I am exploring the various 'brakes' that shut down the critical period of neuroplasticity.
http://www.ncbi.nlm....les/PMC3822369/ "Regulating Critical Period Plasticity: Insight from the Visual System to Fear Circuitry for Therapeutic Interventions" says:
Recent studies using rodent visual cortex have identified multiple structural and functional molecular “brakes” that actively limit plasticity and close the critical period in the adult brain (8, 21). Structural brakes include PNNs (22), myelin-related inhibitory signaling mediated by Nogo receptor (23), and paired immunoglobulin-like receptor B expression (PirB) (24). Functional brakes, such as the nicotinic receptor binding protein Lynx1 act upon excitatory-inhibitory balance within local circuits (25). Importantly, lifting these brakes can induce critical period plasticity in adulthood…
following that underlined link takes us to http://www.ncbi.nlm....cles/PMC3387538 " Lynx1, a cholinergic brake limits plasticity in adult visual cortex"
which states:
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.
So AChEi restore plasticity.
But which ones? Obviously the one that experiment is unsuitable as it requires invasive administration.
I'm aware that Huperzine A is one candidate. But is it the best candidate? Do there exist prescription medications that may be more suitable?
pi