Assuming that sleep allows astrocytes a chance to decompress->externalize data by turning off inputs (and clean up metabolic waste generated by the process), dreams may just be a literal representation of how our ventral streams process information without dorsal stream checking. Dreams are familiar because the data they are based on is our own data generated during the day, and discombobulated because brains are trying to determine valence and engrammatic similarity without the benefit of dorsal “maps” to guide it. Just as in when awake, unchecked ventral streams can predict things incorrectly and start mixing up other heavily valenced data (from psychosis to “unexpected item”). Because these are bad predictions they generate high error states, and it’s that high error state that represents what we see in our dreams (this is the same for “good” or “bad” dreams).
Which leads me to wonder – is dreaming an artifact of the CA2’s global error checking process? Can we check hippocampal CA2 volume or connectivity against dream vividness? Tangentially, is there a link between the hippocampal CA2 and visualization strength?
This parallels the process we experience when awake, items with low “novelty”/valence are removed from the stream regularly and the less novel something is the less likely we are to “remember” it, while high novelty items can stay stuck for weeks, or in particularly vulnerable individuals, months to forever.
All of this of course ignores the brainstem interaction unintentionally, I just don’t have enough data there yet. Considering the brainstem adds another interesting wrinkle to this question, could the function of sleep be a shut down of salience, and if salience needs to be shut down, why? Considering sleep initiates in the brainstem, it follows that maybe this salience function is more important than decompressing astrocytes? Perhaps salience shutdowns prevent astrocytes throughout the CNS from performing behavior (we need a salience and valence signal), and allows metabolic consolidation and clearance throughout the rest of the body.
Does sleep work as our primary anti-inflammatory mechanism?
Interestingly, NSAIDs decrease sleep efficacy. Is there a correlation between NSAIDs and learning efficacy as well?