Andrii
821 posts












A critical period is the early window before age ~5-8 when your brain learns very fast, then plasticity “shuts” when the window closes. It turns out it doesn’t shut because it wears out - the brain actually burns energy to hold plasticity shut - AND neural networks no one designed to have this property actually grow the same critical period on their own, which means the phenomenon might be a computational law. This is another post on my growing obsession with convergence of topics in AI and biology, specifically developmental neuro. The cleanest version of the experiment is to take a normal deep neural net, blur its training images for a little while early on, then un-blur them and let it train on perfect data forever. It never fully recovers from that early blur. The analogous early developmental condition is amblyopia - yes, the same lazy eye damage that some experiments actually induced in kittens (sad, very very sad). It also occurs in kids whose cataracts aren’t caught in time. The network has a sensitive window and no knowledge that the window is sensitive. If you had flipped the images instead of blurring them, there’d be no lasting harm at all. Only the deficits that corrupt low level statistics leave a scar later on. Why? The network front-loads all its commitment. Early in training, the weights grab information fast, then the grabbing collapses, and once it collapses, the network can’t redistribute what it already learned. Locking in early is the price of a clean, stable representation. You spend your adaptability to get there. In human brains, it gets weirder. A human critical period doesn’t close from weight decay. Instead a neural brake actually gets installed in the brain and actively held down. A literal mesh - the perineuronal net - crystallizes around your inhibitory neurons and freezes the wiring in place. If you dissolve that mesh with an enzyme (chondroitinase ABC, specifically), or dose the whole system with Fluoxetine AKA Prozac, you get a plastic brain again. Yes, this also works with psychedelics when it comes to social learning. Ketamine, psilocybin, MDMA, LSD, and ibogaine all reopen social critical period learning levels, which stay open roughly as long as the trip lasts. The closed state is maintained but not permanent. The suspicious part with regard to reopening critical period levels of plasticity is that none of the methods share a mechanism. LSD works through the serotonin receptor; ketamine and ibogaine don't; chondroitinase is just a pair of molecular scissors. What they all converge on is remodeling that same extracellular mesh. Imagine a little man in your head with his foot on the pedal the entire span of your adult life. That’s kinda what’s happening. The Critical Period (and its implications) seems to be a law of information theory. To build something stable, you must pay the price of stopping changing. Then, you keep paying that price to stay that way. This might just be the cost of learning. Moral of the story, if you wanna rewire your brain faster, maybe ask your doctor about prozac lmao. It’s only been studied in the rat visual cortex though, and it only applies if you actually do the work - it’s not just gonna magically change you, and plasticity locks again as soon as you stop taking it. (NOT ADVICE).















