Riley S. Faelan@screwlisp Some such critical periods are known to exist for human language acquisition. The brain's idea of phonetics, in particular, seems to necessarily be constructed relatively early on, and after that, one's somewhat stuck with the phoneomes they learnt early. (This is one of the major factors behing foreign accents.) On a more vague note, humans who don't acquire their first language during a specific critical window (which, luckily, is several years long) will be deprived of a substantial part of their ability to learn any languages later in life. It appears that crucial parts of their brain are just irreversibly pruned away. 'Perfect pitch' is a classic example of a skill that can be acquired through training in childhood, but generally not after the window is missed. There's suggestions that it's related to language acquisition, but we don't quite know for sure yet.
OTOH, there's a very curious class of medicines, histone deacetylase inhibitors, that, somehow — the deep mechanism is poorly understood —, appear to be able to re-open some (but evidently not all) of the critical learning windows in adult humans. The intriguing part is, these have nothing (directly) to do with neurotransmission, like many learning-related medicines do; instead, they affect gene expression regulation. From experiments, they seem to be able to temporarily increse neuroplasticity, allowing some patterns of early brain construction to be repeated. Their primary use is in epilepsy treatment and seizure prevention, and we don't even really know whether that use nd the neuroplasticity modulation are closely related effects or just happen to be triggered by a same class of medicines through a coincidence.
A lot of modern medicines are developed with some advance idea as to how they might be useful, and so, with new medicines, we often have some basic idea as to how they will be working even before the first molecule becomes ready for testing. With the most famous HDAC inhibitors, salts of valproic acid, this his not the case. The molecule was synthesised really early on, back when coal tar was the bleeding edge of medicine research, even earlier than Aspirin(r), but for many decades, it was only believed to be useful as a handy organic solvent for other medicines, not as a medicine in its own right. Even now, we know the basic idea of what it does, and we can measure the effects of its doings, but we don't understand how the two things are connected. It's not like Aspirin(r) at all — another medicine that was first synthesised, then discovered to be useful, and gradually, over time, scientists figured out most of the weird things that it actually does.. For further complication, because valproates mess with gene expression, and are relatively simple molecules capable of passing placenta, they're incompatible with pregnancy. (But it's likely that non-placenta-crossing HDAC inhibitors can be synthesised.)
But, de-digressing, what these medicines do does not have a direct parallel in ANNs, because it deals with a regulatory mechanism that ANNs just don't model. If we understood how these regulatory mechanisms work in biological brains, we might be able to build similar regulatory mechanisms for ANNs, and likely allow ANNs to learn relatively similarly to how mammals learn. Which may or may not be the same way how birds learn. HDAC inhibitors seem to work in a substantially similar way in mice than in humans, but while they improve learning in birds, they have effects on birds' brains that do not appear to have clear counterparts on mammal brains, and we don't yet know why that is, or even very deeply how this is. Even more bizarrrely, HDAC inhibitor overdose can kill, and how it does that that does not make much sense yet, either. Peculiarily, naloxone,which is primarily used to block opioid receptors and thus can reverse acute opioid poisoning, appears to also alleviate sodium valprote overdose's effects, but valproic acid is chemically nothing like opioids, and is not known to bind to opioid receptors, so #MoreStudyIsNeeded on how this actually works.
It might entirely be that the relation beween histone acetylation and neuroplasticity is just coincidental; something on the order of 'histones control the building and pruning of synapses; keeping them acetylated increases the learning reward, and thus promotes learning; if neurons get too much rewards, they start foaming at the mouth and secreting endorphines' We really don't yet know. But understanding whatever it is that histones do to a developing brain is likely useful for understanding how an ANN of useful complex structure could be built out of simple-ish ruls.
On the other hand, if we just threw enough neurons at an ANN, it might be able to do similar things — it'd just be a couple of orders of magnitude more expensive to build and run. There's some suggestions as to this possibility, but we really don't yet know.
Interpolating backwards, the jumping spiders' brain architecture might, likewise, be substantially be DNA-determined. They have histones (the generic idea of histones in cell nuclei is fairly fundamental to Terran life, actually — but there's bacteria who get by without). But there's suggestions that the relationship between their histoines and their brains might be substantially different than in mammals or birds, nd if we figured whether that is, indeed, the case, and if so, why it is the case, we'd have another important clue about structuring brains.