Why do we dream? Psychologists and neuroscientists have been debating the function of desires for generations, but there is still no accepted remedy.
Now, David M. Eagleman and Don A. Vaughn have proposed a new principle. Their preprint post, which has not yet been peer reviewed, is called The Defensive Activation principle: dreaming as a mechanism to protect against takeover of the visual cortex
To my head, it really is a very primary and inventive principle, but I’m not convinced by it.
Here’s Eagleman and Vaughn’s principle in nutshell: the role of desires is to be certain that the brain’s visual cortex is stimulated throughout snooze. In any other case, if the visual method were being deprived of input all evening lengthy, the visual cortex’s function may possibly degrade.
We know that the visual cortex, in the brain’s occipital lobe, can start to respond to non-visual alerts if it is deprived of visual input. In blind persons, for occasion, the occipital lobe strongly responds to contact. This rewiring or repurposing of less than-utilized brain locations is a type of neuroplasticity.
Neuroplasticity is normally thought of a very good factor. But Eagleman and Vaughn position out that for the visual method, neuroplasticity could essentially pose a risk, due to the fact eyesight – not like our other senses – isn’t really lively all the time.
If we are in a dark place, or it really is evening, we get very little or no visual input. So – in principle – our visual cortex would be susceptible to ‘takeover’ by other senses, each and every single evening. Dreams, on this check out, are our brain’s way of defending the integrity of our visual method by maintaining it lively.
As I explained, I like the ingenuity of this principle, but I don’t truly invest in it. We know that desires are affiliated with stimulation of the occipital cortex throughout a snooze phase called REM snooze. So it really is real that desires promote the visual method. But I’m not convinced that this is the primary intent of desires.
For one particular factor, Eagleman and Vaughn’s principle only tends to make sense if neuroplastic repurposing of the cortex takes place very quickly. For the visual cortex to will need defending, dangerous neuroplasticity would will need to occur in the space of a number of hours. The authors do go over proof that rapid neuroplasticity can occur, but they don’t exhibit any proof that these rapid improvements are solid sufficient to be dangerous.
In reality, Eagleman and Vaughn don’t truly go over any immediate proof for the desires-as-protection.
They exhibit a correlation involving quantity of REM snooze and the speed of enhancement among the primate species. Primates whose infants discover to wander a lot quicker and attain maturity a lot quicker, have a tendency to have much less REM. (People, the slowest maturing primates, have the most REM.)
Primate enhancement and REM snooze, from Eagleman and Vaughn (2020)
The concept is that a lot quicker enhancement suggests slower neuroplasticity, and slower neuroplasticity suggests much less will need to safeguard the visual cortex from encroachment. This is very a lot circumstantial. The authors do cite some other indirect proof, but admit that: “The present hypothesis could be analyzed a lot more thoroughly with immediate measures of cortical plasticity.”
I feel this hypothesis could be analyzed fairly conveniently. You would get a team of human volunteers and give them an fMRI scan, at baseline, to establish the extent of their visual cortex and how visually selective it is (i.e. how properly it responds only to visual input, not contact or other senses.)
Then, for 24 hours, half of the volunteers would put on a blindfold to make visual deprivation. 50 % would have REM snooze disrupted that evening (selective REM disruption is doable). At the 24 hour position, they get a second fMRI scan.
Eagleman and Vaughn’s principle would forecast that the eyesight-deprived persons would have much less visually selective visual cortex, and, crucially, that REM disruption would greatly enhance this outcome. The authors suggest a related experiment.