I have read that nicotine promotes neuroplasticity.
Can anyone explain how this works? Also I have heard that there are two variants, and one of them is better to use than the other.
Could anyone explain this?
pi
PS I have been looking through http://www.ncbi.nlm....cles/PMC3387538 which may contain the answer to this enquiry, only I don't understand enough of the technical language to figure it out. Can anyone help?
Lynx1 protein directly binds to nAChRs (Nicotinic acetylcholine receptors) [...] to reduce their sensitivity to ACh (acetylcholine).
Ergo nAChRs of lynx1-knockout mice should retain high sensitivity to ACh, and this increased signalling extends the plasticity window.
Dramatically, lynx1 knockout mice spontaneously recovered visual acuity to normal levels simply by reopening the closed eye [...]. Given the cholinergic basis of this plasticity, we further attempted to induce recovery even in adult wild-type mice by enhancing endogenous ACh signaling. Injection of an acetylcholinesterase inhibitor, physostigmine, during the period of eye re-opening similarly restored vision to wild-type mice initially rendered amblyopic.
Slightly off topic, but this is saying that AChEi restores plasticity.
We did not observe structural changes at the level of perineuronal nets or myelination in lynx1 knockout mice
ok, lynx1-knockout seems to be a separate plasticity mechanism.
But now I am stuck...