How does Sodium Valproate cause neural plasticity
As far as I can see this paper is being a little misleading, by saying "VPA mimics Nogo-66 receptor deletion".

The action of VPA doesn't seem to be related to this receptor.

It seems that blocking this receptor and applying VPA both increase plasticity, but it is like taking a car or taking a train -- entirely different modes of transport that achieve the same effect.

VPA seems to facilitate LTP through increased availability of relevant proteins.

That is unconnected with growing new neural structure.

The principal problem with growing new structure is, as hinted at the end of the question, that the adolescent/adult brain secretes a chemical that gets picked up by Nogo 66 receptor, which signals to collapse the axon growth cone.

It's why adult humans can't recover from spinal injuries. The axons won't reconnect.

It so happens that a small molecule Nogo Antagonist has recently been developed by Professor Strittmatter.  He was kind to reply to my query, and I learned that this molecule is currently in the early stages of FDA approval. It's a very exciting discovery!

I would caution anyone against taking VPA -- I have been encountering chest pains since experimenting with it (even though I dropped the experiment after a week due to pain). It looks as though this pain is inflammation of the stomach lining and a common reaction to VPA (VPA is an acid!).

If someone is determined to take VPA, they should at least investigate taking it together with Omeprazole, which discourages the stomach from producing excess acid.

I am disappointed that I now need to take omeprazole quazi-regularly, it appears that my brief VPA experiment has caused some long-term upset in my chemical balance.

Also of note is that (again discovered by Strittmatter) Ibuprofen has been found to also interrupt the signalling pathway that leads to axon growth collapse. But it requires a high dosage, and ibuprofen also causes a similar imbalance.