of disarray, meaning that we have our “sub-conscious self” activated due to the processes that take place during administering of psychedelic drugs, dreaming, or in meditation. The model does not show meditation since we have yet had enough time to research the processes of meditation enough to base a model on that type of disassociation, but will come soon. The psychedelic influences part of the model is not very detailed because of the same issue. Model 1 also relates the stages of sleep into different conversions that taking place during the phase, those conversions are described in later models.
Model 2 adds in the conversion cycle. With the help of MAO inhibiting beta carbolines, we can see that the midline brainstem neuronal clusters are allowed to create a higher level of serotonin, something that is very important for our long term memory. When lights are turned off, the pineal gland then starts the conversion of serotonin into melatonin which decreases our serotonin levels and increases our melatonin levels making us sleepy. At this time (or relative to it) melatonin is also being converted into tryptamine as well as pinoline, a powerful beta-carboline. The tryptamine, in combination with beta-carbolines such as pinoline, acts as a psychedelic to activate our pontine brainstem.
Model 3 shows the bigger picture of this conversion in the three different stages and shows the core temperature change during the process of waking and disassociation that is apparent right after pontine brainstem activation. As disassociation is activated in the pontine brainstem core temperature is decreased as body temperature is increased. As the cycle of disassociation is completed and the body starts to wake, the opposite happened.
Model 4 shows the different parts of the brain that are activated by the brainstem due to the activation of either the cholinergic system or deactivated by the aminergic system. As the pontine brainstem deactivates the visual cortex of the brain, the pontine sends falsified sensory visual input into the geniculate which helps in creating disassociated visual imagery.
To overview, in our research we have found that dreaming like any other type of disassociation is experienced based on a chemical reaction caused by the formation of tryptamine and beta-carbolines from melatonin and serotonin. The brain is required to shut down and activate different areas of the brain in order to complete the production of tryptamine and beta-carbolines during disassociation. The reason for this process is unknown but can be hypothesized as an important process of preventing the buildup of serotonin. It can also be hypothesized that the production of the tryptamine type psychedelic is an important aspect of our imagination process giving humans the ability be creative during the day. It also could be hypothesized that both previous hypotheses are both equally important to our daily functions. Regardless of the possibilities, it is our opinion that dreaming is a byproduct of this system and anything that is experienced during this time is considered a degree hallucination dependent on the amount of psychedelic released during the disassociation process along with what areas of the brain are activated/deactivated.
This information is not yet completed but I just wanted to show the public what we have been working on. If you have any commits on the models please post them as it would help in our understanding of the sleep design.